Diabetes Mellitus Type 2 Essays - Opinion of professionals

comeInsulin resistance appears to be the best predictor of the development of diabetes in the children of patients with type 2 diabetes, but the mechanism responsible is unknown.

We performed hyperinsulinemic—euglycemic clamp studies in combination with infusions of [6,6- 2 H 2 ]glucose in healthy, young, lean, insulin-resistant offspring of patients with type 2 diabetes and insulin-sensitive control subjects matched for age, height, weight, and physical activity to assess click the following article sensitivity of liver and muscle to insulin.

Proton 1 H magnetic resonance spectroscopy studies were performed to measure intramyocellular lipid and intrahepatic triglyceride content. Rates of whole-body and subcutaneous fat lipolysis were assessed by measuring the rates of [ 2 H 5 ]glycerol turnover in combination with microdialysis measurements of glycerol release from subcutaneous fat. We performed 31 P magnetic resonance spectroscopy studies to assess the rates of mitochondrial oxidative-phosphorylation activity in muscle.

These data support the hypothesis that insulin Diabetes Mellitus Type 2 Essays in the skeletal muscle of insulin-resistant offspring of patients with type 2 diabetes is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in mitochondrial oxidative phosphorylation.

Type 2 diabetes is rapidly becoming a worldwide epidemic. Despite much work, little is known about the factors responsible for insulin resistance in persons at risk. In this regard, studies measuring triglyceride content of muscle-biopsy specimens 6 or intramyocellular lipid content by means of proton 1 H magnetic resonance spectroscopy indicate a strong relation between intramuscular lipid content and insulin resistance in skeletal muscle.

Studies have also identified increases in plasma fatty acid concentrations 10 Diabetes Mellitus Type 2 Essays intramyocellular lipid content 8 in the insulin-resistant offspring of patients with type 2 diabetes, suggesting that dysregulation of fatty acid metabolism may mediate the insulin resistance in these persons.

Increases in the intramyocellular concentration of fatty acid metabolites in turn have been postulated to activate a serine kinase cascade, which decreases the insulin-stimulated activity of insulin receptor substrate 1—associated phosphatidylinositol 3-kinase and results in reduced glucose transport 12 and glycogen synthesis.

In the present study we examined a potential mechanism for the intramyocellular accumulation of lipids in young, lean, insulin-resistant offspring of patients with type 2 diabetes. These subjects are ideal candidates for studies examining the earliest defects leading to insulin resistance, since in contrast to patients with diabetes, they are young, lean, healthy, and unlikely to have other confounding please click for source. Since increases in intramyocellular triglyceride content could occur as a result of the increased delivery of fatty acids from lipolysis, decreased rates of mitochondrial oxidative phosphorylation, or both, we examined these processes in the insulin-resistant offspring of patients with Diabetes Mellitus Type 2 Essays 2 diabetes and in insulin-sensitive control subjects.

We assessed rates of whole-body and subcutaneous fat lipolysis by measuring the rates of [ 2 H 5 ]glycerol turnover in combination with microdialysis measurements of the release of glycerol from subcutaneous fat. We determined the rates of in vivo mitochondrial phosphorylation and the ratio of inorganic phosphate to phosphocreatine in skeletal muscle using phosphorus 31 P magnetic resonance spectroscopy. All subjects were recruited by means of local advertising over a two-year period to and were prescreened to confirm that they were in excellent health, lean, nonsmoking, and taking no medications.

A birth weight above 2. Qualifying subjects more than persons underwent a three-hour oral glucose-tolerance test with a g oral glucose loadafter which two subgroups of subjects were consecutively selected to identify extreme phenotypes for insulin resistance and increased insulin sensitivity. Insulin-resistant subjects 3 men and 11 women were defined as having an insulin sensitivity index 22 of less than 4. Insulin-sensitive control subjects five men and seven women were defined by an insulin sensitivity index of greater than 6.

All qualifying subjects subsequently underwent a complete medical history taking and a physical examination along with blood tests to verify that the following were normal: In addition, subjects underwent 1 H magnetic resonance spectroscopy studies to determine the triglyceride content of liver and muscle. The subjects then underwent a hyperinsulinemic—euglycemic clamp study to assess the responsiveness of liver, muscle, and fat to insulin or 31 P magnetic resonance spectroscopy studies to assess the rates of muscle mitochondrial phosphorylation and the ratio of inorganic phosphate to phosphocreatine.

Owing to the complexity of the protocol, not all the subjects were able to complete both the magnetic resonance spectroscopy and clamp studies.

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Two of the 12 control subjects, who initially qualified on the basis of their insulin sensitivity index, were subsequently excluded after the hyperinsulinemic—euglycemic clamp study identified them as insulin resistant, whereas all subjects who were found to be insulin resistant on the basis of the insulin sensitivity index were also found to be insulin resistant on the basis of the clamp study.

Written consent was obtained from each subject after the purpose, nature, and potential complications of the studies had been explained.

The protocol was approved by the human-investigation committee of Yale University. The subjects were instructed to eat a regular, weight-maintenance diet containing at least g of carbohydrate per day for three days before admission for either the clamp or magnetic resonance spectroscopy study. All subjects were instructed not to perform any exercise other than normal click at this page for the three days before the study.

To minimize changes in glucose metabolism resulting from ovarian hormonal effects, the female subjects were studied during the follicular phase days 0 through 12 of the menstrual cycle.

Plasma concentrations of insulin, glucagon, adiponectin, and Diabetes Mellitus Type 2 Essays were measured with the use of double-antibody radioimmunoassay kits Linco. Plasma fatty acid concentrations were determined with the use of a microfluorometric method. Microdialysate glycerol concentrations in 0. On a separate day, after a hour fast, all subjects were transported by wheelchair to the Yale Magnetic Resonance Center, and localized 1 H magnetic resonance Diabetes Mellitus Type 2 Essays spectra of the soleus muscle and liver were acquired on a 2.

Basal rates of glucose and glycerol turnover were assessed during a three-hour basal period and insulin-stimulated rates were assessed with a three-hour hyperinsulinemic—euglycemic clamp with the use of 20 mU of insulin per square meter of body-surface area per minute, [6,6- 2 H 2 ]glucose, and [ 2 H 5 ]glycerol as previously described. Rates of continue reading phosphorylation were assessed by 31 P magnetic resonance spectroscopy saturation transfer performed at The ratio of Diabetes Mellitus Type 2 Essays phosphate to phosphocreatine in the soleus muscle was measured by 31 P magnetic resonance spectroscopy as previously described.

Statistical analyses were performed with StatView software Abacus Concepts. To detect statistically significant differences between control subjects and insulin-resistant subjects, we used unpaired Student's t-tests for independent samples, with a two-sided P value of less than 0. Non-normally distributed data i. All subjects had normal glucose-tolerance tests, but the plasma concentrations of glucose Figure 1A and insulin Figure 1B before and during the test were significantly higher in the insulin-resistant subjects.

Fasting plasma fatty acid concentrations were similar in the insulin-sensitive control subjects 0.

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Fasting rates of glucose production were similar in the nine insulin-sensitive control subjects 2. In contrast, the rates of glucose infusion required to maintain euglycemia were approximately 60 percent lower in the insulin-resistant subjects than in the insulin-sensitive control subjects during clamping 3. There were no significant differences in fasting or insulin-stimulated rates of whole-body glucose or fat oxidation between the two groups data not shown.

Fasting rates of whole-body energy expenditure tended to be lower in the insulin-resistant group than in the control group Fasting rates of glycerol turnover were similar in the control group and the insulin-resistant group 0. There was no significant difference with respect to intrahepatic triglyceride content between insulin-resistant subjects 2.

The lean, insulin-resistant offspring of patients with type 2 diabetes had severe insulin resistance, as compared with insulin-sensitive control subjects matched for age, height, weight, and activity. The difference could be attributed largely to a reduction of approximately 70 percent in insulin-stimulated nonoxidative muscle glucose metabolism. Using 1 H magnetic resonance spectroscopy to measure intramyocellular lipid content, we found that insulin resistance in muscle was accompanied by an increase of approximately 80 percent in intramyocellular lipid content in the insulin-resistant subjects, as compared with the insulin-sensitive control subjects.

These data are consistent with those of previous studies in humans and Diabetes Mellitus Type 2 Essays, 31,32 which have suggested that dysregulated intramuscular Diabetes Mellitus Type 2 Essays acid metabolism has an important causative role in insulin resistance and may have a similar role in fat-induced insulin resistance in the skeletal muscle of the insulin-resistant offspring of patients with type 2 diabetes. To assess whether the increase in intramyocellular lipid content in the insulin-resistant subjects was due to increased delivery of fatty acids to the muscle, we measured whole-body and localized rates of lipolysis.

Rates of whole-body lipolysis were similar in the control subjects and the insulin-resistant subjects during the basal state and were both suppressed to a similar degree during the hyperinsulinemic—euglycemic clamp study.

In a manner consistent with this finding, we found that the extent of insulin-induced suppression of the localized Diabetes Mellitus Type 2 Essays of lipolysis in subcutaneous fat, as assessed by microdialysis, was also similar in both groups.

More info together, these data suggest that insulin resistance was confined largely to skeletal muscle and that increased basal rates of peripheral lipolysis and defects in insulin-induced suppression of lipolysis do not have a major role in causing the increased intramyocellular lipid content in the insulin-resistant subjects.

To assess whether decreased mitochondrial activity may contribute to the increased intramyocellular lipid content, we also assessed the rates of muscle mitochondrial phosphorylation using 31 P magnetic resonance spectroscopy. We found that the mitochondrial rates of ATP production were reduced by approximately 30 percent in the muscle of the insulin-resistant subjects, as compared with the insulin-sensitive control subjects.

Consistent with this finding of altered mitochondrial function, we also found a reduced ratio of inorganic phosphate to phosphocreatine, which may reflect a lower ratio of type I fibers mostly oxidative to type II fibers mostly glycolytic in the insulin-resistant subjects.

Several studies have also implicated a number of novel adipocyte-derived factors in mediating insulin resistance in patients with obesity and in those with type 2 diabetes. These data suggest that alterations in plasma concentrations of these adipocyte-derived factors do not have continue reading major role in mediating insulin resistance in these persons.

Taken together, our results support the hypothesis that insulin resistance in these young people is due to dysregulation of intramyocellular fatty acid metabolism, which may be caused by an inherited defect in mitochondrial oxidative phosphorylation.

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Such a defect might be due to a reduction in mitochondrial content, which in turn might be attributable to a reduced ratio of type I to type II muscle fibers. These results are similar to those in lean, elderly, insulin-resistant subjects, whose insulin resistance, in contrast to that in insulin-resistant offspring, is most likely attributable to acquired defects in mitochondrial biogenesis, which lead to reductions in source mitochondrial content.

We are http://cocktail24.info/blog/literature-review-on-health-and-safety-at-work.php to Drs. Michael Lehrke and Mitch Lazar for assistance in measuring plasma resistin concentrations; to Dr. From the Departments of Internal Medicine K. Address Diabetes Mellitus Type 2 Essays requests to Dr. Global and societal implications of the diabetes epidemic.

Impaired glucose tolerance as a disorder of insulin action: N Engl J Med ; Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus: Diabetes Care please click for source Slow glucose removal rate and hyperinsulinemia precede the development of type II diabetes in the offspring of diabetic patients.

Ann Intern Med ; Intramuscular triglyceride and muscle insulin sensitivity: Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: Intramyocellular triglyceride content is a determinant of in vivo insulin resistance in humans: Measurement of intracellular triglyceride stores by H spectroscopy: Am J Physiol ; Free fatty acid-induced insulin resistance is associated with activation of protein kinase C theta and alterations in the insulin signaling cascade.

Effect of free fatty acids on glucose transport and IRSassociated phosphatidylinositol 3-kinase activity. J Clin Invest ; Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 IRS-1 -associated phosphatidylinositol 3-kinase activity in muscle. J Diabetes Mellitus Type 2 Essays Chem ; Lipid-induced insulin resistance in human muscle is associated with changes in diacylglycerol, protein kinase C, and IkappaB-alpha. Mechanisms of fatty acid-induced inhibition of glucose uptake.

Mechanism of free fatty acid-induced insulin resistance in humans. Adipose expression of tumor necrosis factor-alpha: Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. Am J Physiol Endocrinol Metab ; The hormone resistin links obesity to diabetes.

The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity.

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Nat Med ;7: A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr ; Insulin sensitivity indices obtained from oral glucose tolerance testing: Glucose metabolism during the menstrual cycle:

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