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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Few data exist on predictors of non-insulin-dependent (type II) diabetes mellitus. We examined body mass index (BMI), ratio of subscapular-to-triceps skin fold (centrality index), and fasting glucose and insulin concentrations as predictors of decompensation to type II diabetes in Mexican Americans, a population at high risk for this disorder. Twenty-eight of 474 initially nondiabetic Mexican Americans developed type II diabetes after 8 yr of follow-up. Converters to diabetes were older and had higher BMIs, centrality indices, and fasting glucose and insulin concentrations than nonconverters. Subjects in the highest quartile of the insulin distribution had 6.6 times the risk of developing type II diabetes as subjects in the remaining three quartiles combined (95% confidence interval [CI] = 3.14-13.7). In multivariate analysis, fasting glucose (odds ratio [OR] = 5.80, 95% CI = 2.57-13.1) and insulin (OR = 3.12, 95% CI = 1.36-7.14) remained significantly related to conversion to diabetes. However, BMI and centrality index, which were significantly related to conversion in the univariate analysis, were no longer significant in the multivariate analysis once glucose and insulin concentrations were taken into consideration, suggesting that the effect of these variables may be mediated by insulin resistance. Nearly half of the incident cases developed in a subset of the population who were simultaneously in the highest quartile of both fasting insulin and glucose concentrations (population-attributable risk 44.2%). Our results support the insulin resistance/pancreatic exhaustion theory of type II diabetes.
Diabetes 1990 Mar
PMID:Incidence of type II diabetes in Mexican Americans predicted by fasting insulin and glucose levels, obesity, and body-fat distribution. 240 81

A study was carried out on 36 geriatric diabetic females (above 60 years). Marked exhaustion and significant loss of weight were common presenting complaints (60%) besides usual symptomatology. Only 25% patients were asymptomatic for diabetes. Generalised itching (20%) and pruritus vulvae (33.3%) were other common presenting complaints. Neuropathy was found to be the commonest complication being present in 77.7% patients, followed by retinopathy (50%) and nephropathy (27.7%). Hypertension was found to be associated in 44% patients and evidence of ischaemic heart disease was found in 42%. Development of nephropathy, retinopathy, neuropathy, and hypertension showed direct correlation with duration of illness ie, longer the history of diabetes higher was the incidence of complications.
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PMID:Diabetes mellitus in geriatric females. 258 30

In 79 diabetic patients, 37 patients with diabetes mellitus type I and 42 patients with diabetes mellitus type II, the HLA-A, B and DR antigens were examined. An association of diabetes mellitus type I with HLA-B8, DR3 and DR4 was found. For the first time a relation between diabetes mellitus type I and HLA-B21 antigen was established. The early onset of the disease and the exhaustion of the endogenic insulin secretion are linked with B8 and DR3 carrier state while the late manifestations of diabetes mellitus and the preservation of one's own insulin production correlate with antigen B21. In the patients with diabetes mellitus Type II the frequency of antigen B21 and DR1 is increased and the carriers of B21 develop in the course of the disease relative insulin insufficiency and a secondary resistance toward sulfanilurea drugs.
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PMID:[The relationship of HLA antigens to certain clinical forms of diabetes mellitus]. 266 40

Sixty-seven subjects with moderate obesity (50 +/- 3 percent above ideal body weight) were given an oral glucose tolerance test with the simultaneous measurement of rates of glucose and lipid oxidation by continuous indirect calorimetry. When the subjects were stratified into nine 5-year classes of duration of obesity, the prevalence of impaired glucose tolerance (IGT) and overt diabetes both increased with increasing duration of obesity. Both basal and post-OGTT lipid oxidation rates were, however, similar in all classes. To assess the independent influence of IGT, diabetes, age, and duration of obesity on glucose metabolism, the data were subjected to analysis of variance using a factorial design with metric covariates. Age by itself was found to be associated (P less than 0.05) with a decline in total post-OGTT glucose oxidation. Both IGT and diabetes, on the other hand, were associated with increased plasma insulin and free fatty acid (FFA) levels, both in the fasting state and following glucose ingestion (P = 0.05-P less than 0.002). Only diabetes, however, was associated with a drastic reduction in nonoxidative glucose disposal, which marked the appearance of, and strongly correlated with (r = -0.81, P less than 0.001), fasting hyperglycemia. Duration of obesity had significant metabolic consequences in its own right: a fall in the insulin response to glucose (P = 0.05) and in the rate of total glucose oxidation (P = 0.03), and a rise in post-OGTT glucose levels (P = 0.04). We conclude that: (a) increased lipid oxidation is common in obesity, but is not sufficient to explain the deterioration of glucose tolerance in long-term obesity; (b) very-long-term obesity may be associated with partial exhaustion of the beta cell, and the resultant insulinopenia may cause depressed glucose oxidation and impaired glucose tolerance, and (c) a defect in nonoxidative glucose disposal is a characteristic feature of frank diabetes at any stage of obesity.
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PMID:The metabolic consequences of long-term human obesity. 306 64

In this study, in vitro B-cell models are described, which may be applicable for studying the reported B-cell desensitization produced by hyperglycemia in IDDM and NIDDM. Using a programmable perifusion/perfusion system, insulin secretion from perifused islets was measured at 10-30-min intervals for 24-50 h. After 3-4 h continuous glucose (11 mM), a new phase of insulin release occurs in which secretion declines to, and remains at, approximately 25% maximal release. Results were similar when using: perifused islets embedded in Cytodex 3, or Bio-Gel P-2, 100-200 mesh; batchincubated islets with hourly changes of medium; and the isolated pancreas perfused for 8 h. Three different media, Hana HB 104 (fortified, fully defined medium), RPMI-1640 + 10% FBS, and perfusion bufferalbumin, were used. Despite reduced secretion to continuous glucose, each system responded vigorously to an acute stimulation with glucose-forskolin. Decreased secretion was primarily caused by decreased secretagogue efficiency (reduced fractional secretion). Prolonged stimulation with glucose or glucose-IBMX produced a similar waning of secretion regardless of the amount of insulin released. It is concluded that the third phase of insulin secretion may represent a secret-agogue-induced, signal desensitization of the B-cell, rather than exhaustion of a B-cell compartment of stored insulin.
Diabetes 1986 Mar
PMID:The third phase of in vitro insulin secretion. Evidence for glucose insensitivity. 351 47

Groups of young adult rats with body weights of 125-135 g (group A) or 300-400 g (group B) were subjected to one bout of prolonged exercise to exhaustion on a treadmill and were studied 2 h postexercise. Liver glycogen levels were markedly depleted in the exercised rats. Adipocytes from group A exercised rats showed a significantly greater increase in pyruvate dehydrogenase (PDH) activity in response to insulin than those from sedentary controls. Incubation with insulin of liver particulate fractions from exercised group A rats resulted in an increased production of a mitochondrial PDH activator compared with preparations from sedentary controls. The tissues of both exercised and sedentary group B rats were less responsive to insulin than those of the smaller rats. A significant effect of exercise on increased production of a PDH activator in response to insulin was found only in experiments in which adipocyte plasma membranes were coincubated with mitochondria and insulin. For group B rats exercise provided no significant enhancement of insulin activation of intact adipocyte PDH or stimulation of the production of a PDH activator by liver particulate preparations. Insulin binding to fat cells was not affected by exercise. Group A rats made insulin resistant by a high-fat diet did not respond to exercise by significantly increasing the insulin stimulation of PDH activator by liver membranes. The enhancing effect of a single bout of exercise on insulin response was not readily demonstrable in rats resistant to insulin either in association with age and weight or with a high-fat diet.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1986 Jul
PMID:Effect of acute exercise on insulin generation of pyruvate dehydrogenase activator by rat liver and adipocyte plasma membranes. 352 20

Plasma glucose, insulin, glucagon and growth hormone responses to both oral glucose and iv arginine were evaluated in 15 heroin addicts and 15 control subjects matched for age, sex and weight. The heroin users had an exaggerated rise in plasma glucose concentrations following oral sugar, which persisted until the end of the study (102 +/- 5 mg/dl in addicts vs 72 +/- 3 mg/dl in controls at 240 min, p less than 0.01) and significantly lower insulin responses (insulin peak 28 +/- 4 microU/ml in addicts vs 67 +/- 8 microU/ml in controls, p less than 0.01). The inhibitory effect of glucose on glucagon concentrations was less evident in addicts than in controls. The responses of plasma glucose, insulin and glucagon to arginine were not significantly different between addicts and controls, while the growth hormone rise was significantly greater in addicts. These results demonstrate that heroin users have impaired insulin secretion to oral glucose but not to arginine and suggest that: the impaired insulin secretion in heroin addicts is not dependent on beta-cell exhaustion, and a selective inhibition of glucose-induced insulin secretion is operative in these subjects, as it happens in patients with noninsulin-dependent diabetes mellitus.
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PMID:Impaired insulin response to glucose but not to arginine in heroin addicts. 354 79

Sulfonylureas seem to have similar mechanisms of action, including an acceleration and increase of insulin secretion, an increase of the systemic availability of insulin, and probably indirectly, an increase of insulin action. Sulfonylureas may postpone the development of impaired glucose tolerance (IGT) to manifest non-insulin-dependent diabetes mellitus (NIDDM), and all NIDDM subjects should benefit from sulfonylurea treatment except those in whom insulin secretion has been attenuated. The most effective use is the combination of diet restriction and sulfonylurea introduced in NIDDM subjects soon after transition from IGT to NIDDM. A simple screening procedure has been devised to find the subjects at this early stage. Newer sulfonylureas, such as glipizide and glyburide, are more potent than the older ones, such as tolbutamide and chlorpropamide. During chronic treatment, glipizide and glyburide seem to be equally effective in reducing blood glucose levels, and they do so without causing a chronic elevation of insulin secretion, signifying that they do not increase the risk of pancreatic B cell exhaustion. Glipizide has rapid and complete absorption, as well as a rapid distribution and elimination. This may explain why it is less liable than other sulfonylureas to provoke long-lasting hypoglycemia, which is the major danger when using sulfonylureas. Despite its rapid elimination, 7.5 to 15 mg glipizide can be administered once daily without loss of therapeutic efficacy. This may be due in part to enterohepatic recirculation of the drug in response to meals. The therapeutic efficacy is increased if glipizide is received half an hour before breakfast.
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PMID:Clinical pharmacology of sulfonylureas. 354 16

The effect of the oral hypoglycemic agent methylpalmoxirate (methyl-2-tetradecylglycidate), a selective inhibitor of long-chain fatty acid oxidation, on the exercise capacity of diabetic rats was evaluated. Rats were made diabetic by injection of streptozocin (75 mg/kg i.p.), which was confirmed by 4+ glucosuria. Daily oral administration of 2.5 mg/kg for 5 days, or a single dose of 10 mg/kg, of methylpalmoxirate produced a slight, nonsignificant decrease in the ability of diabetic rats to perform strenuous exercise of an intensity that caused exhaustion in less than 30 min. The ability of diabetic rats to perform prolonged, moderately strenuous exercise of an intensity that could be maintained for more than 60 min was not affected by methylpalmoxirate treatment. Methylpalmoxirate normalized plasma glucose concentrations, with resting glucose levels reduced 71% compared with nontreated controls, and did not cause hypoglycemia during prolonged exercise to exhaustion. Hepatic glycogen content was significantly reduced in methylpalmoxirate-treated rats in the fed, resting state, and during exercise, suggesting that liver was forced to oxidize carbohydrate at the expense of carbohydrate storage. Blood ketone levels of methylpalmoxirate-treated rats were reduced by 82% at rest, and exercise-induced ketosis was prevented by drug treatment. Muscle glycogen concentration and the rate of muscle glycogen depletion during exercise were not altered by methylpalmoxirate. It appears that the liver is the major site of action of methylpalmoxirate in diabetic rats when given in low doses.
Diabetes 1986 Jul
PMID:Effects of oral hypoglycemic agent methylpalmoxirate on exercise capacity of streptozocin diabetic rats. 372 Oct 61

The effects of prior high-intensity cycle exercise (85% VO2 max) to muscular exhaustion on basal and insulin-stimulated glucose metabolism were studied in obese, insulin-resistant, and normal subjects. Six obese (30.4% fat) and six lean (14.5% fat) adult males underwent two separate, two-level hyperinsulinemic-euglycemic clamp studies (100-min infusions at 40 and 400 mU/m2/min), with and without exercise 12 h earlier. Carbohydrate oxidation was estimated by indirect calorimetry using a ventilated hood system, and endogenous glucose production by D-(3-3H)-glucose infusion. Glycogen content and glycogen synthase activity (GS %l) were measured in vastus lateralis muscle biopsies before and at the end of each insulin clamp procedure. After exercise, the obese and lean subjects had comparably low muscle glycogen concentrations (0.10 versus 0.08 mg/g protein, respectively), and equal activation of muscle GS activity (54.4 versus 45.3 GS %l, respectively). In the obese subjects, insulin-stimulated glucose disposal was increased significantly, but not totally corrected to normal. In both groups there was a comparable increase in nonoxidative glucose disposal (NOGD), whereas glucose oxidation was decreased and lipid oxidation was increased. Thus, the major effect of prior exercise was to increase insulin-stimulated glucose disposal in the obese subjects and to alter the pathways of glucose metabolism to favor NOGD and decrease glucose oxidation. No correlation was found between the exercise-induced increase in GS %l and NOGD, except in the normal subjects during maximal insulin stimulation. Thus, glycogen synthase activity does not appear to be rate-limiting for NOGD at physiologic insulin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Oct
PMID:Effects of prior high-intensity exercise on glucose metabolism in normal and insulin-resistant men. 393 Mar 21


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