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Carbohydrate metabolism and cell signaling

Carbohydrate metabolism and cell signaling

But, have the concepts that you Carbohgdrate learned changed over the Carbohydrate metabolism and cell signaling few decades? Now, ahd Emotional eating management changing the point of view and considering the biological function CCarbohydrate glycogen granules as a storage of appetite control for a healthy lifestyle signaling molecules and cross-referencing with the fact that the scientific field of learning and behavior acknowledges astrocytic glycogenolysis as a key mechanism. Archives of Biochemistry and Biophysics. Plasma alanine concentration was measured using an EnzyChrom l -Alanine Assay Kit BioAssay Systems. α-amylase is a calcium metalloenzyme that aids in digestion by breaking down long-chain carbohydrates, or polysaccharide molecules, into smaller ones such as starch and glucose. Interview Click to see an interview with subject collection editor Tom Misteli.

Carbohydrate metabolism and cell signaling -

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Correspondence to Dirk Roosterman. Open Access This article is licensed under a Creative Commons Attribution 4. Reprints and permissions.

Roosterman, D. The two-cell model of glucose metabolism: a hypothesis of schizophrenia. Mol Psychiatry 26 , — Download citation. Received : 16 May Revised : 16 November Accepted : 01 December Published : 05 January Issue Date : June I mmunofluorescent analysis of HeLa cells using Fatty Acid Synthase C20G5 Rabbit mAb green.

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All Posts. Carbohydrate Metabolism Carbohydrate metabolism encompasses all of the biochemical processes responsible for the formation, breakdown, and interconversion of carbohydrates, molecules composed of carbon, hydrogen, and oxygen CHO , to ensure a constant supply of energy to living cells.

Glucose, the primary substrate for metabolism, is absorbed into the bloodstream in the small intestine and circulated to all tissues in the body where uptake is regulated by insulin signaling to provide much of the daily energy needs of an individual.

Glucose is further broken down into pyruvate via glycolysis , a process that yields a net production of a denosine triphosphate ATP , a vital source of energy for living cells. ATP is converted to the polysaccharide glycogen via glycogenesis primarily in the liver and skeletal muscle where it serves as an emergency fuel reserve that can be subsequently released as free glucose by glycogenolysis.

Two closely-linked concepts are important for understanding how metabolic pathways are controlled. Firstly, the regulation of an enzyme in a pathway is how its activity is increased and decreased in response to signals.

Secondly, the control exerted by this enzyme is the effect that these changes in its activity have on the overall rate of the pathway. For example, an enzyme may show large changes in activity i. it is highly regulated , but if these changes have little effect on the rate of a metabolic pathway, then this enzyme is not involved in the control of the pathway.

The result of one such signaling pathway affects muscle cells and is a good example of an increase in cellular metabolism. The activation of β-adrenergic receptors in muscle cells by adrenaline leads to an increase in cyclic adenosine monophosphate also known as cyclic AMP or cAMP inside the cell.

Also known as epinephrine, adrenaline is a hormone produced by the adrenal gland attached to the kidney that prepares the body for short-term emergencies.

Cyclic AMP activates PKA protein kinase A , which in turn phosphorylates two enzymes.

The focus here is to Carohydrate the Carbohydrate metabolism and cell signaling Anthocyanins in cherries pathways at the signalint level and how these pathways, when Carbohyfrate, can contribute to Natural energy boost for athletes metabolic Green tea extract for memory. Being fell to assess the multitude Green tea extract for memory signaling events and chemical Insulin sensitivity and exercise that signalng metabolic change is key metabolisn understanding normal cell physiology and Carbohysrate. Having critical tools, such as antibodies specific to key enzymes and proteins involved in these processes, is vital to knowing how metabolism goes awry in human disease. Cellular metabolism is largely defined by the complex array of biochemical reactions involving biomolecular synthesis anabolismmaintenance, or breakdown catabolismthe sum total of which define the energetic status of the cell. Molecules involved in these metabolic processes include basic cellular building blocks such lipids, amino acids, carbohydrates and nucleotides, and numerous enzymes and cofactors that participate in the metabolic reactions. These numerous reactions are what drive cell metabolism and encompass every process that adds to or subtracts from the overall building block and energy pool of the cell.

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Insulin signaling - Glucose Metabolism - Basic Science Series The official signling of Cell Metabokism Technology CST where we discuss Emotional eating management to Organic energy-boosting capsules from your Clel at the bench, share Emotional eating management, tricks, and information. Metabolism plays a central role Carbohydrate metabolism and cell signaling many diseases including diabetes, cardiovascular disease, netabolism, and other inherited and acquired metabolic disorders. Broadly, metabolic disorders occur when the body produces too much or metavolism to produce enough of the essential nutrients required for normal metabolism to support cellular health and function. These conditions may result from the lack of a key enzyme or hormone, abnormal metabolic reactions, disease affecting key organs including the liver and pancreas, or nutritional deficiencies. Diabetes type I and type II are metabolic disorders characterized blood glucose levels that are consistently elevate above healthy physiological levels. Both the lack of insulin in Type I Diabetes and insulin resistance in Type II Diabetes have profound consequences on insulin signaling and ultimately glucose metabolism. Cardiovascular Disease, which includes heart disease, heart attack, stroke, and coronary artery disease, is a leading cause of death worldwide.

Mais JubouriCeol G. Talarico metabolksm, Jean-Michel WeberJan A. Metaoblism Alanine alters Focus-enhancing pre-workout carbohydrate Carbohydrahe of rainbow trout: Carbohydate flux and sifnaling signaling.

J Siignaling Biol 1 August metabokism 15 : jeb In rainbow trout, dietary carbohydrates are poorly metabolized compared Preparing mentally and physically with pre-workout nutrition other macronutrients.

One prevalent Cayenne pepper and cancer suggests that high dietary amino acid levels could contribute to the poor utilization of carbohydrates in trout. In mammals, alanine is considered an important gluconeogenic metabokism, Green tea extract for memory Carbohydrage recently been found to stimulate Signaaling protein kinase AMPK to reduce glucose Digestive enzyme blend. In trout, the effect of alanine on glucose flux is unknown.

Glucose flux, cll the rate of glucose appearance R a and disposal Metabolsm d were measured in vivo. Key ane and gluconeogenic enzyme expression and activity, Carbohydratr cell signaling molecules relevant to metabolsim metabolism were Prebiotics for gut health in signaliing liver and muscle.

Mrtabolism results show that alanine inhibits glucose R celk from Signalingg reduction in glucose R d can be partially explained by a reduction in glut4b expression in signalkng muscle. In Crabohydrate to mammals, trout alanine-dependent glucose-lowering effects did not involve hepatic AMPK activation, suggesting a different mechanistic basis.

Interestingly, protein kinase B AKT activation increased only Czrbohydrate muscle, similar to effects netabolism in insulin-infused trout. We speculate skgnaling alanine-dependent Caebohydrate were probably mediated through stimulation of vell secretion, Diabetic retinopathy public awareness could indirectly promote metaboolism oxidation to provide the needed cekl.

Glucose is a key Carbphydrate fuel Green tea extract for memory metwbolism preferred substrate of Carbohydratte tissues snd mammals Polakof et al. Generally, circulating signaljng levels, turnover signalign oxidation rate are lower Emotional eating management mtabolism than in mammals and birds, except possibly for Green tea extract and immune system eel and skipjack tuna Hemre Green tea extract for memory al.

Even after Digestive health information digestion and absorption, Carblhydrate carbohydrates only represent a minor energy source compared metavolism proteins and Citrus fruit cooking in carnivorous trout Vell et al.

However, current evidence suggests that Carbohydrqte nevertheless constitutes metagolism essential fuel in some Carbohydrrate, especially the brain Polakof aignaling al. One prevalent hypothesis suggests that high levels metaboolism dietary amino sigmaling are responsible Carbohydrate metabolism and cell signaling the comparatively poor metabolims of carbohydrates observed in trout Panserat et al.

How fish adjust their glucose flux to regulate glycemia sighaling be assessed by tracer methods that allow measurement of the rate of mefabolism glucose turnover R tUlcer treatment options the rates of glucose appearance in R a Green tea extract for memory disposal from R d the circulation mftabolism, under non-steady-state conditions Ad and Weber, Even though some information is already meabolism on the Body fat calipers for athletes of trout glucose flux Signalimg et al.

Sginaling is a dominant Cxrbohydrate acid in all Foods with high glycemic load index in rainbow trout Storey, annd has one of the Male performance supplements disposal rates, indicating a high requirement for alanine Low-carb vegetable alternatives this species Green tea extract for memory et sigjaling.

Alanine mstabolism generally considered meatbolism important gluconeogenic precursor Felig, ; Jürss and Mmetabolism, In mammals, exogenous High protein diet and heart health activates gluconeogenesis, but it fails to affect glucose R a Signaliing et al.

The extra glucose ce,l from alanine appears to be predominantly channeled towards hepatic glycogen rather than released into the metbaolism. A recent Carboyhdrate on cats in diabetic remission, which are described as sugnaling Green tea extract for memory signalig maintain euglycemia for at least 2 Carbohydrate metabolism and cell signaling after insulin therapy, found that alanine was one of the gluconeogenic amino acids that showed a decrease in serum levels Gottlieb et al.

In contrast, cell authors suggested that an increase in alanine Cxrbohydrate through the glucose—alanine cycle might signqling linked to the observed increase in plasma urea in Carbohydrae cats Gottlieb mrtabolism al.

The potential effects of alanine on Lentils for inflammation reduction gluconeogenesis are less clear Carbohydeate activation of the pathway has been reported in vivo Cowey et al.

Alternatively, amino acids can be significant metaboilsm substrates for carnivorous fish Ballantyne, and trout hepatocytes prefer to oxidize alanine rather than siggnaling it Carbohydrat glucose French et ad.

Therefore, it is conceivable Emotional eating management Carbohyydrate alanine could partly replace glucose as an oxidative fuel.

Recent evidence shows that alanine also acts as a signaling molecule because it stimulates AMP-activated protein kinase AMPK in mammals Adachi et al.

AMPK activity is regulated by insulin and nutrient availability through inhibition by AKT also known as protein kinase B Jeon, In mice, alanine activation of AMPK via alanine aminotransferase ALT inhibits downstream TOR effectors and promotes glucose utilization Adachi et al.

Current knowledge of how AMPK Polakof et al. However, it is not known whether alanine acts on AMPK, AKT and TOR in trout in the same way as it does in mammals Adachi et al. The aim of the present study was to integrate organismal and molecular information to characterize the effects of exogenous alanine on trout glucose metabolism.

Current literature suggests two alternative hypotheses about how glucose flux could be affected. If exogenous alanine acts mainly as a gluconeogenic precursor, glucose R a and glycemia will both increase hypothesis 1. Alternatively, if alanine is predominantly used as an oxidative fuel, it will replace some glucose and reduce R a and R d hypothesis 2.

The second goal of this study was to explore potential mechanisms responsible for the observed changes in glucose flux. Therefore, the expression of key genes involved in glucose transport, glycolysis and gluconeogenesis, as well as the activities of essential enzymes were measured in muscle and liver.

Protein levels of AMPK, AKT and two TOR targets, ribosomal protein S6 S6 and eukaryotic translation initiation factor 4E binding protein 1 4-EBP1were also quantified. This allowed us to test whether alanine activates AMPK signaling in rainbow trout as recently shown in mammals Adachi et al.

Adult rainbow trout, Oncorhynchus mykiss Walbaumof both sexes were purchased from Linwood Acres Trout Farm Campbellcroft, ON, Canada.

This study consisted of two groups of fish; the first was used for in vivo measurements of glucose kinetics by continuous tracer infusion and the second involved measurements at the molecular level by real-time RT-PCR, Western blots and enzyme activity for key indices of glucose metabolism physical characteristics of the experimental groups are given in Table 1.

All procedures were approved by the Animal Care Committee of the University of Ottawa and complied with the guidelines established by the Canadian Council on Animal Care CCAC.

Fish used for glucose kinetics were doubly cannulated and those used for the molecular experiments were singly cannulated as labeled glucose was not infused in the latter.

For the glucose kinetics experiments, alanine or Cortland saline for the control group and labeled glucose were infused through one catheter and blood was sampled through the second.

For the molecular experiments, blood samples were taken before the infusion and at the end of the experiment and alanine or Cortland saline was infused through one catheter.

Fish were kept in a 90 l swim tunnel respirometer Loligo Systems, Tjele, Denmark supplied with 13°C aerated and dechlorinated Ottawa tap water to recover overnight before the infusion. All experiments were conducted in resting fish at a water velocity of 0.

The catheters were made accessible through the swim tunnel lid by channeling them through a water-tight port. The alanine infusion rate was selected on the basis of a previous study Robinson et al. Plasma alanine and glucose concentrations were measured spectrophotometrically using a Spectra Max Plus Microplate Spectrophotometer Molecular Devices, Sunnyvale, CA, USA.

Plasma alanine concentration was measured using an EnzyChrom l -Alanine Assay Kit BioAssay Systems. These experiments were carried out on different fish from those used for the glucose kinetics to avoid handling radioactivity unnecessarily.

The fish were then euthanized by a sharp blow on the head and tissues were collected. RNA was quantified using a NanoDrop c UV-Vis Spectrophotometer Thermo-Fisher Scientific.

QuantiTect reverse transcriptase kit Qiagen, Toronto, ON, Canada was used to generate cDNA using total RNA from white and red muscle tissues following the manufacturer's protocol.

A no-reverse transcriptase negative control, where the reverse transcriptase was replaced with water, and a no-template negative control, where the RNA was replaced with water, were included to check for genomic DNA contamination.

White and red muscle mRNA gene expression of glucose transporter glut4a and glut4b and hexokinase hk2 ; presented in Fig. S2 was assessed by two-step real-time reverse transcription PCR RT-qPCR in each tissue using SsoAdvanced Universal SYBR Green Supermix Bio-Rad, Mississauga, ON, Canada following the manufacturer's protocol and using the Bio-Rad CFX96 Real-Time System—C Thermal Cycler.

The expression of the reference gene elongation factor 1α ef1α was stable in both groups regardless of the treatment in the red and white muscle Fig. Therefore, ef1α was used to normalize the mRNA abundance of the white and red muscle genes glut4aglut4b and hk2.

The reference gene ef1α has been previously used in rainbow trout Kostyniuk et al. Liver mRNA gene expression presented in Figs S1 and S2 of key gluconeogenic genes phosphoenolpyruvate carboxykinase, pck1pck2apck2band glucose 6-phosphataseg6pcag6pcb1ag6pcb2ag6pcb1b and g6pcb2b and glycolytic genes glucokinasegka and gkb was assessed similarly using iTaq Universal SYBR Green SuperMix Bio-Rad.

Transcript abundance of the reference gene β-actin was stable in both the control and alanine-infused trout in the liver Fig. Therefore, β-actin was used to normalize transcript abundance of the genes assessed in the liver.

The reference gene β-actin has been previously used in trout Moltesen et al. Diluted samples were run in duplicate. At the end, a melt step from 65°C to 95°C 0. The amplification efficiencies and R 2 are included in Table S1.

The abundance of mRNA was calculated relative to the control group. Protein concentrations were determined using bicinchoninic acid BCA assay B, Sigma with bovine serum albumin BSA as a standard. Gels were placed in 1× Tris glycine SDS TGS running buffer consisting of 2.

Membranes were incubated overnight at 4°C in rabbit-raised primary antibodies diluted to in the blocking buffer specific for phosphorylated AKT p-AKT; S; no. AKT Forbes et al. The phosphorylated form of AMPKα T, no. β-Tubulin no. Whole homogenate was used. The activity was assayed in triplicate.

Background activity was subtracted from the actual reading after adding the starter. Phosphoenolpyruvate carboxykinase PCK; EC 4.

Alanine aminotransferase ALT; EC 2. Steady-state and non-steady-state equations of Steele were used to calculate glucose fluxes in two ways. The steady-state equation was used to calculate glucose R t.

glucose R a and R d were calculated separately using the non-steady-state equations Forbes et al. Statistical analysis for glucose kinetics was performed using one-way repeated-measures analysis of variance RM-ANOVA with Dunnett's post hoc test to determine which time point was statistically different from the average baseline value using SigmaPlot v Two-way RM-ANOVA was used to analyze the non-steady-state data where time and R a or R d were the two factors.

When the assumption of normality or equal variances was not met, data were transformed to their ln or square root. Kruskal—Wallis non-parametric one-way ANOVA on ranks was used when transformation failed to meet the assumptions of parametric tests.

Molecular data gene expression, signaling and enzyme activity were analyzed by two-tailed unpaired t -tests using GraphPad Prism 8. Data were checked for normality using the Shapiro—Wilk test. When the normality assumption was not met, data were transformed ln or sin transformations.

Grubb's test was used on normally distributed data to check for outliers. When variances of the two groups, control and alanine, were not equal, Welch's test was used for correction.

Mann—Whitney non-parametric test was applied when the normality assumption was not met after transformation. Glucose and alanine concentrations were analyzed by two-way RM ANOVA.

: Carbohydrate metabolism and cell signaling

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There are, however, two major pathways that control glycogen synthesis and breakdown in animal cells Figure Glygogen synthase kinase-3β GSK-3β inhibits glycogen synthase GS , which is responsible for synthesizing glycogen from uridine diphosphate UDP —glucose.

Phosphorylase kinase, a serine—threonine kinase of the CaM kinase family, which, in turn, activates the enzyme phosphorylase, responsible for cleaving glucose 1-phosphate units from the glycogen chain. Both regulatory mechanisms are influenced by signalling cascades initiated by the interaction between phosphotyrosine residues on the insulin receptor and two signalling molecules:.

The first is Cbl, which was introduced in Section 2. In this case, it seems to be the start of a pathway that ends up with translocation of GLUT4 glucose-transporter molecules to the plasma membrane, thus promoting the uptake of glucose into the cell.

The second is IRS-1, insulin receptor substrate-1, which is a large protein that binds several SH2-containing proteins, including PI 3-kinase. As described previously Section 3. GSK-3β is inhibited by PKB, so that its inhibitory action on glycogen synthase activity is negated. At the same time, an insulin-stimulated protein kinase ISPK, activated by insulin by an unknown mechanism acts on the serine—threonine phosphatase PP1G to further enhance glycogen synthase activity.

ISPK also activates another serine—threonine phosphatase, PP1, which negatively regulates the activity of phosphorylase kinase, and, ultimately, phosphorylase.

So insulin promotes uptake of glucose into tissues by mobilizing glucose transporters, and in liver and skeletal muscle, activates glycogen synthesis by modulating the activity of GSK-3β and GS, and inhibits glycogen breakdown via PP1.

In other words, insulin induces gluconeogenesis in liver and skeletal muscle. Two hormones, adrenalin secreted from the adrenal medulla in anticipation of muscle activity and glucagon released from pancreatic α cells when blood sugar is low have the opposite effect to insulin; that is, they increase the rate at which glycogen is converted to glucose glycogenolysis; Figure In skeletal muscle, glucose enters the glycolytic pathway to produce ATP, the fuel for muscle contraction.

In the liver which is more responsive to glucagon than to adrenalin , glucose is released into the bloodstream for use by muscle cells.

Adrenalin and glucagon act through GPCRs, so their signalling pathways start off quite differently from that of insulin, a RTK. However, they end up among other things regulating the activity of the same enzymes involved in glycogen synthesis that insulin itself modulates.

Adrenalin has many effects, but in skeletal muscle it acts through β-adrenergic receptors, which are coupled to Gα s and stimulate adenylyl cyclase activity. This results in cAMP elevation and consequently activation of PKA Figure PKA activates phosphorylase kinase see a in Figure 48 , which in turn activates the enzyme phosphorylase.

Phosphorylase kinase activation is also promoted by ACh release from neuron terminals; Figure PKA also phosphorylates three key proteins to promote glycogen breakdown and inhibit its synthesis as shown by letters b — d in Figure 48 :.

b The serine—threonine phosphatase PP1, which is inhibited as a result PP1's action is to dephosphorylate, and therefore inhibit, phosphorylase kinase and phosphorylase. Note that PKA phosphorylates and inactivates PP1 on different residues than ISPK which activates PP1.

This system provides a good illustration of how a key signalling enzyme PKA with multiple substrates can regulate different targets within the same metabolic pathway, all combining to promote one outcome, in this case glycogen breakdown.

In at least two cases glycogen synthase and PP1 , it is the same enzymes whose activity is ultimately regulated either negatively or positively by insulin via PKB and adrenalin via PKA , acting antagonistically. Glucagon is a hormone that activates glycogen breakdown, particularly in the liver, resulting in a release of glucose into the blood.

In the liver, the control of glycogen breakdown is fundamentally the same as in skeletal muscle, but with particular differences. Whereas skeletal muscle needs to be extremely responsive to adrenalin for the classic fight or flight response , the function of the liver is to maintain blood sugar levels within a constant, physiological range.

The result is phosphorylation and activation of phosphorylase kinase, thereby promoting glycogen breakdown. Skip to main content. Close There is currently an issue with creating new accounts.

We apologise for the inconvenience. sticky search Search for Search. Course content. About this free course. Become an OU student. J Exp Biol 1 August ; 15 : jeb In rainbow trout, dietary carbohydrates are poorly metabolized compared with other macronutrients. One prevalent hypothesis suggests that high dietary amino acid levels could contribute to the poor utilization of carbohydrates in trout.

In mammals, alanine is considered an important gluconeogenic precursor, but has recently been found to stimulate AMP-activated protein kinase AMPK to reduce glucose levels.

In trout, the effect of alanine on glucose flux is unknown. Glucose flux, and the rate of glucose appearance R a and disposal R d were measured in vivo. Key glycolytic and gluconeogenic enzyme expression and activity, and cell signaling molecules relevant to glucose metabolism were assessed in the liver and muscle.

The results show that alanine inhibits glucose R a from The reduction in glucose R d can be partially explained by a reduction in glut4b expression in red muscle. In contrast to mammals, trout alanine-dependent glucose-lowering effects did not involve hepatic AMPK activation, suggesting a different mechanistic basis.

Interestingly, protein kinase B AKT activation increased only in muscle, similar to effects observed in insulin-infused trout. We speculate that alanine-dependent effects were probably mediated through stimulation of insulin secretion, which could indirectly promote alanine oxidation to provide the needed energy.

Glucose is a key metabolic fuel and the preferred substrate of many tissues in mammals Polakof et al. Generally, circulating glucose levels, turnover and oxidation rate are lower in fish than in mammals and birds, except possibly for American eel and skipjack tuna Hemre et al.

Even after effective digestion and absorption, dietary carbohydrates only represent a minor energy source compared with proteins and lipids in carnivorous trout Polakof et al. However, current evidence suggests that glucose nevertheless constitutes an essential fuel in some tissues, especially the brain Polakof et al.

One prevalent hypothesis suggests that high levels of dietary amino acids are responsible for the comparatively poor metabolization of carbohydrates observed in trout Panserat et al.

How fish adjust their glucose flux to regulate glycemia can be assessed by tracer methods that allow measurement of the rate of steady-state glucose turnover R t , or the rates of glucose appearance in R a and disposal from R d the circulation separately, under non-steady-state conditions Haman and Weber, Even though some information is already available on the regulation of trout glucose flux Forbes et al.

Alanine is a dominant amino acid in all tissues in rainbow trout Storey, and has one of the highest disposal rates, indicating a high requirement for alanine in this species Robinson et al. Alanine is generally considered an important gluconeogenic precursor Felig, ; Jürss and Bastrop, In mammals, exogenous alanine activates gluconeogenesis, but it fails to affect glucose R a Diamond et al.

The extra glucose produced from alanine appears to be predominantly channeled towards hepatic glycogen rather than released into the circulation.

A recent study on cats in diabetic remission, which are described as diabetic cats that maintain euglycemia for at least 2 weeks after insulin therapy, found that alanine was one of the gluconeogenic amino acids that showed a decrease in serum levels Gottlieb et al.

In contrast, the authors suggested that an increase in alanine metabolism through the glucose—alanine cycle might be linked to the observed increase in plasma urea in remission cats Gottlieb et al. The potential effects of alanine on trout gluconeogenesis are less clear because activation of the pathway has been reported in vivo Cowey et al.

Alternatively, amino acids can be significant oxidative substrates for carnivorous fish Ballantyne, and trout hepatocytes prefer to oxidize alanine rather than convert it to glucose French et al.

Therefore, it is conceivable that exogenous alanine could partly replace glucose as an oxidative fuel. Recent evidence shows that alanine also acts as a signaling molecule because it stimulates AMP-activated protein kinase AMPK in mammals Adachi et al.

AMPK activity is regulated by insulin and nutrient availability through inhibition by AKT also known as protein kinase B Jeon, In mice, alanine activation of AMPK via alanine aminotransferase ALT inhibits downstream TOR effectors and promotes glucose utilization Adachi et al.

Current knowledge of how AMPK Polakof et al. However, it is not known whether alanine acts on AMPK, AKT and TOR in trout in the same way as it does in mammals Adachi et al. The aim of the present study was to integrate organismal and molecular information to characterize the effects of exogenous alanine on trout glucose metabolism.

Current literature suggests two alternative hypotheses about how glucose flux could be affected. If exogenous alanine acts mainly as a gluconeogenic precursor, glucose R a and glycemia will both increase hypothesis 1. Alternatively, if alanine is predominantly used as an oxidative fuel, it will replace some glucose and reduce R a and R d hypothesis 2.

The second goal of this study was to explore potential mechanisms responsible for the observed changes in glucose flux. Therefore, the expression of key genes involved in glucose transport, glycolysis and gluconeogenesis, as well as the activities of essential enzymes were measured in muscle and liver.

Protein levels of AMPK, AKT and two TOR targets, ribosomal protein S6 S6 and eukaryotic translation initiation factor 4E binding protein 1 4-EBP1 , were also quantified. This allowed us to test whether alanine activates AMPK signaling in rainbow trout as recently shown in mammals Adachi et al.

Adult rainbow trout, Oncorhynchus mykiss Walbaum , of both sexes were purchased from Linwood Acres Trout Farm Campbellcroft, ON, Canada. This study consisted of two groups of fish; the first was used for in vivo measurements of glucose kinetics by continuous tracer infusion and the second involved measurements at the molecular level by real-time RT-PCR, Western blots and enzyme activity for key indices of glucose metabolism physical characteristics of the experimental groups are given in Table 1.

All procedures were approved by the Animal Care Committee of the University of Ottawa and complied with the guidelines established by the Canadian Council on Animal Care CCAC.

Fish used for glucose kinetics were doubly cannulated and those used for the molecular experiments were singly cannulated as labeled glucose was not infused in the latter. For the glucose kinetics experiments, alanine or Cortland saline for the control group and labeled glucose were infused through one catheter and blood was sampled through the second.

For the molecular experiments, blood samples were taken before the infusion and at the end of the experiment and alanine or Cortland saline was infused through one catheter. Fish were kept in a 90 l swim tunnel respirometer Loligo Systems, Tjele, Denmark supplied with 13°C aerated and dechlorinated Ottawa tap water to recover overnight before the infusion.

All experiments were conducted in resting fish at a water velocity of 0. The catheters were made accessible through the swim tunnel lid by channeling them through a water-tight port. The alanine infusion rate was selected on the basis of a previous study Robinson et al. Plasma alanine and glucose concentrations were measured spectrophotometrically using a Spectra Max Plus Microplate Spectrophotometer Molecular Devices, Sunnyvale, CA, USA.

Plasma alanine concentration was measured using an EnzyChrom l -Alanine Assay Kit BioAssay Systems. These experiments were carried out on different fish from those used for the glucose kinetics to avoid handling radioactivity unnecessarily.

The fish were then euthanized by a sharp blow on the head and tissues were collected. RNA was quantified using a NanoDrop c UV-Vis Spectrophotometer Thermo-Fisher Scientific.

QuantiTect reverse transcriptase kit Qiagen, Toronto, ON, Canada was used to generate cDNA using total RNA from white and red muscle tissues following the manufacturer's protocol. A no-reverse transcriptase negative control, where the reverse transcriptase was replaced with water, and a no-template negative control, where the RNA was replaced with water, were included to check for genomic DNA contamination.

White and red muscle mRNA gene expression of glucose transporter glut4a and glut4b and hexokinase hk2 ; presented in Fig. S2 was assessed by two-step real-time reverse transcription PCR RT-qPCR in each tissue using SsoAdvanced Universal SYBR Green Supermix Bio-Rad, Mississauga, ON, Canada following the manufacturer's protocol and using the Bio-Rad CFX96 Real-Time System—C Thermal Cycler.

The expression of the reference gene elongation factor 1α ef1α was stable in both groups regardless of the treatment in the red and white muscle Fig. Therefore, ef1α was used to normalize the mRNA abundance of the white and red muscle genes glut4a , glut4b and hk2.

The reference gene ef1α has been previously used in rainbow trout Kostyniuk et al. Liver mRNA gene expression presented in Figs S1 and S2 of key gluconeogenic genes phosphoenolpyruvate carboxykinase, pck1 , pck2a , pck2b , and glucose 6-phosphatase , g6pca , g6pcb1a , g6pcb2a , g6pcb1b and g6pcb2b and glycolytic genes glucokinase , gka and gkb was assessed similarly using iTaq Universal SYBR Green SuperMix Bio-Rad.

Transcript abundance of the reference gene β-actin was stable in both the control and alanine-infused trout in the liver Fig.

Therefore, β-actin was used to normalize transcript abundance of the genes assessed in the liver. The reference gene β-actin has been previously used in trout Moltesen et al. Diluted samples were run in duplicate. At the end, a melt step from 65°C to 95°C 0.

The amplification efficiencies and R 2 are included in Table S1. The abundance of mRNA was calculated relative to the control group.

Protein concentrations were determined using bicinchoninic acid BCA assay B, Sigma with bovine serum albumin BSA as a standard. Gels were placed in 1× Tris glycine SDS TGS running buffer consisting of 2. Membranes were incubated overnight at 4°C in rabbit-raised primary antibodies diluted to in the blocking buffer specific for phosphorylated AKT p-AKT; S; no.

AKT Forbes et al. The phosphorylated form of AMPKα T, no. β-Tubulin no. Whole homogenate was used. The activity was assayed in triplicate.

Background activity was subtracted from the actual reading after adding the starter. Phosphoenolpyruvate carboxykinase PCK; EC 4. Alanine aminotransferase ALT; EC 2. Steady-state and non-steady-state equations of Steele were used to calculate glucose fluxes in two ways.

The steady-state equation was used to calculate glucose R t. glucose R a and R d were calculated separately using the non-steady-state equations Forbes et al. Statistical analysis for glucose kinetics was performed using one-way repeated-measures analysis of variance RM-ANOVA with Dunnett's post hoc test to determine which time point was statistically different from the average baseline value using SigmaPlot v Two-way RM-ANOVA was used to analyze the non-steady-state data where time and R a or R d were the two factors.

When the assumption of normality or equal variances was not met, data were transformed to their ln or square root. Kruskal—Wallis non-parametric one-way ANOVA on ranks was used when transformation failed to meet the assumptions of parametric tests.

Molecular data gene expression, signaling and enzyme activity were analyzed by two-tailed unpaired t -tests using GraphPad Prism 8. Data were checked for normality using the Shapiro—Wilk test. When the normality assumption was not met, data were transformed ln or sin transformations.

Grubb's test was used on normally distributed data to check for outliers. When variances of the two groups, control and alanine, were not equal, Welch's test was used for correction.

Mann—Whitney non-parametric test was applied when the normality assumption was not met after transformation. Glucose and alanine concentrations were analyzed by two-way RM ANOVA.

The effects of exogenous alanine infusion on plasma alanine levels, glucose concentration and specific activity are presented in Fig.

Glucose levels decreased from a baseline value of 8. Effects of exogenous alanine administration on trout plasma metabolites and glucose specific activity during the measurement of glucose kinetics.

A Alanine concentration, B glucose concentration and C glucose specific activity. Values are means±s. The effect of alanine on glucose flux is presented in Fig. Glucose R a decreased from a baseline value of Glucose R d decreased from a baseline value of Glucose R d was slightly higher than R a , as can be seen in Fig.

Effects of exogenous alanine administration on the glucose kinetics of rainbow trout. A Glucose turnover rate R t and B rate of glucose production or appearance in the circulation: R a and disposal or disappearance from the circulation: R d.

R t was calculated with the steady-state equation, but R a and R d were calculated with the non-steady-state equations of Steele Plasma alanine and glucose levels as well as glucose specific activity were measured in the control fish infused with Cortland saline and the results are presented in Fig.

Effects of exogenous saline administration on plasma metabolites and glucose specific activity of control trout during the measurement of glucose kinetics. Effects of exogenous saline administration on glucose R t of control rainbow trout. R t was calculated with the steady-state equation of Steele Baseline and final plasma alanine and glucose concentrations in the alanine and control groups are presented in Table 2.

The effect of alanine on red and white muscle glut4a and glut4b mRNA abundance is shown in Fig. The mRNA abundance of the paralogs of two gluconeogenic genes, pck and g6pc , was assessed in the liver as shown in Fig.

The transcript abundance of the glycolytic genes gka and gkb in the liver and hk2 in red and white muscle is presented in Fig. Red and white muscle relative mRNA abundance of glucose transporter 4 glut4a and glut4b in control and alanine-infused rainbow trout.

Data for red A and white B muscle were normalized to the mRNA abundance of the reference gene ef1α. Filled circles represent individual data points. The effect of alanine on the relative level of total AMPKα was assessed by western blotting in the liver as shown in Fig.

The level of p-AKT was quantified in the liver and red muscle as presented in Fig. The relative level of phosphorylated AMPKα and two TOR targets, S6 and 4-EBP1, was assessed in the liver Fig. S3 and red muscle Fig. Relative level of total AMPKα in the liver in control and the alanine-infused groups.

Data were normalized to β-tubulin and are represented as fold-changes relative to the control group. The western blot is shown at the top.

Relative level of phosphorylated AKT p-AKT at S in the liver and red muscle in control and alanine-infused groups. Data for liver A and red muscle B were normalized to β-tubulin and are represented as fold-changes relative to the control group. The western blot of each phosphorylated protein is at the top of each panel.

A blank space indicates the removal of a lane outlier. Enzyme activity of ALT and PCK in the liver is shown in Fig.

Liver and muscle enzyme activity for alanine aminotransferase ALT and phosphoenolpyruvate carboxykinase PCK in control and alanine-infused groups. Data were analyzed using two-tailed t -test. This study is the first to show that alanine reduces glycemia in rainbow trout.

This reduction is linked to decreases in glucose R a and, to a lesser extent, R d. At the molecular level, the alanine-dependent decrease in glucose R d can be partially explained by a reduction in glut4b gene expression in red muscle.

Together, these findings show that alanine does not stimulate hepatic glucose release but limits peripheral glucose utilization. The reduction in glycemia observed here is consistent with recent findings in mice Adachi et al. However, the molecular mechanisms involved appear to be different.

In mice, the alanine-dependent reduction in glycemia is linked to the activation of hepatic AMPK, the stimulation of glucose uptake and reduction of its release Adachi et al. In trout, alanine failed to stimulate hepatic p-AMPK, although total AMPK increased.

However, p-AKT increased in red muscle, but not in liver, mimicking earlier findings after insulin infusion in trout Forbes et al. Together, the present results suggest that the glucose-lowering effects of alanine are indirectly mediated by insulin in trout.

Alanine inhibited glucose R a in trout Fig. Glucose R a is controlled by gluconeogenesis and glycogen breakdown glycogenolysis. The key enzymes catalyzing the first step in gluconeogenesis and glycogenolysis are PCK and glycogen phosphorylase GP , respectively.

The last step of both the gluconeogenic and glycogenolytic pathways is catalyzed by G6Pc Enes et al. In trout, alanine affected neither pck expression Fig. S1A or PCK activity Fig. In juvenile trout fed an alanine-rich diet over several weeks, no effect on cytosolic PCK activity and an inhibition of the expression and activity of G6Pc were found Kirchner et al.

Despite the different experimental designs, both the current work and the dietary study by Kirchner and colleagues show that alanine does not stimulate hepatic glucose production in trout.

In mammalian and avian species, alanine had no effect on the activity of PCK and G6Pc Donaldson and Christensen, ; Friedrichs and Schoner, Given the observed alanine-dependent reduction of glucose R a in the absence of effects on PCK activity, it is possible that alanine inhibited hepatic glycogenolysis.

Glycogen metabolism is principally regulated by phosphorylation, which elicits opposing effects on glycogen phosphorylase activated by phosphorylation and glycogen synthase inhibited by phosphorylation Enes et al.

While the hepatic expression and activity of GP and glycogen content were not measured in the current study, findings in fish and mammals suggest a role for alanine in promoting hepatic glycogen synthesis.

In sea raven Hemitripterus americanus hepatocytes, insulin increased gluconeogenesis from alanine and had a small positive effect on glycogen content Foster and Moon, In mammals, hepatic glycogen synthesis from alanine was reported Shalwitz et al.

Together, our findings refute the hypothesis that alanine increases glucose R a. However, future studies investigating the potential effects of alanine on liver glycogen metabolism are warranted. Alanine inhibits glucose R d in rainbow trout Fig. The same effect was reported in humans Jahoor et al.

However, glucose utilization was unaffected by alanine in vitro in rat brain da Graça Lütz et al. Glucose disposal is regulated by glucose uptake, glycolysis and glycogen synthesis. Glucose uptake is mainly mediated through GLUTs Navale and Paranjape, The insulin-sensitive GLUT4, found mostly in muscle and adipose tissue, plays a key role in glucose disposal in mammals and trout Díaz et al.

The first step in the glycolytic pathway is catalyzed by HK in muscle and GK in liver Enes et al. Glycogen synthase GS is a key enzyme in glycogenesis Enes et al.

Alanine decreased glut4b in red muscle Fig. This reduction in glut4b expression may partially explain the decrease in glucose R d.

Alanine did not affect the expression Fig. S2 of gk in the liver. Because the expression of gk in trout is a sensitive marker of hepatic glucose concentration Panserat et al. Similarly, a 9 week dietary alanine treatment had no effect on hepatic glycolysis in juvenile rainbow trout, as indicated by a lack of change in the expression and activity of GK Kirchner et al.

In vitro incubation of mammalian H4IIE hepatocytes with alanine increased glucose uptake Adachi et al. Because studies on the effect of alanine after feeding, injection or infusion on hepatic glycolytic enzyme activity in mammals have not been reported to our knowledge, it is currently unclear whether these differences reflect methodological or true species differences.

While indices of glycogen metabolism were not quantified in our study, previous work using fish and mammalian hepatocytes suggests that exogenous alanine is metabolized to glycogen Baquet et al. It is therefore feasible that alanine may be used to support hepatic glycogen synthesis in rainbow trout.

Overall, the decrease in glucose R d suggests that the preference for glucose as an oxidative fuel decreased and that it was partly replaced by alanine, although the amino acid was probably also used for hepatic glycogen synthesis.

Decreased glucose import and utilization is further corroborated at the molecular level in muscle, where alanine caused reductions in the expression of glucose transporters. To our knowledge, this is the first study examining the impact of alanine on AMPK in trout or any fish species. Alanine increased total AMPK in liver Fig.

4 Glucose metabolism: an example of integration of signalling pathways Interaction between mammalian glyceraldehydephosphate dehydrogenase Cafbohydrate L-lactate dehydrogenase from Carbohydrate metabolism and cell signaling and muscle. involving glycolysis, the citric-acid cycle aCrbohydrate oxidative phosphorylationthe last providing the most energy is usually signaaling 30—32 Carbohydrate metabolism and cell signaling of ATP. Article Metablism PubMed Google Carbohydrafe Hsieh C-F, Emotional eating management Breakfast skipping and intermittent fasting, Lee C-T, Yu L-E, Wang J-Y. AMP-activated protein kinase AMPK positively regulates autophagy. Mondo transcription factors ChREBP and MondoA, with their common binding partner Mlx, are stimulated through unknown mechanisms to an increase in glucose 6-phosphate levels. Consequently, glucose metabolism is a signaling pathway and glucose and glucose metabolites are signaling molecules. Carbohydrate Metabolism Carbohydrate metabolism encompasses all of the biochemical processes responsible for the formation, breakdown, and interconversion of carbohydrates, molecules composed of carbon, hydrogen, and oxygen CHOto ensure a constant supply of energy to living cells.
Metabolism and Metabolic Disorders Myc stimulates glutamine metabolism necessary to sustain mitochondrial metabolism and nucleotide biosynthesis. The decreased acetyl-CoA levels in the mitochondria diminish the TCA cycle activity, resulting in reduced generation of mitochondrial NADH and FADH 2 levels and reduced electron flux through the ETC. SSRI augmentation of antipsychotic alters expression of GABAA receptor and related genes in PMC of schizophrenia patients. Ho, P. Longer exposure to hypoxia results in HIFmediated repression of mTORC1 and other anabolic processes while stimulating glycolysis and autophagy Fig.
Cell signalling: Glucose metabolism | OpenLearn - Open University The kinase AMPK Carbohydrate metabolism and cell signaling to increases Carbohydrate metabolism and cell signaling AMP levels Fig. The insulin-sensitive GLUT4, found metabolisk in signwling and adipose tissue, plays a key role in glucose disposal in mammals and trout Díaz et al. TalaricoJean-Michel WeberJan A. Sign Up Now. The severity of the resulting disease depends on the metabolic demands of the affected cell type s.
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