Energy metabolism and thyroid function -
While some research has found that water may increase the amount of energy you burn at rest by as much as 30 percent, another study found no connection between water and energy burned.
However, your body needs enough water to work well, and that means getting about 2. See your doctor before starting any supplements.
There are no dietary supplements that can treat hypothyroidism in place of thyroid hormone, McAninch says. And some supplements, such as those that contain iodine, can worsen hypothyroidism. Get enough shut-eye. Not getting enough sleep can lower your metabolic rate, according to the Sleep Foundation , which recommends that most adults get about seven to nine hours of sleep a night.
Making these changes in your life can help you manage hypothyroidism and overcome the effects of slow metabolism that accompany it. Everyday Health follows strict sourcing guidelines to ensure the accuracy of its content, outlined in our editorial policy.
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Brett, MD. If you imagine that your metabolism is a revving engine, thyroid hormone would be the gas. A slower metabolism can make weight loss difficult, but it causes other symptoms too, such as fatigue and weakness. Try these tips: Take thyroid hormone. Editorial Sources and Fact-Checking. Resources Can You Boost Your Metabolism?
June 22, Cleveland Clinic. April 19, The Truth About Metabolism. Harvard Health Publishing. May 30, Boschmann M et al. Water-Induced Thermogenesis.
Twenty-four hours after a habituation trial, during which the rats were allowed to explore an empty container, the animals were placed in the same area with two identical objects set at an equal distance for 3 min. After 1 h, the rats were placed in the same container in the presence of the familiar object and a novel object similar in size and height but different in shape and appearance.
The time spent by every animal exploring each object was measured. All biochemical experiments were carried out under exactly the same conditions for every sample, regardless of the type of animal treatment.
The rats were sacrificed under non-stressful conditions between a. and a. The plasma concentrations of TSH Demeditec, Kiel, Germany , free T3 and free T4 both: DiaMetra, Perugia, Spello, Italy were assayed using ELISA according to the instructions provided by the manufacturer.
The T3 level in the frontal cortex and hippocampus was measured using the ELISA assay described above. Biochemical analyses of plasma glucose and lipid profiles were performed on a Mindray BS Chemistry Analyzer Mindray, Shenzhen, Guangdong, China.
Conversion into cDNA was performed by a High-Capacity cDNA Reverse Transcription Kit Thermo Fisher Scientific, Waltham, MA, United States using a T Thermal Cycler Bio-Rad, Hercules, CA, United States. Quantitative real-time PCR was performed using TaqMan probes and primers for the thra , thrb , rxra , rxrb , dio2 , dio3 , and thrsp genes Thermo Fisher Scientific, Waltham, MA, United States and the FastStart Universal Probe Master Rox kit Roche, Basel, Switzerland using the CFX96 Real-Time System Bio-Rad, Hercules, CA, United States.
The following thermal cycling conditions were used: 2 min at 50°C, 10 min at 95°C, followed by 40 cycles of 95°C for 15 s and 60°C for 1 min. The C t values for each sample were measured in the exponential phase of the PCR, and the ΔΔ C t method was used for data analysis.
hprt1 Thermo Fisher Scientific, Waltham, MA, United States was used as the reference gene. To measure the activities and amounts of selected mitochondrial enzymes, mitochondria-enriched membrane fractions were isolated from the frontal cortex and hippocampus by using the procedure described by Wernicke et al.
After the supernatants were collected, the remaining pellet was rinsed twice with homogenization buffer and centrifuged at 1, × g for 4 min at 4°C to increase mitochondrial yield. SDS-PAGE was performed under a constant voltage of V.
Proteins were transferred to PVDF membranes at a constant current of mAmp for 2 h in CAPS buffer. Some membranes were cut to allow simultaneous incubation with different antibodies. The next day, after rinsing 3 × 10 min with PBS with 0.
Chemiluminescence was visualized with a luminescence image analyzer Fujifilm LAS System and quantified using Fujifilm Multi Gauge software Fujifilm, Tokyo, Japan. For some blots, antibody stripping was performed by incubation in mL of Tris—HCl pH 6.
Then, the membranes were washed 3 × 10 min in TBST, blocked, and reprobed with an antibody against β-actin 1: 15,; Sigma-Aldrich, Saint Louis, MO, United States diluted using a SignalBoost Enhancer Kit as an internal loading control Merck, Darmstadt, Germany.
The intensity of each target protein band was divided by the intensity of the internal loading control β-actin for that sample to adjust the target protein signals with respect to small, unavoidable variations in sample loading.
The ratio of the intensity of the target protein band to that of β-actin was used to compare target protein abundance in different samples. The level of lactate in the samples was measured with a colorimetric assay kit BioVision, Milpitas, CA, United States. The mitochondria-enriched membrane fraction and cytosolic fraction were transferred to a well plate and mixed with the reaction mix.
A fluorimetric assay kit BioVision, Milpitas, CA, United States was used to measure the concentration of pyruvate in the cytosolic fraction isolated from the frontal cortex and hippocampus.
The concentrations of pyruvate dehydrogenase, PDK2, and PDK4 in the mitochondria-enriched fractions of the frontal cortex and hippocampus were determined using an ELISA method PDH: EIAab Science Co.
Samples and standards were dispensed in precoated well ELISA plates and incubated. Mitochondrial respiration was measured at 37°C by high-resolution respirometry with an Oxygraph-2k Oroboros Instruments, Innsbruck, Austria as described Pesta and Gnaiger, ; Sebastian et al.
Frontal cortices and hippocampi isolated from rats were homogenized in ice-cold homogenization buffer [0. Tissue homogenates were centrifuged at 1, rpm for 10 min at 4°C. After the supernatant SN1 was collected, the remaining pellet was resuspended in 4 volumes of homogenization buffer and centrifuged under the same conditions to maximize mitochondrial yield.
The obtained supernatant SN2 was then mixed with SN1, and the supernatant mixture was centrifuged at 9, × g for 15 min. After gentle resuspension of the pellet containing the mitochondria, the protein concentration was measured using the BCA method Smith et al.
Three hundred micrograms of isolated mitochondria suspended in 2 mL of MiR05 respiration buffer 0. All respiration measurements were made with the following protocol: glutamate 10 mM and malate 2 mM without ADP [L: LEAK CI ]; respiration assessed by the addition of 2.
Then, the uncoupling control was measured by the titration of the protonophore carbonylcyanide trifluoromethoxy -phenylhydrazone FCCP FCCP-uncoupled state, max ETS Pesta and Gnaiger, ; Sebastian et al.
Finally, rotenone 1 μM, E: ETS CII state and antimycin A 2. The inhibition of respiration in uncoupled mitochondria allows for the evaluation of oxygen flux due to oxidative side reactions residual oxygen consumption, ROX.
The protein concentration in tissue homogenates was measured with the bicinchoninic acid method Smith et al. Statistical evaluations were performed using the Statistica The ANOVA results are reported as an F -statistic and its associated degrees of freedom.
All graphs were prepared using GraphPad Prism 8. Weight gain was significantly lower in the WKY rats than in the Wistar rats, and PTU significantly reduced this parameter in both strains Figure 1A. Figure 1.
The effects of strain and PTU treatment on weight gain A , immobility B , and swimming times C measured in the forced swim test and on the preference index measured in the novel object recognition test D.
The results are expressed as the mean ± SEM. the WKY group. The duration of immobility and the climbing time in the forced swim test was measured for 5 min on the second day of the test. The administration of PTU had no effect on immobility or climbing time in either strain.
Short-term memory was investigated with a new object recognition test and is presented as the preference index Figure 1D. Plasma TSH levels did not differ significantly between the tested strains, although an upward trend was observed in the WKY rats.
Figure 2. The effects of strain and PTU treatment on fT3 A , fT4 B , TSH C , and corticosterone D levels measured in the plasma and T3 E,F levels measured in the frontal cortex and hippocampus. the WKY group; Λ vs. the Wistar PTU group. Moreover, post hoc analysis indicated that the T3 level in the frontal cortex of the WKY rats was lower than that of the Wistar rats.
PTU increased the level of HDL in the WKY rats compared with those of the other groups Figure 3B. Figure 3. The effects of strain and PTU treatment on the total cholesterol A , HDL B , LDL C , and triglyceride D levels measured in the plasma.
The expression of this receptor was significantly lower in the WKY rats both with and without PTU administration than in the Wistar rats Figure 4A. There were no differences in TRβ1 or RXRα expression in this brain structure regardless of strain or PTU administration Figures 4C,E.
Figure 4. The effects of strain and PTU treatment on the gene expression of the thyroid receptors TRα thra A,B and TRβ thrb C,D and the retinoid receptors RXRα rxra E,F , and RXRβ rxrb G,H in the frontal cortex and hippocampus. The results are expressed as the average fold change ± SEM. The expression of DIO2, the enzyme that converts T4 to active T3, was significantly lower in the WKY rats than in the Wistar control rats, whereas in animals receiving PTU, there was no difference in the expression of DIO2 between the rat strains tested Figure 5A.
Figure 5. The effects of strain and PTU treatment on the gene expression of deiodinase 2 dio2 , A,B deiodinase 3 dio3 C,D , and thyroid hormone responsive protein thrsp E,F in the frontal cortex and hippocampus.
Figure 6. The effects of strain and PTU treatment on the pyruvate level in cytosolic fraction A,B and lactate level in cytosolic and mitochondria-enriched fraction C,D in the frontal cortex and hippocampus. There was no difference in the level of lactate in the cytosol in either the frontal cortex or hippocampus of the WKY and Wistar rats.
The lactate concentration in the mitochondrial fraction of the frontal cortex did not differ between the tested rat strains and was not changed in the animals that received PTU.
Figure 7. The effects of strain and PTU treatment on the pyruvate dehydrogenase level A,B and aconitase activity C,D in the mitochondria-enriched fraction of the frontal cortex and hippocampus. There were no differences in aconitase activity between the WKY and Wistar rats in either the frontal cortex or the hippocampus.
In the Wistar rats, PTU administration significantly diminished the level of PDK2 compared with those in the control Wistar animals and in the WKY rats treated with PTU Figures 8A,B. Figure 8. The effects of strain and PTU treatment on PDK2 and PDK4 in the mitochondria-enriched fraction of the frontal cortex A,C and B,D hippocampus.
There were no changes in the protein levels of respiratory chain complexes in the hippocampus Figure 9B.
Figure 9. The effects of strain and PTU treatment on the expression of oxidative phosphorylation complexes I—V in the mitochondria-enriched fraction of the frontal cortex A and hippocampus B. Representative immunoblots of proteins studied and β-actin in the frontal cortex A and hippocampus B.
The bands from the left: Wistar, WKY, Wistar PTU, WKY PTU. High-resolution respirometry HRR was used to measure mitochondrial respiration in both selected brain structures. In the hippocampus, there were no differences in these two respiratory states among the groups Figures 11A,B.
Figure The results are expressed as the average fold change ± SEM A—D or as the mean ± SEM. No significant changes in ETS coupling efficiency were observed in the frontal cortex Figure 10E. There were no changes in the level of mitofusin 2 between the WKY and Wistar rats in either the frontal cortex or the hippocampus.
PTU also had no effect on the expression of this protein. In the hippocampus, the level of UCP4 did not differ among any of the examined groups.
The level of VDAC1 in either brain structure did not differ between the tested rat strains and was not changed in the animals that received PTU. Table 1. The effects of strain and PTU treatment on the level of Mitofusin 2, UCP4, VDAC1, and HK1 in the mitochondria-enriched fraction of frontal cortex and hippocampus.
In addition, the decreased metabolism in the frontal cortex in depression may result from decreases in the levels of T3 and TRα1 and in the expression of DIO2, an enzyme that catalyzes the conversion of T4 to the active T3 hormone.
As in previous studies, in the forced swim test, we observed a longer duration of immobility and a shorter climbing time in the WKY rats than in the control Wistar animals Aleksandrova et al.
Additionally, in agreement with previous data, the WKY rats showed short-term memory impairment and reduced weight gain. The administration of PTU had no effect on immobility or climbing time but attenuated the memory impairment of the WKY rats and intensified the decrease in weight gain.
It is difficult to explain that in contrast to our predictions, the administration of PTU did not lead to prolonged immobility time in the Porsolt test in either the Wistar or WKY rats.
Although behavioral tests, including the Porsolt test, have been widely used to screen potential antidepressant drug effects, whether they can assess depression in rodents remains a matter of debate Yu et al. It is still unknown which of the numerous changes observed in the human brain or in animal models of depression e.
It is also unresolved why in many animal models of depression based on stress procedures, not all animals develop depression-like behavioral changes despite the use of identical stressors, whereas the biochemical changes are most often similar Kolasa et al.
Since depression is a highly heterogeneous disorder with diverse pathogenic origins, the lack of changes in depression-like behavior does not exclude the participation of other factors, including hypothyroidism, that do not affect the time of immobility but affect other processes e.
For thyroid hormones, data on their effects on depression-like and anxiety-like behaviors are very ambiguous because both hypothyroidism and hyperthyroidism can induce such behaviors. Additionally, concerning hypothyroidism, some studies found an increase in depression-like behavior in rats, but others found decreased depression-like behavior Yu et al.
Furthermore, hypothyroidism in humans does not necessarily lead to depression but increases the risk of this disease, and the administration of a high dose of T4 to patients with drug-resistant depression produces a therapeutic effect, probably by normalizing any significant changes that have occurred in depression.
We also verified the hypothyroidism model by determining the plasma lipid levels. Total cholesterol and low-density lipoprotein cholesterol were significantly increased under hypothyroidism conditions in both rat strains; however, high-density lipoprotein cholesterol was elevated only in the WKY rats.
In agreement with previous data, the lowered thyroid hormone levels in rats of both strains decreased triglyceride levels in the blood, which contrasts with the effect observed in humans Popović et al.
The results obtained in the current research confirmed and extended the data showing the presence of hypothalamic—pituitary—thyroid HPT axis disturbance in WKY rats and indicated the possible causes of the weaker action of these hormones in the brain compared to their action in peripheral tissue.
In the blood, both TSH and fT3 levels tended to be higher in the WKY rats than in control animals, and although these changes did not reach statistical significance, they suggested a weakening of the inhibitory effect of T3 on TSH secretion i. As in the current research, Redei et al.
In a previous study, the level of total T3 was measured, whereas we studied the free fraction of this hormone, which not only confirmed previous data but also excluded the effects of potential differences in thyroid hormone-binding protein levels on the active fraction of this hormone in the WKY and Wistar rats.
The total T4 hormone levels were slightly but not significantly lower in WKY rats than in Wistar rats in the Redei study Redei et al. The fact that thyroid hormone levels in the blood do not correlate with their concentrations in the brain is known, and it follows that the T3 content in the brain depends not only on its synthesis in the thyroid gland but also, to a large extent, on the expression of transporters and deiodinase enzymes in particular brain structures.
Since the expression of DIO2 in the frontal cortex was lower in the WKY rats than in the Wistar rats, this could be one of the reasons for the lower T3 concentration we observed in the frontal cortex of the WKY rats. However, it should be noted that many factors affect the levels of thyroid hormones and deiodinases in the brain, and additionally, the roles of iodothyronine derivatives other than T3 and T4 are poorly known Pinna et al.
The predominant mechanism for the biological action of TH involves the regulation of gene transcription through nuclear TH receptors. The effects of TH depend mainly on the expression of specific isoforms of TH receptors and their dimerization with RXR.
The decreased expression of the TRα1 isoform in the frontal cortex of the WKY rats suggested weaker TH activity in this brain structure because this receptor isoform is widely distributed and is the predominant TH receptor in the adult brain.
TRα1 presumably mediates most of the effects of TH, and some studies show that mutation of this receptor increases depressive and anxiety behaviors, evokes memory impairment, and reduces glucose utilization in the brain Cheng, ; Vallortigara et al.
Moreover, in a chronic mild stress model of depression, a decrease in TRα1 mRNA expression in the brain and its reversal by imipramine suggest that this receptor may play a role in stress-induced depressive behavior and in antidepressant action Stein et al. In contrast to the frontal cortex of the WKY rats, in which changes in the levels of DIO2 and TRα1 receptor suggest that a decrease in thyroid hormone action, in the hippocampus, the severe reduction in the expression of DIO3, the T3- and T4-metabolizing enzyme, and the increase in the expression of TRβ1 and RXRα indicate the enhancement of thyroid hormone function.
However, the comparison of selected metabolic markers in these brain structures in the WKY and Wistar rats indicated that a decrease in metabolism occurred not only in the frontal cortex but also in the hippocampus. A decrease in glycolysis was evidenced by the finding that the level of pyruvate, the end product of glycolysis, was lower in both brain structures studied in the WKY rats than in the Wistar rats; additionally, the level of pyruvate was lower in both strains with hypothyroidism than in the strains under control conditions.
In the frontal cortex in the hypothyroidism models but not in the depression model, reduced levels of pyruvate may be caused by the increased conversion of pyruvate to lactate.
However, in the WKY rats receiving PTU, a simultaneous decrease in pyruvate dehydrogenase levels and pyruvate levels suggested the weakening of the Krebs cycle by limiting both its substrate and the enzyme linking glycolysis with the Krebs cycle.
Moreover, in addition to a reduction in pyruvate dehydrogenase levels, a decrease in pyruvate dehydrogenase kinase 4, the enzyme that inhibits pyruvate dehydrogenase, was observed only in the model of depression with hypothyroidism.
These changes indicate that lower levels of pyruvate dehydrogenase in the frontal cortex can be partially compensated by an increase in its activity. In contrast to the cortex, in the hippocampus, there was no decrease in the level of pyruvate dehydrogenase; however, the increased PDK4 level suggested that the activity of this enzyme could have been decreased.
In the hippocampus, the decreased pyruvate levels were accompanied by reduced lactate concentrations in the mitochondrial fractions of all treated animal groups compared to that of the control Wistar rats; moreover, in the model of depression with hypothyroidism, lactate concentrations in the hippocampus were also reduced in the cytosolic fraction, which was even more clear than in the case of the frontal cortex, indicating a decrease in glycolysis efficiency.
Furthermore, a significant decrease in the level of lactate, which can act as a gliotransmitter in addition to being an energy substrate mainly for neurons, may lead to a reduction in norepinephrine release and disturbances in long-term memory Suzuki et al.
Some existing data indicate that hypothyroidism induces the detachment of hexokinase 1 HK1 from the outer mitochondrial membrane by lowering the expression of voltage-dependent anion channel 1 VDAC1 , and this action may be an important cause of the disrupted coordination between glycolysis and oxidative phosphorylation Regenold et al.
In our study, the levels of VDAC1 in the mitochondrial fraction in both brain structures examined did not change, and the HK1 concentration did not decrease or even increased in the hippocampus of the WKY rats treated with PTU; therefore, we excluded the participation of this mechanism in the models we examined.
In the frontal cortex, the decreased expression of complex II and complex V in rats with hypothyroidism suggested that in this brain structure, not only glycolysis but also oxidative phosphorylation could be reduced. However, since no differences in the expression of these enzymes were observed between the rat strains, only slight downward trends in these levels were observed in the WKY rats, and because PTU decreased the levels of these enzymes in the WKY and Wistar rats to a similar extent, the changes in complexes II and V may be associated with hypothyroidism but not with differences between the tested rat strains.
Additionally, functional assays of mitochondrial respiration showed the impact of PTU, but not of strain, on the leak and OXPHOS states. The intensification of the leak state in animals with hypothyroidism could indicate the uncoupling of oxidative phosphorylation from ATP synthesis in these animals.
In the leak state, when ATP synthase is not active, oxygen consumption is mainly used to compensate for proton leakage. Thus, the increase in oxygen consumption in the leak state in animals receiving PTU suggested that in the rats with hypothyroidism, the inner mitochondrial membrane was more permeable to protons, and consequently, oxidative phosphorylation may have become uncoupled from ATP synthesis.
This change is difficult to explain because T3 is known to activate thermogenesis by uncoupling electron transport from ATP synthesis in brown adipose tissue BAT mitochondria, whereas the level of this hormone in the frontal cortex in rats treated with PTU was decreased.
However, the action of thyroid hormones in BAT is relatively well studied, and it is known that T3 increases fatty acid oxidation and mitochondrial respiration and also affects the processes of mitophagy and biogenesis.
However, little is known about the effect of thyroid hormones on mitochondrial function in adult brain cells. Neural tissue shows a very high respiratory activity that may exceed several times those of other metabolically active peripheral tissues, and the action of thyroid hormones on metabolic activity, the process of mitochondrial disintegration fission and mitophagy , and the process of mitochondrial formation biogenesis and fusion in brain cells is poorly studied.
Thus, differences in the action of thyroid hormones on the mitochondrial uncoupling states of the brain and peripheral tissues may result from many factors; for example, thyroid hormone deficiency can cause differences in the expression and function of uncoupling proteins and low contents of antioxidant enzymes in the brain as well as affect the mitochondrial membrane potential of intracellular signaling pathways.
Additionally, we found that the uncoupling of oxidative phosphorylation from ATP synthesis did not result from the overexpression of uncoupling protein 4 UCP4. The main UCP isoforms expressed in the brain are UCP2, UCP4, and UCP5, and it has been found that overexpression of UCP4 and UCP5, but not UCP2, reduces mitochondrial membrane potential, decreases ATP production and reduces the release of H 2 O 2 by astrocytes Lambert et al.
Moreover, in some cellular models, UCP4 has been shown to increase mitochondrial complex II activity and glucose uptake and shift ATP production from mitochondrial respiration to glycolysis Ramsden et al.
The reduction in UCP4 expression in the frontal cortex in the model of the co-occurrence of hypothyroidism and depression seems to be an adaptive mechanism caused by the weakening of oxidative phosphorylation in this brain structure.
The adverse effects of decreased thyroid hormone levels on mitochondrial respiration were also evidenced by reductions in the ETS CII state in the frontal cortex and hippocampus.
Moreover, PTU decreased the ETS coupling efficiency and OXPHOS coupling efficiency. Since a significant decrease in these parameters after PTU treatment was observed only in the WKY rats, it seems that although decreased coupling efficiency is mainly an effect of hypothyroidism, in the presence of hypothyroidism and depression, this decrease was more pronounced.
Summarizing the metabolic effects in the brain caused by the decreased synthesis of thyroid hormones, it seems that, similar to peripheral tissues, oxidative phosphorylation is reduced, since we observed decreased expression of complex II and V in the frontal cortex and decreased ETS CII capacity in both brain structures examined.
Regarding the earlier stages of metabolism, the process of glycolysis was also decreased in both brain structures, but the Krebs cycle was only reduced in the frontal cortex, while in the hippocampus, it was intensified.
This suggests that in the hippocampus, in contrast to the frontal cortex but similar to the case of changes in the expression of T3 receptors, metabolic compensatory mechanisms were also activated.
It is known that the proper function of mitochondria depends on maintaining a balance between fusion and fission. In the case of mitochondrial dysfunction, the intensification of fusion increases the production of ATP and is considered a neuroprotective mechanism Martorell-Riera et al.
We did not observe changes in the expression of mitofusin 2 in any of the animal groups studied, which suggests that there are no changes in the mitochondrial fusion process in the model of depression applied in this study or in animals with hypothyroidism. An interesting result of the current research was that the gene encoding thyroid hormone-responsive protein THRSP was more highly expressed in the hippocampus of the WKY rats than in the hippocampus of the Wistar rats.
THRSP is one of the few genes in the adult brain that are sensitive to thyroid hormones, and its activation by thyroid hormones is considered to cause the cytotoxic effect of thyroid hormones observed in primary neuronal cell cultures Haas et al.
However, most studies indicate that thyroid hormones have a neuroprotective effect and suggest that the hippocampus is especially sensitive to their action.
For example, hypothyroidism is associated with decreases in the number of neurons in CA1, CA3, and the dentate gyrus; in the volume of the granular cell layer; in hippocampus-dependent cognitive function; in cholinergic system activity; and in adult hippocampal neurogenesis Madeira et al.
Thus, increased THRSP expression in the hippocampus of WKY rats could be connected with the disturbances in synaptic plasticity demonstrated in this rat strain Aleksandrova et al.
Animals with increased THRSP concentrations in the striatum exhibited inattention behavior, but the function of this protein in the hippocampus has not yet been studied Custodio et al.
However, it should be taken into account that both impaired synaptic plasticity, which is considered crucial in the pathogenesis of depression, and hypothyroidism-induced disturbances in mitochondrial function can be caused by many factors, e.
HFD consumption is known to cause systemic and central inflammation, mitochondrial dysfunction, and excessive ROS production, which can lead to disturbances in synaptic plasticity and consequently increase the risk of developing mental and neurodegenerative disease Crispino et al.
Our study has some limitations. The first limitation is that only two behavioral tests were performed: the forced swim test and the novel object recognition test.
Perhaps for this reason, we did not find an impact of PTU on depression-like behavior or on recognition memory in the WKY rats.
However, greater numbers of behavioral tests, especially the sucrose preference test, increase the probability of the tests affecting metabolic markers in the brain, which were the main parameters measured in this research.
Additionally, the substantial decrease in weight gain in the WKY rats and in both strains after PTU administration can be interpreted as a symptom of depression; however, its impact on the behavioral tests and the metabolic parameters cannot be excluded.
Another significant limitation of the current research is the use of only male rats, which did not allow us to determine the sex-related differences in the parameters tested.
Finally, the physiological importance of the reduced level of the gliotransmitter lactate and the increased expression of cytotoxic THRSP in the hippocampus in the model of depression used in this study should be determined in further studies.
In summary, the obtained results suggested that in both the depression and hypothyroidism models, a reduction in glycolysis and in the connection between glycolysis and the Krebs cycle occurred, while the weakening of oxidative phosphorylation was mainly due to a lower level of thyroid hormones.
However, the co-occurrence of hypothyroidism and depression led to changes in the presence or abundance of some metabolic markers, such as decreased pyruvate dehydrogenase levels in the frontal cortex, decreased lactate levels in the cytosolic fraction of the hippocampus, increased PDK4 expression in the hippocampus, and decreased ETS and OXPHOS coupling efficiency.
We have also found that the changes observed in the studied models depend on which brain structure is evaluated. Alterations in markers that determine the effect of thyroid hormones in the frontal cortex clearly indicated that in the studied model of depression, their function could be weakened as shown by the decreases in T3, TRα1, and DIO2 , while in the hippocampus, only a downward trend in the T3 level was observed, while the changes in TRβ1, RXRα, and DIO3 suggested the induction of compensatory mechanisms for enhancing T3 action.
Similarly, in the rats receiving PTU, the expression of T3 receptors was increased in the hippocampus but not in the frontal cortex, probably as a mechanism to compensate for the lower concentration of this hormone.
These changes are consistent with many results indicating that, under the influence of unfavorable factors, protective mechanisms are induced to a greater extent in the hippocampus than in the frontal cortex Kucharczyk et al.
Comparing the metabolic changes, a greater reduction in the glycolysis process was observed in the hippocampus than in the frontal cortex; in contrast, the Krebs cycle was weakened only in the frontal cortex.
Additionally, changes in oxidative phosphorylation were present mainly in the frontal cortex, but these disturbances were related to a deficiency of thyroid hormones rather than depression. Thus, the weakening of the glycolysis process occurred in both brain structures examined, while changes in the later stages of metabolism prevailed in the frontal cortex.
The data supporting the conclusions of this article will be made available by the authors, without undue reservation, to any qualified researcher. Requests to access the datasets should be directed to KG, glombik if-pan.
The animal study was reviewed and approved by Local Ethics Committee in Kraków, Poland permission no. KG and BB: conceptualization, writing—original draft, and writing—review. KG, JD, and BB: formal analysis. KG, JD, and AK: investigation.
KG: methodology and visualization. All authors contributed to the article and approved the submitted version. This research was funded by Grant No.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The manuscript has been edited by the American Journal Experts for proper English language, grammar, punctuation, spelling, and overall style.
Verification code: 0BB-EB7DD0B. Aleksandrova, L. Evaluation of the Wistar-Kyoto rat model of depression and the role of synaptic plasticity in depression and antidepressant response. doi: PubMed Abstract CrossRef Full Text Google Scholar. Alzoubi, K. Levothyroxin restores hypothyroidism-induced impairment of hippocampus-dependent learning and memory: behavioral, electrophysiological, and molecular studies.
Hippocampus 19, 66— Antunes, M. The novel object recognition memory: neurobiology, test procedure, and its modifications. Bauer, M. Levothyroxine effects on depressive symptoms and limbic glucose metabolism in bipolar disorder: a randomized, placebo-controlled positron emission tomography study.
Psychiatry 21, — Regional cerebral glucose metabolism and anxiety symptoms in bipolar depression: effects of levothyroxine. Psychiatry Res.
This reduces the thyroie of tyhroid your Energy metabolism and thyroid function Fat burning exercises and often leads to weight gain. Conversely, when your thyroid is producing too metabbolism hormones hyperthyroidism Energy metabolism and thyroid function, funcction metabolism goes into overdrive, thyeoid more calories funcion normal and likely resulting in weight loss. However, this is a simplistic picture of the various factors that are involved in these processes. Your metabolism involves a series of processes that break down food and convert it into the energy your body needs to run. It also determines how quickly or slowly your body uses calories. Some of how efficiently your metabolism runs is determined by genetics. You burn calories through physical activity and by performing your daily activities.Energy metabolism and thyroid function -
These hormones regulate growth, development, metabolism, and energy production. The intricate connection between thyroid function and energy metabolism is pivotal for maintaining overall physiological balance in the body.
The thyroid gland, located in the neck, plays a central role in regulating metabolism by producing thyroid hormones , primarily thyroxine T4 and triiodothyronine T3. These hormones influence the metabolic rate the speed at which the body converts food into energy and thermogenesis heat generation.
By increasing basal metabolic rate, thyroid hormones modulate the metabolism of fats, carbohydrates, and proteins; influence blood glucose levels; and contribute to maintaining lean body mass.
Thyroid hormones affect nearly every cell in the body, influencing the utilization of nutrients and the production of ATP, the primary energy currency of cells. In a hypothyroid state, the metabolic rate slows down. This can result in the classic symptoms of hypothyroidism, including fatigue, weight gain, sensitivity to cold, muscle weakness, constipation, and hair loss, as the body struggles to convert nutrients into energy efficiently.
The primary cause of hypothyroidism is an autoimmune disorder known as Hashimoto's thyroiditis , where the immune system attacks the thyroid gland.
Other potential causes include iodine deficiency, certain medications , hypothalamic or pituitary disorders, and thyroid radiation treatment. Understanding the root cause is essential for effective management. Traditional treatment for hypothyroidism typically involves hormone replacement therapy with synthetic thyroid hormones, such as levothyroxine.
This medication aims to supplement the deficient thyroid hormones and restore normal bodily functions. Regularly monitoring thyroid hormone levels through blood tests is essential to adjust medication dosage as needed. While thyroid replacement therapy is a crucial aspect of maintaining optimal thyroid balance and preventing unwanted consequences of hypothyroidism, functional medicine approaches may also be considered.
Functional medicine encourages using nutrition, lifestyle modifications, dietary and herbal supplements, and stress management techniques to correct suboptimal nutrient levels, dampen inflammation, and support other body systems influencing thyroid hormone production.
L-carnitine levocarnitine is one form of carnitine, a derivative of amino acids, which are the building blocks of proteins. It plays a vital biological role in facilitating the transport of fatty acids into the mitochondria, where they undergo oxidation to generate energy. Mitochondria are responsible for producing adenosine triphosphate ATP , the energy currency of cells.
L-carnitine is a carrier molecule that transports long-chain fatty acids across the mitochondrial membrane. This process is essential for the beta-oxidation of fatty acids, a metabolic pathway that breaks down fats into acetyl-CoA, a precursor for ATP synthesis.
L-carnitine is a conditionally essential nutrient, meaning that while the body can generally make enough of it to support metabolism, there are certain instances such as during intense physical exertion in which the body will require exogenous sources of carnitine through foods or supplements.
The liver and kidneys create L-carnitine from the amino acids lysine and methionine. The kidneys can store L-carnitine and eliminate the excess through urine. Dietary sources of L-carnitine include red meat, poultry, fish, dairy, avocados, tempeh, seeds, and nuts.
Studies suggest that despite adequate thyroid hormone replacement and normalization of TSH levels, many hypothyroid patients will continue to experience persistent fatigue. In a recent study published in , researchers used fatigue severity scale FSS scores and clinical and biochemical characteristics of 92 patients with primary hypothyroid to evaluate the effects of levothyroxine on hypothyroid-associated fatigue.
Researchers noted a decrease in the frequency of fatigue in participants after six months of levothyroxine therapy compared to before treatment However, these results show that nearly half of the participants were still experiencing fatigue despite adequate thyroid replacement.
Carnitine deficiency in hypothyroid patients may be a causative factor for persistent fatigue. In a study, 60 patients experiencing hypothyroid-related fatigue were given L-carnitine mg twice daily or a placebo for 12 weeks.
After 12 weeks, researchers noted that the experimental group receiving L-carnitine experienced improvements in fatigue. Patients younger than 50 and those who had a history of thyroidectomy experienced the most significant results.
The metabolic effects of inadequate thyroid hormone can, in part, be linked to this high prevalence of muscle complaints. Deficiencies in T4 and T3 impair muscle energy metabolism, leading to selective atrophy of type 2 muscle fibers and slowed muscle contraction.
However, research also indicates a trend for lower muscle carnitine content in hypothyroid patients, with levels improving upon thyroid hormone treatment. L-carnitine is most commonly used at a dose of 2 grams daily.
Doses ranging from grams daily, most often in divided doses, have been used safely for up to one year. The bioavailability of dietary carnitine can vary depending on dietary composition. This means that the body will absorb and utilize no more than one-quarter of the dose. Because of its ability to support mitochondrial function and energy production, the implications of using carnitine as adjunctive support in treating other conditions associated with metabolic dysfunction have been explored.
In cardiovascular health, L-carnitine has demonstrated the potential to improve lipid profiles and positively affect blood vessel function. Its ability to facilitate the transport of fatty acids into mitochondria may contribute to the metabolism of fats, potentially aiding individuals with conditions related to lipid metabolism.
Carnitine also acts as an antioxidant, preventing oxidative damage, which is implicated as a strong risk factor for cardiovascular disease. L-carnitine has been used successfully to assist recovery from heart attack , treat symptoms of congestive heart failure , and improve insulin resistance.
L-carnitine has gained attention for its role in optimizing energy production in the setting of athletic performance. L-carnitine may assist athletes in exercise recovery , increasing oxygen supply to the muscles, improving stamina by delaying muscle discomfort and fatigue, increasing the production of red blood cells 13 , 14 , and improving high-intensity athletic performance.
Its involvement in fatty acid metabolism suggests a potential role in supporting weight loss efforts by aiding the utilization of fat stores for energy.
However, it's important to note that while some studies suggest positive outcomes, results can vary. L-carnitine should be considered as part of a comprehensive approach to weight management, including a healthy diet and regular exercise.
In one review of L-carnitine's safety profile, doses of 2 grams daily were deemed safe for long-term use. The authors did note reports of mild side effects, including heartburn and indigestion, at this dose. L-carnitine supplements can also raise blood levels of trimethylamine-N-oxide TMAO.
TMAO is a gut microbe-derived metabolite of carnitine suggested to be pro-atherogenic. High levels of TAMO are linked to an increased risk of atherosclerotic cardiovascular disease and future cardiac events.
Managing hypothyroidism and enhancing energy metabolism necessitates a holistic approach encompassing various aspects of lifestyle, nutrition, and targeted supplementation.
While L-carnitine plays a role in supporting energy metabolism, its integration into a broader therapeutic plan enhances overall effectiveness. Working with a functional and integrative healthcare provider can help you to identify specific triggers for thyroid dysfunction.
Using specialty labs and a comprehensive patient intake, a personalized treatment approach that removes obstacles to achieving a euthyroid state and restores a healthy thyroid signaling cascade can be implemented. This may include modifying diet to emphasize nutrient-dense, anti-inflammatory foods while removing potential thyroid dietary triggers; managing stress and optimizing sleep; reducing exposure to endocrine-disrupting chemicals; balancing other endocrine systems; addressing gut dysbiosis and intestinal permeability; treating infections; and using additional supplements to reduce inflammation, support thyroid hormone production, and manage symptoms of hypothyroidism.
The benefits of L-carnitine in metabolic health underscore its potential to enhance energy metabolism. L-carnitine's role in facilitating the transport of fatty acids into mitochondria positions it as a valuable component in optimizing energy production. In individuals with hypothyroidism, where reduced thyroid hormone levels impact energy metabolism, L-carnitine supplementation may offer support.
However, recognizing the importance of personalized approaches is crucial, as responses can vary. Consulting with healthcare professionals becomes essential to tailor L-carnitine use effectively, considering individual needs and potential interactions.
This emphasizes the need for a comprehensive and personalized strategy, integrating L-carnitine into broader health applications for optimal metabolic well-being. Documents Tab. Redesigned Patient Portal.
Simplify blood panel ordering with Rupa's Panel Builder. Sign in. Sign in Sign up free. Subscribe for free to keep reading! If you are already subscribed, enter your email address to log back in. Are you a healthcare practitioner? Yes No. While it could be gathered that weight loss disentangles the relationship between thyroid activity and REE, from the standpoint of energy balance and weight control our short-term results should be confirmed in long-term studies to add further evidence of an activating relationship between thyroid, adiposity and energy homeostasis during weight loss.
FFM exerts a predictive effect on REE and its inter-individual variability over a broad range of BMIs [ 39 ]. In obese subjects, values of absolute resting and total energy expenditure are conventionally higher than in lean controls, but these differences disappear when FFM is accounted for, suggesting that intrinsic energy expenditure is not altered in obese individuals [ 40 ].
On the other hand, qualitative and quantitative changes of FFM instigated by caloric restriction are capable of decreasing REE to values below the prediction models, implying the intervention of body composition-unrelated components [ 27 , 30 , 41 — 45 ]. Nonetheless, REE and FFM were tightly associated and both decreased after weight loss but the magnitude of their losses was not interrelated, while a marginal but significant association related percent variations in REE and BMI.
BMI decreased by 5. In individual analysis, however, REE increased a third of patients after weight loss. In comparison to patients with decreased REE, these patients showed similar gender distribution and equivalent changes in weight and body composition, but were generally older and harbored lower baseline REE both as absolute values and normalized for pREE or FFM.
At odds with these findings, a Whether differences in population sample, obesity degree, study design, diet regimen, macronutrients composition, and protein sparing may play a role in the discrepancies between these and our results remains unclear. Further more specifically designed studies should clarify the effect of physical activity regimens on REE during weight loss.
In addition to body composition-related variables, adaptive thermogenesis is modulated by metabolic, neuroendocrine, autonomic, and behavioral responses [ 47 ]. Changes in insulin [ 29 ], leptin [ 48 ], and sympathetic tone [ 49 ] all play a role on REE modifications after weight loss.
Thyroid elicits its effects on energy expenditure by acting on white and brown adipocytes, spontaneous motor activity, mitochondria thermogenesis and hypothalamic control of the sympathetic nervous output to the brown adipose tissue [ 50 , 51 ].
In untreated obesity, the relationship between REE and thyroid function is generally null [ 52 , 53 ], and our baseline results confirm this gap. Adaptive thermogenesis in response to weight loss has been associated with changes in serum TSH or T3 in some but not all studies [ 29 , 45 , 48 , 49 , 54 — 56 ].
The current analysis revealed that weight loss, while producing diverging effects on TSH and FT3 on one side and FT4 on the other [ 3 ], disclosed a significant association between REE and FT4 as well as FT3, regardless of changes in body composition. This interaction suggests the intervention of body composition-independent neuroendocrine signals controlling energy metabolism via THs.
Because our study did not include the measurement of circulating leptin, which is rapidly responsive to weight loss [ 57 ] and regulates the thermogenic activity through central mechanisms involving TRH [ 3 , 58 , 59 ] our results provide no insight on neuroendocrine control of TH-REE association during weight loss.
As weight loss significantly reduced TSH and FT3 levels, while enhancing FT4 ones, a lowering of type II deiodinase activity could be involved in a such variations [ 60 ].
However, changes in FT3 and FT4 could also be due to variations in serum levels of total T3 and T4, or thyroid hormones binding proteins, which were not measured in this study.
Other study limitations should be acknowledged as potentially affecting our results. First, body composition was calculated from BIA. Although patients with fluid overload, which overestimates fat mass, were excluded from the study, BIA is indeed of modest diagnostic value when compared to more refined techniques, such as CT or MRI, and shows its limits mostly in abdominally obese subjects [ 64 ].
however, previous studies from our laboratory [ 65 ] and others [ 66 ] suggested that BIA results are more similar to DEXA and BOD POD results in severe obesity than in lean or overweight subjects. Secondly, our study duration was calculated conceivably to circumvent the period of 6—8 weeks required for the physiological resetting of the HPT axis [ 67 , 68 ].
Thus, the significance of our findings remains to be proved in longer studies. Thirdly, the standard multidisciplinary approach used herein comprised 5 weekly sessions of non-vigorous physical activity, which could mitigate the natural loss in FFM occurring with caloric restriction.
However, vigorous exercise does not prevent the loss in FFM occurring during caloric restriction [ 45 ], suggesting that metabolic adaptation persists even upon combination treatments of obesity.
Lastly, our study participants were selected as euthyroid and severely obese, such that current findings may not fully apply to people with normal bodyweight or mild obesity, as well as those with thyroid dysfunctions.
Nevertheless, we consider the homogeneous study sample, the controlled inpatient regimen, the balanced diet and the controlled weight management schedule as potential points of strength of this study.
In conclusion, we observed an association between REE and thyroid hormones in severe obesity after a short-term, mildly hypocaloric multidisciplinary weight loss program. How thyroid hormone impacts energy expenditure during long-term calorie restriction warrants further investigation, as it could frustrate weight loss attempts of obese individuals.
Long-term studies are awaited to add further evidence of an activating relationship between thyroid, adiposity and energy homeostasis during weight loss.
S1 Table legend. For abbreviations: BMI, body mass index; REE, resting energy expenditure; pREE, predicted REE; FM, fat mass; FFM, fat-free mass. S2 Table legend: Significance between the two subgroups was obtained by ANOVA. The contribution of the nurse staff at the Division of Metabolic Diseases, Istituto Auxologico Italiano, Piancavallo VB for valuable contribution in clinical research is kindly acknowledged.
Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments. Abstract Background Regulating thermogenesis is a major task of thyroid hormones THs , and involves TH-responsive energetic processes at the central and peripheral level.
Methods We enrolled euthyroid subjects with severe obesity who were equally distributed between genders. Results Baseline REE was lower than predicted in 70 obese patients, and overall associated with BMI, FFM and FM but not thyroid-related parameters. Conclusions In severe obesity, short-term weight loss discloses a positive relationship between REE and THs.
Funding: The authors received no specific funding for this work. Introduction The functions of the hypothalamic-pituitary-thyroid HPT axis are influenced by environmental and physiological factors, the most relevant of which are external temperature, iodine intake, reproduction and aging [ 1 ].
Although the mechanisms responsible for this changes are incompletely understood, the main neuroendocrine signal governing the response of the HPT axis to adiposity involves actions of leptin on TRH activity in the brain and hindbrain [ 10 , 15 — 18 ] The effects of HTP on facultative thermogenesis entail both central and peripheral actions, on cellular processes governing triiodothyronine-responsive energetic mechanisms [ 19 — 23 ].
Body measurements Both at the beginning and at the end of the study, all testing procedures were performed between am in fasting conditions and after voiding.
Laboratory Thyroid function was tested by analysis of FT4, FT3, TSH, anti-Tg antibodies TgAb and anti-TPO antibodies TPOAb levels. Statistical analysis Data were tested for normality of distribution by the Kolmogorov-Smirnov test and log-transformed when needed, to correct for skewness. Results Results obtained at baseline and at the end of study are summarized in S1 Table.
Discussion Growing attention has recently focused on the ability of weight loss to restore thyroid function parameters in obesity. Supporting information. S1 Table. Baseline data in the obese population obtained at baseline and at the end of the 4-week study, and expressed as percent variation over baseline values.
s DOCX. S2 Table. Data summary in the obese population at study entry stratified according to REE measured as lower vs higher than predicted REE. S3 Table. Data summary obtained at baseline and at the end of the 4-week study in the obese population subgrouped by gender.
S4 Table. Bivariate correlation analysis between thyroid function parameters and REE at baseline and at the study end. S4 Table legend: For abbreviations: REE, resting energy expenditure.
S5 Table. Data summary in the obese population stratified according to percent REE variation below decreased REE or above increased REE baseline values recorded at the end of the study.
Acknowledgments The contribution of the nurse staff at the Division of Metabolic Diseases, Istituto Auxologico Italiano, Piancavallo VB for valuable contribution in clinical research is kindly acknowledged.
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Although hypothyroidism appears metagolism be metabolsim important factor in the pathogenesis of depression, the impact Energy metabolism and thyroid function thyroid Energy metabolism and thyroid function on the bioenergetics of the Eneryg brain is still Energy metabolism and thyroid function known. Since metabolic changes are reported Metabllism be a key player in the manifestation Immunity enhancing supplements depressive disorder, we functin whether there are differences in thygoid metabolic markers in functikn frontal cortex and hippocampus Fnuction Wistar Kyoto rats Mettabolism an animal model of depression merabolism to those of control Wistar Nutritional periodization for triathletes and Energgy the induction tjyroid hypothyroidism metaboliwm propylthiouracil PTU elicits similar effects in these animals or intensifies some parameters in the WKY rats. In our study, we used WKY rats as a model of depression since this strain exhibits lower levels of monoamines in the brain than control rats and exhibits behavioral and hormonal alterations resembling those of depression, including increased reactivity to stress. The findings indicate a decrease in glycolysis intensity in both brain structures in the WKY rats as well as in both strains under hypothyroidism conditions. Furthermore, hypothyroidism disrupted the connection between glycolysis and the Krebs cycle in the frontal cortex and hippocampus in the depression model used in this study. Decreased thyroid hormone action was also shown to attenuate oxidative phosphorylation, and this change was greater in the WKY rats. Our results suggest that both the depression and hypothyroidism models are characterized by similar impairments in brain energy metabolism and mitochondrial function and, additionally, that the co-occurrence of hypothyroidism and depression may exacerbate some of the metabolic changes observed in depression. For more information about PLOS Subject Areas, Energy metabolism and thyroid function here. Regulating thermogenesis is a major task Muscle-building nutrition thyroid hormones THs thyriod, and involves Treat muscle stiffness energetic tgyroid at First aid for DKA central and mettabolism level. Energy metabolism and thyroid function annd obesity, little znd known on the relationship between THs and resting energy expenditure REE before and after weight loss. We enrolled euthyroid subjects with severe obesity who were equally distributed between genders. Each was examined before and after completion of a 4-wk inpatient multidisciplinary dieting program and subjected to measurement of thyroid function, REE, fat-free mass FFM, kg and percent fat mass FM. Baseline REE was lower than predicted in 70 obese patients, and overall associated with BMI, FFM and FM but not thyroid-related parameters. 
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