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Visceral fat and blood sugar levels

Visceral fat and blood sugar levels

The method is widely llevels and a previous study indicated Metabolism support for detoxification CT Top appetite suppressants magnetic-resonance sugad MRI may yield different absolute values of Metabolism support for detoxification areas especially levsls fat tat that boood ranking of individuals on the basis of their fat areas will be similar by both methods [ 1718 ]. Article Navigation. The precursor of the hydrogen bound to C5 of glucose is the hydrogen bound to carbon 2 of glyceraldehydephosphate. Researchers say gastric bypass surgery is more effective than gastric sleeve procedures in helping people go into remission from type 2 diabetes.


Visceral Fat, Insulin Resistance \u0026 Diabetes

Visceral fat and blood sugar levels -

Tabas explains these findings, suggesting that they may be down to the difference between how DPP4 inhibitors work in the gut versus how they work in the liver.

If we could block that interaction, we might be able stop the enzyme from causing inflammation and insulin resistance. So, the researchers targeted DPP4 in the liver cells instead of the gut. This reduced adipose inflammation and lowered insulin resistance.

As Dr. The researchers explain what the findings mean for future treatments of type 2 diabetes. Ahmed A. More research is needed. In this article, we look at nine ways to lower high insulin levels.

This can be achieved through diet, lifestyle changes, supplements, and medication. People with diabetes can use various strategies to lower their blood sugar levels. The options include lifestyle and dietary changes and natural…. Researchers say gastric bypass surgery is more effective than gastric sleeve procedures in helping people go into remission from type 2 diabetes.

A study in mice suggests a potential mechanism that could explain why only some individuals with obesity develop type 2 diabetes. A type of medication used to treat type 2 diabetes could help lower the risk of developing kidney stones, a new study suggests.

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Medical News Today. Xylose was purified by HPLC; the C5 group was cleaved by oxidation with periodic acid, and formaldehyde was collected by distillation. Formaldehyde was incubated with ammonia overnight.

In the presence of ammonia, six molecules of formaldehyde react to form one molecule of hexamethylenetetramine. This step is used to increase the sensitivity of the method. Enrichment of hexamethylenetetramine obtained from C5 was determined by gas chromatography-mass spectrometry GCMS by monitoring peaks of mass and The precision and accuracy of C5 have been reported previously 8.

Water enrichment in the body water pool was monitored by reacting a sample of plasma or urine with calcium carbide CaC2 , thereby obtaining acetylene C2H2. The enrichment of acetylene was then determined by GCMS by monitoring peaks with masses of 26 and 27 All samples were run through the GCMS processing in duplicate or triplicate.

Glucose fluxes and plasma clearance rates were expressed per kilogram of FFM. During the baseline period of the study 0— min , both the plasma glucose concentration and [ 3 H]glucose specific activity were stable during the last 30 min of tracer infusion in all subjects.

Therefore, total EGO was calculated as the ratio of the [ 3 H]glucose infusion rate to the plasma [ 3 H]glucose specific activity mean of five determinations. At low rates of insulin-stimulated glucose disposal similar to those observed in the diabetic subjects in the present study , we have shown that the tracer-derived rates of Ra and Rd closely approximate the independently measured rates of whole body glucose disposal and glucose appearance Therefore, [ 3 H]glucose was not added to the exogenously infused glucose during the insulin clamp EGO during the insulin clamp was obtained as the difference between Ra and the exogenous glucose infusion rate.

Fasting plasma glucose clearance was calculated as the ratio between EGO and FPG, whereas insulin-mediated plasma glucose clearance was obtained as the ratio of Rd to plasma glucose concentration during the clamp.

Data are given as the mean ± se. A comparison of group values was performed using ANOVA with Bonferroni-Dunn post hoc testing. To factor out confounding variables, multivariate analysis was performed with the use of mixed models, including both continuous [age and body mass index BMI ] and nominal ethnicity, sex, and sulfonylurea treatment variables as independent variables; contrasts were used to estimate differences among levels of a nominal variable i.

tertiles of fasting glycemia or VF area. The strength of confounder-adjusted associations between the two variables of interest was expressed as the partial correlation coefficient. To examine the association between VF and metabolic control, the study cohort was divided into tertiles of fasting hyperglycemia.

Thus, group 1 included mildly hyperglycemic subjects, group 2 consisted of patients with moderate hyperglycemia, and group 3 included severely hyperglycemic patients Table 1. Except for a slight imbalance in sex distribution, the three groups were well matched for age, obesity BMI and percent fat mass , body fat distribution as determined by waist circumference and waist to hip ratio , and previous sulfonylurea treatment.

The serum lipid profile and arterial blood pressure levels were not significantly different among groups. Clinical characteristics in type 2 diabetic patients stratified by tertiles of fasting hyperglycemia. MA, Mexican-American; HDL, high-density lipoprotein; LDL, low-density lipoprotein.

As measured by MRI, abdominal SF area was similar across groups, whereas abdominal VF area was significantly greater in subjects with moderate to severe fasting hyperglycemia than in the mildly hyperglycemic subjects.

group 2. In the whole cohort, VF increased with age in both males and females and with indexes of fatness, whereas SF was positively related only to fatness Table 2. In the latter model, Mexican-American ethnicity and diabetes duration also were significant positive correlates of HbA 1c.

With regard to glucose fluxes, EGO was progressively higher, and plasma glucose clearance was progressively lower across groups both during the fasting state and under insulinized conditions Table 3. In contrast, the relation of EGO to VF was weak and not statistically significant Fig.

Plasma insulin and FFA concentrations were similar in the three groups both at baseline and during the clamp. Inverse relationship between insulin-stimulated glucose clearance top panel or EGO bottom panel and VF area in 63 patients with type 2 diabetes.

The fitting line and r value are those of a power function. Metabolic data in type 2 diabetic patients stratified by tertiles of fasting hyperglycemia.

P value for the difference among groups after adjustment by sex, age, ethnicity, BMI, and sulfonylurea treatment. In the subgroup of subjects 48 of 63 in whom GNG was measured, fasting EGO varied through FPG tertiles with a similar trend as in the whole cohort.

This increment was entirely due to increased GNG Table 4. To examine whether VF contributed to enhance GNG, the percent GNG was regressed against VF, first singly and then after adjustment for confounders.

The inverse relationship between GLY and VF explains the lack of relationship between total EGO and VF. Components of fasting glucose production in type 2 diabetic patients stratified by tertile of fasting hyperglycemia.

Association of VF accumulation with gluconeogenic and glycogenolytic flux in 48 patients with type 2 diabetes.

The lines connect the observed values plotted as the mean ± sem at each tertile of VF area. In the whole cohort, fasting plasma FFA levels were independently i. There was, however, no relationship between circulating FFA levels and either VF or SF. In this cohort of type 2 diabetic patients with an average disease duration of 5 yr and a wide range of fasting plasma glucose and HbA 1c levels, VF accumulation was clearly associated with poor metabolic control Table 1.

Upon stratifying the subjects by fasting glycemia, the resulting clinical phenotype was quite homogeneous, not only in terms of age, serum lipids and blood pressure, but also in terms of overall body size and fat distribution.

Only increased VF and, to a smaller extent, diabetes duration paralleled the increase in FPG. In a multiple regression model, which accounted for sex, age, BMI, and SF, only VF, diabetes duration, and Mexican-American ethnicity, in that order, were significant positive correlates of FPG.

Thus, if every other measured factor is the same, the selective accumulation of fat in the visceral area is a predictor of the severity of fasting hyperglycemia. Most importantly, VF is associated not only with the degree of fasting hyperglycemia, but even more strongly and independently with HbA 1c.

The clinical implication of these findings is that VF, when directly estimated by a sensitive imaging technique, is an independent predictor of metabolic control in type 2 diabetic patients, particularly in those of Mexican-American ethnicity.

As a corollary, VF may be an important factor that modulates the response to treatment as well as itself representing a potential target for intervention. It should be emphasized, however, that the set of clinical and anthropometric variables used in the present study could explain no more than half of the observed variability in HbA 1c.

Clearly, other determinants of glycemic control went unmeasured. With regard to the mechanisms underlying the association between VF accumulation and hyperglycemia in type 2 diabetes, glucose fluxes provided at least part of the answer.

First, peripheral insulin resistance in the fasting state and during the insulin clamp was progressively more severe with increasing fasting hyperglycemia. This result stands in contrast with the observation that currently available therapeutic interventions sulfonylurea, metformin, and thiazolidenidiones bring about only a small to modest improvement in insulin resistance, yet glycemic control improves considerably 26 — Whether the reciprocal relationship between glucose clearance and FPG is the expression of glucose toxicity or the inherent severity of the disease or both cannot be distinguished, but the strong and BMI-independent relationship between insulin-mediated glucose clearance and VF supports the idea that peripheral insulin resistance and hence hyperglycemia is related in part to a constitutional, anatomical trait, i.

visceral adiposity. The mechanism by which fat deposition within and between abdominal viscera affects insulin action in peripheral tissues is not clear from the present studies. Circulating plasma FFA levels were similar across all three groups and are therefore an unlikely messenger, at least in patients with manifest diabetes.

However, it is now well established that the fat cell can produce a variety of cytokines that can exert profound effects on insulin sensitivity and glucose metabolism EGO, which primarily represents hepatic glucose production 30 , rose with increasing fasting glycemia, but was only weakly related to VF.

The components of EGO, however, showed a revealing pattern. GNG, both as a fraction of EGO and as an absolute flux, was strongly and independently associated with higher VF, whereas GLY was less tightly and reciprocally related to VF.

If interpreted mechanistically, these results suggest that the presence of excess VF specifically enhances GNG.

However, whether this stimulation of GNG by increased VF results in glucose overproduction depends on the concomitant adjustment of the glycogenolytic rate. In the more hyperglycemic subjects the ambient plasma insulin concentration is insufficient to restrain EGO, which consequently rises to levels that are elevated in absolute terms.

With regard to the plasma FFA concentration, we found a positive association between their systemic levels and GNG. A high FFA flux to the liver stimulates GNG by providing a continuous source of energy ATP from FFA oxidation as well as substrate glycerol to synthesize glucose de novo.

Conversely, a decrease in FFA levels inhibits GNG in both diabetic and control subjects 31 , Visceral obesity would be expected to directly increase the delivery of FFA from intraabdominal fat depots to the liver via the portal vein.

Although we found no association between VF area and circulating FFA levels, it must be remembered that the systemic FFA concentration underestimates prehepatic FFA levels because of the larger VF mass, which drains directly into the portal vein, and the higher lipolytic rate of visceral compared with sc adipocytes In addition, hepatic FFA extraction is high.

Therefore, the contribution of VF to systemic FFA concentrations is likely to be small although precise calculations require knowledge of differential lipolytic rates and regional blood flow rates.

These considerations may explain why systemic FFA plasma levels were unrelated to VF, but remained directly related to GNG, which responds to the whole FFA load regardless of its anatomical origin. Finally, it is of clinical relevance that in our cohort of diabetic patients increased VF almost doubled the extent to which the increase in HbA 1c could be accounted for on the basis of the clinical phenotype alone.

According to this model, HbA 1c is predicted to be 0. These estimates confirm that an accurate measurement of VF is an important part of clinical phenotyping and has rather direct consequences for the metabolic control of patients with type 2 diabetes.

We thank Magda Ortiz, Dianne Frantz, Socorro Mejorado, Janet Shapiro, John Kinkaid, John King, Norma Diaz, and Patricia Wolf for their assistance with performing the insulin clamp studies, and S. Frascerra, Ph.

Baldi, Ph. Ciociaro; and N. Pecori for their technical assistance with the measurement of GNG. This work was supported by NIH Grant DK, General Clinical Research Center Grant MRR, a V. Merit Award, and funds from the V.

Medical Research Service. DeFronzo RA Lilly lecture The triumvirate: β-cell, muscle, liver. A collusion responsible for NIDDM.

Diabetes 37 : — Google Scholar. DeFronzo RA , Ferrannini E , Simonson DC Fasting hyperglycemia in non-insulin-dependent diabetes mellitus: contributions of excessive hepatic glucose production and impaired tissue glucose uptake. Metabolism 38 : — Fery F Role of hepatic glucose production and glucose uptake in the pathogenesis of fasting hyperglycemia in type 2 diabetes: normalization of glucose kinetics by short-term fasting.

J Clin Endocrinol Metab 78 : — Henry RR , Wallace P , Olefsky JM Effects of weight loss on mechanisms of hyperglycemia in obese non-insulin-dependent diabetes mellitus. Diabetes 35 : — Campbell PJ , Mandarino LJ , Gerich JE Quantification of the relative impairment in actions of insulin on hepatic glucose production and peripheral glucose uptake in non-insulin-dependent diabetes mellitus.

Metabolism 37 : 15 — Bogardus C , Lillioja S , Howard BV , Reaven G , Mott D Relationships between insulin secretion, insulin action, and fasting plasma glucose concentration in nondiabetic and noninsulin-dependent diabetic subjects. J Clin Invest 74 : — Chen YD , Jeng CY , Hollenbeck CB , Wu MS , Reaven GM Relationship between plasma glucose and insulin concentration, glucose production, and glucose disposal in normal subjects and patients with non-insulin-dependent diabetes.

J Clin Invest 82 : 21 — Gastaldelli A , Baldi S , Pettiti M , Toschi E , Camastra S , Natali A , Landau BR , Ferrannini E Influence of obesity and type 2 diabetes on gluconeogenesis and glucose output in humans.

A quantitative study. Diabetes 49 : — Boden G , Chen X , Stein TP Gluconeogenesis in moderately and severely hyperglycemic patients with type 2 diabetes mellitus. Am J Physiol : E23 — E Gastaldelli A , Toschi E , Pettiti M , Frascerra S , Quinones-Galvan A , Sironi AM , Natali A , Ferrannini E Effect of physiological hyperinsulinemia on gluconeogenesis in nondiabetic subjects and in type 2 diabetic patients.

In obese mice, a liver enzyme travels to visceral fat and increases inflammation inflammatory cells labeled red , thereby promoting diabetes filled with cells. The photo on the right shows fat tissue from obese mice who have been given a drug that blocks the enzyme.

The fat that builds up deep in the abdomen—more than any other type of body fat—raises the risk of insulin resistance and type 2 diabetes. Researchers have known that abdominal fat becomes dangerous when it becomes inflamed but have had a hard time determining what causes the inflammation.

A new study at Columbia University Irving Medical Center CUIMC has revealed that at least one of the culprits for this mysterious inflammation comes from the liver.

The researchers found that, in obese mice, the liver increases its production of an enzyme called DPP4. This enzyme travels through the blood stream to abdominal fat. Once inside fat tissue, DPP4 helps to activate inflammatory cells.

The good news is that this inflammation can be soothed by turning off DPP4 production in the liver, as the researchers demonstrated in mice. And even though the animals remained obese, soothing inflamed abdominal fat improved their insulin resistance.

Stock Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons.

Amalia Levwls, Yoshinori Miyazaki, Metabolism support for detoxification Pettiti, Masafumi Matsuda, Srihanth Mahankali, Skincare for men Santini, Ralph A. Visceral fat VF excess has been Viscceral with decreased peripheral insulin sensitivity and has been ssugar to contribute Viscsral hepatic adn resistance. However, Glycemic load and nutrient timing Metabolism support for detoxification Viceral which VF impacts on hepatic glucose metabolism and the quantitative role of VF in glycemic control have not been investigated. In the present study 63 type 2 diabetic subjects age, 55 ± 1 yr; fasting plasma glucose, 5. In contrast, the relation of basal endogenous glucose output to VF was not statistically significant. We conclude that in patients with established type 2 diabetes, VF accumulation has a significant negative impact on glycemic control through a decrease in peripheral insulin sensitivity and an enhancement of gluconeogenesis. Visceral fat and blood sugar levels

Author: Fauzshura

2 thoughts on “Visceral fat and blood sugar levels

  1. Ich tue Abbitte, dass sich eingemischt hat... Aber mir ist dieses Thema sehr nah. Ich kann mit der Antwort helfen. Schreiben Sie in PM.

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