Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of graded, physiologic hyperinsulinemia (+5, +15, +30, +70, +200 microU/ml) on oxidative and nonoxidative pathways of glucose and FFA metabolism was examined in nine lean non-insulin dependent diabetic patients (NIDDM) and in eight age- and weight-matched control subjects. Glucose and FFA metabolism were assessed using stepwise insulin clamp in combination with indirect calorimetry and infusion of [3H]3-glucose/[14C]palmitate. The basal rate of hepatic glucose production (HGP) was higher in NIDDM than in control subjects, and suppression of HGP by insulin was impaired at all but the highest insulin concentration. Glucose disposal was reduced in the NIDD patients at the three highest plasma insulin concentrations, and this was accounted for by defects in both glucose oxidation and nonoxidative glucose metabolism. In NIDDs, suppression of plasma FFA by insulin was impaired at all five insulin steps. This was associated with impaired suppression by insulin of plasma FFA turnover, FFA oxidation (measured by [14C]palmitate) and nonoxidative FFA disposal (an estimate of reesterification of FFA). FFA oxidation and net lipid oxidation (measured by indirect calorimetry) correlated positively with the rate of HGP in the basal state and during the insulin clamp. In conclusion, our findings demonstrate that insulin resistance is a general characteristic of glucose and FFA metabolism in NIDDM, and involves both oxidative and nonoxidative pathways. The data also demonstrate that FFA/lipid and glucose metabolism are interrelated in NIDDM, and suggest that an increased rate of FFA/lipid oxidation may contribute to the impaired suppression of HGP and diminished stimulation of glucose oxidation by insulin in these patients.
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PMID:Glucose and free fatty acid metabolism in non-insulin-dependent diabetes mellitus. Evidence for multiple sites of insulin resistance. 266 89

Decreased serum zinc levels and hyperzincuria occur in some non-insulin dependent diabetic subjects (NIDDM). Zinc deficiency was demonstrated in various tissues of animal models for NIDDM. Serum zinc and 24-hr urine zinc of subjects with NIDDM were compared with that of age- and sex-matched healthy volunteers. Zincuria was significantly increased in the diabetic group. Thirteen diabetic subjects with hyperzincuria and hypozincemia were supplemented with zinc sulfate 220 mg x 3/day for 7-8 weeks. At the end of the study, glucose disposal (evaluated by kg) decreased significantly from 0.562 +/- 0.03 to 0.414 +/- 0.05 (p less than 0.05) and fasting glucose and fructosamine were significantly increased from 177 +/- 10 mg/dl to 207 +/- 15 mg/dl (p less than 0.05) and from 2.7 +/- 0.2% to 3.2 +/- 0.28% (p less than 0.05), respectively. T-lymphocyte response to phytohemagglutinin was increased significantly. We conclude that zinc supplementation to NIDD patients with hypozincemia and hyperzincemia might aggravate their glucose intolerance. More accurate methods to assess zinc deficiency in NIDD patients is needed to justify the supplementation of zinc in these patients.
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PMID:The influence of zinc supplementation on glucose homeostasis in NIDDM. 269 82

The majority of zinc, copper and magnesium is either intracellular or associated with the bones. It is therefore unlikely that the plasma concentration of these trace elements will reflect their whole body content. Blood cells might be more representative of lean tissue and are also easy to obtain. The concentration of zinc, copper and magnesium was measured in the leukocytes and hemoglobin of 42 subjects with non insulin dependent diabetes mellitus (NIDDM) and in 22 subjects with insulin dependent diabetes mellitus (IDDM) and was compared with that of 44 age-matched healthy volunteers. Zinc was found to be deficient in the serum (p less than 0.001), leukocyte (p less than 0.001) and hemoglobin (p less than 0.05) of the IDDM subjects, while copper and magnesium were increased in the serum, leukocytes and hemoglobin of the IDDM subjects (p less than 0.001). There was no zinc deficiency in the leukocytes of NIDD subjects. These results are opposite to the findings on zinc concentration in various tissue of animal models for IDDM and NIDDM and with our present knowledge on zinc status in IDDM and NIDDM subjects. Thus, we conclude that the concentration of zinc in blood cells of diabetic subjects might not reflect its concentration in various tissues.
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PMID:Trace elements in blood cells of diabetic subjects. 275 38

Insulin resistant, Type II diabetes mellitus (NIDD) in a rat animal model results in profound changes in basal and insulin-stimulated membrane (Ca2+ +Mg2+)-ATPase activity in kidney basolateral membrane (BLM) preparations. We find that NIDD in these animals does not result in similar changes in membrane (Na+ +K+)-ATPase activity. Basal enzyme activity was the same in diabetic and control animals. Insulin treatment of diabetic animals in vivo resulted in hyperinsulinemia and increased BLM (Na+ +K+)-ATPase, while food restriction for 18 hr resulted in lowered enzyme activity. There was no direct effect of insulin on (Na+ +K+)-ATPase activity in isolated membranes from any of the animal groups. Thus, physiologic perturbations which alter insulin sensitivity and glucose homeostasis are accompanied by altered levels of (Na+ +K+)-ATPase activity. Lower levels of this membrane enzyme activity appear to be associated with optimal insulin action.
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PMID:(Na+ +K+)-ATPase activity in kidney basolateral membranes of non insulin dependent diabetic rats. 302 Nov 55

In order to evaluate whether the hypoglycaemic action of glibenclamide during chronic treatment of obese subjects with NIDDM is primarily due to changes in the daytime insulin level, in insulin secretion or to changes in tissue sensitivity to insulin, we studied eight NIDD's (age 43 +/- 3 years, body mass index 31.4 +/- 2.6 kg/m2) inappropriately controlled by dietary treatment alone. Before and after three months of glibenclamide treatment, plasma glucose, insulin and C-peptide were measured hourly (0800 to 1600 hours) and in vivo insulin sensitivity was evaluated using the sequential euglycaemic clamp (insulin infusion: 0, 0.8, 3.2 mU/kg/min) in combination with 3-3H-glucose tracer technique. During glibenclamide treatment the mean daytime glucose level was reduced (11.2 +/- 0.5 versus 7.1 +/- 0.4 mmol/l, p less than 0.001) but not to normal (5.2 +/- 0.2 mmol/l, p less than 0.001). Before treatment the mean daytime insulin level was higher than normal (38 +/- 58 versus 24 +/- 2 microU/ml, p less than 0.05) and was increased by 79% (67 +/- 8 microU/ml, p less than 0.001) after three months of treatment. In contrast the mean C-peptide level was unchanged (1.40 +/- 0.13 versus 1.30 +/- 0.17 nmol/l, p = NS), although it was higher than normal on both occasions (0.84 +/- 0.09 nmol/l, p less than 0.05). The basal hepatic glucose production rate was normal before treatment (86 +/- 4 versus 82 +/- 3 mg.m-2.min-1 in normals, p = NS), and unchanged after glibenclamide treatment (80 +/- 3 mg.m-2.min-1, p = NS versus pretreatment level).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo action of glibenclamide in obese subjects with mild type 2 (non-insulin dependent) diabetes. 314 30

In order to better understand the role of A- and B-cell function in diabetic pregnancy, we studied four groups of pregnant women at week 34-36 of gestation. Seventeen were healthy controls (C), 24 had gestational diabetes (GD), 16 had type 2 diabetes (NIDD) and 37 had type 1 diabetes (IDD). At times -20, 0, 20, 30, 45, 60, 90 and 120 min from the beginning of a 30 min infusion of 30 g of arginine intravenously, plasma glucose, glucagon (IRG) and C-peptide (CPR) were measured. Plasma glucose was higher in diabetic than in control subjects. IRG values were also higher in the GD and the NIDD women. CPR values were similar to, or slightly higher than control values in the GD and the NIDD and were much lower in the IDD women. All three variables increased during the arginine infusion in all groups, with the exception that CPR remained unchanged in the IDD. The CPR/IRG molar ratio was similar in control, GD and NIDD women; in the IDD, it was much smaller than in the other groups and was not affected by arginine. In all the diabetic patients, IRG was negatively correlated with the maternal weight gain and in the IDD IRG was positively correlated with the increase in the insulin need and with the CPR levels. In conclusion diabetes appeared to enhance the A-cell function also in pregnancy, possibly impairing the 'facilitated anabolism' and stressing the 'accelerated starvation' which are typical of normal pregnancy. Glucagon was confirmed as one possible determinant of the insulin resistance seen in diabetic pregnancy.
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PMID:Endocrine pancreatic function in insulin-dependent diabetic pregnant women. 353 67

There are residual ambiguities between the two main current glycaemic definitions of the categories of DM, IGT and normal GT which should be resolved. IGT is clearly a highly heterogeneous category and could with advantage be resolved into its identifiable subsets though adequate data for this is not yet available. The concept of insulin dependency requires clearer definition for operational purposes. Biochemical parameters (e.g. C-peptide responses) may help. Attempts to combine clinical manifestations and pathogenic mechanisms in a single classification (e.g. IDDM/NIDD versus Type I/Type II) should be handled with care. If the term Type I is to be retained, it should be applied to a defined pathogenic process, not to a clinical type of DM. The term Type II is inadequately defined at present. IDDM and NIDDM, clinical descriptive terms, may be provoked by a variety of pathogenic mechanisms (i.e. they are 'heterogeneous'). They could be subclassified by mechanism (when known). More visibility should be given in classification to non-Europid forms of DM (e.g. 'Tropical or 'Nutritional' DM). A staging dimension should be recognised in classifications of DM. Future classifications will benefit from the incorporation of the presence or absence of susceptibility/resistance factors to diabetes itself or to its severe long term sequelae. There remain uncertainties about the definitions and clinical implications of gestational DM (and gestational IGT) not discussed above. It should be accepted that different user groups may need different subclassification of diabetes and glucose intolerance to meet their specific requirements and so long as this is made clear and definitions are adequate this should not be a problem. However, for the present, all groups should accept the proposed glycaemic definitions of DM or IGT for the purposes of comparability.
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PMID:Limitations and problems of diabetes classification from an epidemiological point of view. 403 18