Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phenomenon called paradoxical undressing has been described from 33 cases of hypothermia collected from Swedish police reports. The cases were almost evenly distributed with regard to sex, age, and geographical distribution. The cases occurred more frequently in open land although cases from town areas were also found. Most incidents were recorded from November to February at low ambient temperatures, although cases were also reported at temperatures above 0 degree C. Arteriosclerosis and chronic alcoholism were important concomitant illnesses, the latter being frequent in middle-aged men. Epilepsy, diabetes, and pregnancy were present in single cases. Ethanol and other drugs were present in 67% of the males and in 78% of the females, ethanol predominating in men and various psychotropic agents in women. The mean blood ethanol concentration in males was 0.16% and in females, 0.18%. Most frequent findings at necropsy were purple spots or discoloration on the extremities, pulmonary edema, and gastric hemorrhages. It is concluded that paradoxical undressing might be explained by changes in peripheral vasoconstriction in the deeply hypothermic person. It represents the last effort of the victim and is followed almost immediately by unconsciousness and death.
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PMID:"Paradoxical undressing" in fatal hypothermia. 54 27

Ethanol at an average blood concentration of 1 mg. per milliliter enhanced the immediate (first-phase) and prolonged (second-phase) insulin response to an intravenous glucose load in nonfasting normal human subjects. Simultaneously, the glucose disposal rate was increased and the postglucose hypoglycemia was accentuated, resulting in definite hypoglycemic symptoms in some individuals. Oral glucose tolerance was not changed by ethanol administration, but the thirty-minute blood glucose and plasma insulin values were increased, suggesting that alcohol might accelerate the absorption of glucose from the gut. Ethanol given orally during evening hours (1.5 gm. per kilogram) caused a nocturnal hyperinsulinemia and a decrease of blood glucose, but not an actual hypoglycemia. Oral glucose tolerance and plasma insulin response tested the next morning, when ethanol had disappeared from the blood, were not influenced by drinking the previous evening. The K-value of intravenous glucose was increased at this time, however. When alcohol was administered for one week at a dose corresponding to 25 per cent of daily calories and substituting for fat, both the oral and intravenous glucose tolerances were impaired in each subject but the insulin response remained unchaged. In obese nondiabetic subjects, ethanol did not potentiate the early insulin response to intravenous glucose but it increased the second phase of insulin secretion in response to sustained hyperglycemia. In contrast to conditions in nonobese subjects, the glucose disposal rate was not incresed and postglucose hypoglycemia was not accentuated by ethanol in overweight subjects. In insulin-deficient diabetic patients the absent early insulin response could not be restored by ethanol, and the late component of insulin release was little increased by alcohol infusion. Ethanol did not improve the glucose utilization of diabetic patients.
Diabetes 1975 Oct
PMID:Ethanol-induced alterations of glucose tolerance, postglucose hypoglycemia, and insulin secretion in normal, obese, and diabetic subjects. 110 Apr 61

Several autoimmune diseases have been linked to an aberrant expression of major histocompatibility complex (MHC) products Ethanol enhances Class I and Class II products on a variety of cell types, and there is evidence for an autoimmune etiology in numerous pathologies associated with alcoholism. We examined whether ethanol alters the expression of Class I and Class II MHC products on human fetal islet-like cell clusters. Incubation of islet-like clusters for 48 hr in ethanol at a starting concentration of 1.5% increased the percentage of single cells expressing Class I. The percentage of cells expressing Class II did not change, but their relative mean fluorescence increased significantly. These findings suggest that alcohol ingestion could alter MHC expression on pancreatic islet cells in vivo perhaps affecting the development of diabetes in genetically predisposed individuals. These findings also support the hypothesis that the rising incidence of type 1 diabetes seen in areas of the world where the per capita consumption of alcohol is also increasing may be a consequence of the immunological effects of alcohol intake.
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PMID:Ethanol influences class I and class II MHC antigen expression on human fetal islet-like cell clusters. 192 54

Increased gluconeogenesis has been suggested to account for all of the increase in basal glucose production in patients with non-insulin-dependent diabetes mellitus (NIDDM). We studied the effect of inhibition of gluconeogenesis with ethanol on total hepatic glucose output (HGO) in patients with NIDDM. Fourteen patients with NIDDM (mean +/- SE age 61 +/- 2 yr, fasting plasma glucose 11.4 +/- 0.8 mM; body mass index 27 +/- 1 kg/m2) were studied twice after an overnight fast, once during ethanol administration (blood ethanol approximately 12 mM) and once during saline administration. Total HGO rate was measured with [3H]glucose. Inhibition of gluconeogenesis by ethanol was followed qualitatively with [U-14C]lactate (n = 8) and [U-14C]glycerol (n = 6) as tracers. Ethanol inhibited gluconeogenesis from lactate by 71 +/- 5% (0.5 +/- 0.2 vs. 1.8 +/- 0.1 mumol glucose.kg-1.min-1, 240-300 min, P less than 0.001; ethanol vs. saline, P less than 0.001) and from glycerol by 65 +/- 6% (0.8 +/- 0.2 vs. 2.3 +/- 0.6 mumol glucose.kg.min-1, P less than 0.001). Total HGO rate remained unchanged and averaged 12.8 +/- 1.8 and 11.8 +/- 2.1 mumol.kg-1.min-1 in the saline and ethanol studies, respectively (NS). We concluded that inhibition of gluconeogenesis by ethanol does not decrease total HGO in patients with NIDDM. Our results suggest the existence of a regulatory mechanism in the liver that maintains constant total HGO despite inhibition of gluconeogenesis.
Diabetes 1991 Oct
PMID:No reduction in total hepatic glucose output by inhibition of gluconeogenesis with ethanol in NIDDM patients. 193 94

The effects of alcohol on insulin action are not yet clearly established. To assess the effects of intravenously administered ethanol on insulin mediated glucose disposal, euglycaemic clamps at 3 different plasma insulin levels and insulin receptor binding studies on circulating monocytes after alcohol infusion were performed. Ethanol infusion leads to a significant reduction of insulin mediated glucose disposal (7.08 +/- 0.4 vs 8.6 +/- 0.6 mg/Kg/min; 9.8 +/- 0.7 vs 13.4 +/- 0.7; 14.7 +/- 0.7 vs 18.1 +/- 0.7 at 33, 73 and 760 mU/m2/min insulin infusion rate respectively). Monocyte insulin-receptor binding was decreased in all the subjects from 30 to 60% after ethanol infusion. These results demonstrate that alcohol can adversely influence the insulin mediated glucose disposal.
Diabetes Res 1987 May
PMID:Alcohol impairs insulin sensitivity in normal subjects. 362 2

Methodologies for T and B lymphocyte quantitation, lymphocyte blast transformation (LBT) and carbohydrate (CHO) metabolism are important for assessing host lymphocyte response in the clinical laboratory. Modifications of methods for each of these techniques are presented. Results from studies of normal ambulatory adults, patients with diabetes mellitus, sickle cell disease and hyperlipidemia are reported. LBT of normal lymphocytes before and after ethanol exposure are examined. LBT during pregnancy is evaluated. T cell populations are abnormally high in black diabetics and decreased in patients with sickle cell anemia. B cell subpopulations are increased in patients with sickle cell anemia. LBT responses are decreased in maturity onset diabetes, during pregnancy and in patients with sickle cell disease. Ethanol in amounts attainable during human consumption results in significantly decreased LBT response. CHO metabolism (especially hexose monophosphate shunt [HMPS] and HMPS by pentose sugar recycling) is abnormal in diabetic lymphocytes. The low HMPS activity is partially reversible by treatment with prostaglandin synthetase inhibitors. Information related to lymphocytes in normal states remains to be collected by further clinical application of these techniques of quantitation and in vitro function.
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PMID:B and T lymphocytes: quantitation, function, and clinical applicability. 696 70

The effects of varying concentrations of ethanol (1, 10, and 30 mM) and its metabolites (1 mM acetate and 1 and 10 mM acetaldehyde) on insulin and glucagon secretion induced by glucose (11.1 mM) and arginine (20 mM) were studied in isolated perfused pancreas of Sprague-Dawley rats. Ethanol and its metabolites did not significantly modify basal secretion of the two hormones. Ethanol reduced glucose-induced insulin secretion by means of a dose-related effect. Arginine-induced insulin output did not seem to be influenced to any significant degree. Acetate and acetaldehyde significantly inhibited glucose and arginine-induced insulin secretion. While ethanol (10 and 30 mM ) did not modify glucagon output during arginine perfusion, acetate and acetaldehyde markedly enhanced it. The block of insulin secretion and the increased secretion of glucagon could explain the diabetogenic effect of ethanol demonstrated in vivo. The mechanism by which ethanol acts on the pancreatic beta- and alpha-cells is discussed.
Diabetes 1981 Sep
PMID:Effect of ethanol, acetaldehyde, and acetate on insulin and glucagon secretion in the perfused rat pancreas. 702 Dec 70

We have previously reported that in young men, ethanol caused acute insulin resistance, but compensatory insulin secretion prevented deterioration of glucose tolerance (1). In this study, we tested the hypothesis that elderly men, because of their pre-existing insulin resistance and compromised insulin secretory capacity, may experience worsening of their glucose tolerance after ethanol. Nine elderly men (65.7 +/- 0.8 yr, BMI 25.8 +/- 1.4 kg/m2) received ethanol (13 mmol/kg for 30 min i.v.) or saline followed 30 min later by i.v. glucose (2.8 mmol/kg for 5 min). To determine the mechanism of the ethanol effect, six of the men underwent euglycemic-hyperinsulinemic (approximately 350 pM) clamping with simultaneous infusion of ethanol or saline. Muscle biopsies were obtained before and 1 and 4 h after insulin infusion. In all nine men, glucose concentrations after i.v. glucose were higher after ethanol than after saline, whereas insulin was the same and glucose tolerance decreased by 23% (Kg 2.41 +/- 0.2 vs. 1.86 +/- 0.1%/min, P < 0.01). Ethanol reduced insulin-stimulated glucose uptake from 40.6 +/- 3.1 to 25.6 +/- 1.9 mumol.kg-1.min-1 (-37%, P < 0.05), glucose oxidation from 11.7 +/- 1.1 to 7.0 +/- 0.7 mumol.kg-1.min-1 (-33%, P < 0.01), and glucose storage from 28.7 +/- 2.4 to 18.6 +/- 1.7 mumol.kg-1.min-1 (-35%, P < 0.01). Ethanol increased muscle lactate concentration from 0.49 +/- 0.14 to 1.99 +/- 0.99 mumol/mg protein (P < 0.05), but had no effects on muscle concentration of free glucose, G-6-P, and citrate concentrations, nor did it affect muscle GS activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Jan
PMID:Effects of ethanol on carbohydrate metabolism in the elderly. 842 Aug 19

Whether urine samples used in forensic science DUI testing can be compromised by endogenous ethanol production is a recurrent and yet unresolved issue. This study first assessed unpreserved urine samples that were collected, processed, and analyzed repeatedly over 13 to 41 days using a standard gas chromatographic procedure for ethanol analysis. Despite extensive microbial growth, ethanol was not detected in any test sample. The extent of ethanol production in samples supplemented with glucose, Candida albicans, or both was determined to evaluate the potential for ethanol production in urine samples associated with pathological conditions such as urinary tract yeast infections and diabetes mellitus. Ethanol production under each of the above treatment conditions was assessed in the presence and absence of 1% sodium fluoride as a microbial suppressant. Mean ethanol concentrations were determined for unpreserved samples containing urine only (0.003 +/- 0.005 g%), urine plus yeast (0.006 +/- 0.009 g%) and urine plus glucose (0.067 +/- 0.070 g%). Unpreserved samples supplemented with both yeast and glucose attained mean ethanol concentrations of 0.164 +/- 0.057 g% (P < 0.01). Ethanol could not be detected in any corresponding duplicate samples, which were preserved with 1% sodium fluoride. A lack of ethanol production in any of the unpreserved urine samples indicates that false DUI convictions due to endogenous ethanol production are very unlikely. And while endogenous ethanol production is possible in the presence of both glucose and contaminating C. albicans, 1% sodium fluoride completely eliminated microbial fermentation.
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PMID:Efficacy of 1% sodium fluoride as a preservative in urine samples containing glucose and Candida albicans. 845 87

Ethanol consumption has been associated with glucose intolerance and insulin resistance and is suggested to be an independent risk factor in the development of non-insulin-dependent diabetes mellitus. We have investigated the long-term effects of ethanol consumption on insulin-regulated glucose transport in rat adipocytes. Male Wistar rats were fed a high-fat liquid diet containing 35% ethanol (ethanol fed) or a control diet that isocalorically substituted maltose dextrin for ethanol (ad libitum). A third group was pair fed the control diet. Basal rates of 2-deoxyglucose uptake were similar in adipocytes from all three groups. Treatment with insulin increased 2-deoxyglucose uptake in ad libitum- and pair-fed rats but did not stimulate uptake in ethanol-fed rats. Similarly, although okadaic acid increased 2-deoxyglucose uptake in pair-fed rats, it had no effect in ethanol-fed rats. GLUT-1 quantity was greater in pair-fed and ethanol-fed rats compared with ad libitum controls. GLUT-4 was decreased in ethanol-fed compared with pair-fed rats but was not different from ad libitum controls. In ad libitum- and pair-fed rats, insulin increased the translocation of GLUT-4 to the cell surface by 2.0-fold. In contrast, translocation of GLUT-4 was not observed after insulin stimulation of ethanol-fed rats, paralleling the loss of insulin-stimulated glucose uptake. In ethanol-fed rats, GLUT-4 protein quantity was negatively associated with increased Gs alpha protein and isoproterenol-stimulated adenosine 3',5'-cyclic monophosphate production. These data suggest that loss of insulin-stimulated glucose uptake in rat adipocytes after chronic ethanol feeding is at least partially due to decreased movement of GLUT-4 to the cell surface after insulin stimulation.
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PMID:Chronic ethanol feeding in a high-fat diet decreases insulin-stimulated glucose transport in rat adipocytes. 884 41


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