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

Endogeneous hyperglucagonemia is observed in experimental diabetes mellitus and semistarvation, conditions associated with an increased intestinal absorptive function. To examine whether glucagon might exert a similar adaptive response on intestinal digestive-absorptive function like experimental diabetes mellitus the effect of chronic glucagon administration on intestinal transport of 3-0-methyl-D-glucose, water, sodium, potassium, and D-glucose induced transmural potential difference (PD) was examined by an in vivo perfusion technique in rat small intestine. Chronic administration of glucagon (100 mug twice daily) for 5 days resulted in increased absorption of 3-0-methyl-D-glucose, water, sodium and potassium as well as in an increase of D-glucose induced PD. A similar, but more pronounced augmentation of D-glucose induced PD was observed in the jejunum of streptozotocin-diabetic rats. Disaccharidase (maltase, sucrase, trehalase, lactase) and alkaline phosphatase activities were not affected in intestinal mucosa of glucagon-treated rats compared to controls. It cannot be decided from these results whether hyperglucagonemia is responsible for the adaptive intestinal changes observed in experimental diabetes mellitus.
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PMID:Effect of chronic glucagon-administration on the digestive and absorptive function of rat small intestine in vivo. 98 1

By means of a glucose-controlled insulin- and glucose-infusion system (GCIGIS) we examined the effect of somatostatin on insulin and glucose requirements following meals or oral glucose loads in juvenile diabetics. In six of seven patients the insulin requirement with somatostatin was remarkably reduced to between 38 per cent and 79 per cent of that of otherwise identical control experiments. No reduction could be found in the seventh case, fed only 575 kcal. In all cases we observed an increase in dextrose demanded from the GCIGIS ranging between 28 per cent and 192 per cent of the control amounts. In addition, a lowering and smoothing of postprandial blood glucose curves caused by somatostatin application was a general finding. It seems to us most likely that the well-known suppression of the secretion of growth hormone and glucagon, both insulin antagonists, is responsible for the antidiabetic action of somatostatin.
Diabetes 1975 Nov
PMID:Antidiabetic action of somatostatin--assessed by the artificial pancreas. 110 69

Glomerular basement membrane (GBM) and tubular basement membrane (TBM) were prepared from human kidneys of diabetics and non-diabetics, and their chemical composition was compared. GBM from diabetics contained a larger amount of hydroxyproline than that from non-diabetics, and smaller amounts of half-cystine, glucose, mannose and sialic acid. On the other hand, TBM from diabetics contained larger amounts of hydroxylysine, methionine, galactose, hexosamine and phospholipid phosphorus than non-diabetics, and smaller amounts of half-cystine, valine, leucine, lysine and histidine. No significant difference was observed in the contents of other components examined in this study between the corresponding membrane obtained from diabetics and non-diabetics. The observed changes may be due to alteration of the tissues in diabetes mellitus.
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PMID:Comparison of the chemical composition of glomerular and tubular basement membranes obtained from human kidneys of diabetics and non-diabetics. 113 45

In vivo studies were undertaken in rats to provide evidence of the neural nature, tentative localization and mode of excitation of the insulin-sensitive central nervous system (CSN) glucoregulator center. In rats under light barbiturate anesthesia minute amounts of insulin injected into the carotid artery resulted in an immediate decrease of the systemic blood sugar. This hypoglycemic action of regional insulinzation of the CSN was lost when the animals were subjected to prolonged, deep barbiturate narcosis. Competitive inhibition of glucose utilization in the CSN region by intracarotid administration of 2-deoxy-D-glucose did not block the systemic hypoglycemic effect of subsequent intracarotid insulin injection. Chronic endogenous hyperinsulinemia produced by daily growth hormone treatment resulted in an insensitivity of the CNS glucoregulator center to exogenous insulin. The ratio of the quantity of the injected insulin and the pre-existent plasma insulin concentration showed direct correlation with the systemic hypoglycemic response that followed intracarotid injection. Present data support the hypothesis that the insulin-sensitive glucoregulator center located in the area supplied by the carotid artery is neural in nature, because of its inhibition by barbiturate anesthesia. The data are compatable with the working hypothesis that the center is located in the hypothalamus, since light cortical barbiturate anesthesia did not, but deep anesthesia did have an inhibitory effect on it. Marked interference by chronic hyperinsulinemia suggests that the receptor center estimates the metabolic status of the animal through means related to physicochemical binding of insulin to specific receptors. However, since our attempt to inhibit glucose utilization in the CNS was without effect on the activity of the center, it appears that the singal for the glucoregulatory impulse is not insulin facilitation of glucose utilization in the receptor area, but another parameter of insulin action.
Diabetes 1975 Apr
PMID:Studies on the nature and mode of action of the insulin-sensitive glucoregulator receptor in the central nervous system. 113

The efficacy of alpha and beta-D-glucose in causing insulin release and suppressing glucagon release from the isolated perfused rat pancreas was tested. In order to allow simultaneous assessment of glucose effect on both alpha and beta-cells, the pancreas was continually perfused with a physiological amino acid mixture (10 mM) which provokes glucagon secretion and also stimulates the beta-cells, provided glucose is present. Under these conditions the alpha-anomer of D-glucose at 3 and 6 mM proved significantly more potent than the beta-anomer in inducing insulin release and in inhibiting glucagon secretion. These data lend further support to the concept that alpha-cells and beta-cells contain glucoreceptors controlling glucagon and insulin seckretion and show that certain physiochemical properties of these receptors are alike in both types of cells.
Diabetes 1975 Apr
PMID:Differential effects of alpha- and beta-D- glucose on insulin and glucagon secretion from the isolated perfused rat pancreas. 113 3

1. The in vitro transport of 3-0-methyl-D-glucose was measured in the small intestine of obses-hyperglycemic (ob/ob) mice and their lean littermates, fed or fasted for 48 hrs. 2. Transport was much increased in the jejunum of obese animals and, to a lesser extent, in obese mice on a chronic restricted diet. 3. Kinetic studies indicate that the Vmax of transport was significantly greater in obese than in lean mice, whether fed or fasting. Fasting increase the Vmax in lean but not in obese animals. These changes were more prominent in the jejunum. The apparent Km of transport was the same in all four groups. 4. These findings are discussed in relation to the increase in intestinal absorptive functions in diabetes and in some conditions of food restriction or starvation. The results are consistent with the hypothesis that the effects of diabetes and of starvation on intestinal sugar transport reflect an alteration in the same controlling factor.
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PMID:Sugar transport in the small intestine of obese hyperglycemic, fed and fasted mice. 118 64

Free and protein-bound serum sugars and serum lipids were analyzed in 65 adult diabetic patients, 10 age-matched controls, and 24 male medical students for correlation of carbohydrate changes with the extent of retinal, renal, and cardiovascular disease. In diabetic sera, both protein-bound sugars and free mannose, fucose, and hexosamine were significantly elevated; free galactose and inositol were elevated in some diabetic patients, and essentially undetectable in sera from controls. Serum triglycerides and pre-beta-lipoproteins were also elevated in diabetics, but alpha-lipoproteins decreased. Although no specific relationships were observed with the extent of retinal and renal disease, bivariate analyses by Pearson coefficients of correlation showed correlations between levels of serum-free mannose and systolic blood pressure, free hexosamine and duration of diabetes, and serum protein-bound fucose and age. Serum triglycerides and pre-beta-lipoprotein levels correlated with insulin therapy. These are preliminary leads of laboratory studies related to carbohydrate macromolecular changes which might aid in a better understanding of the cardiovascular complications associated with diabetes.
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PMID:Serum-free and protein-bound sugars and cardiovascular complications in diabetes mellitus. 124 17

Human umbilical vein endothelial cells (HUVEC) cultured in high glucose exhibit delayed replication and colchicine-resistant microtubules. Tubulin dysfunction and stabilization, brought about by acetylation of the NH2-terminal residues, loss of the C-terminal tyrosine and binding of microtubular-associated proteins (MAPs) may be involved in the above phenomenon. The effects of L-tyrosine on HUVEC replication in high glucose were tested and the hypothesis that non-enzymatic glycosylation might impair tubulin depolymerization was also checked by growing the cells in the presence of L-glucose, which binds to intracellular proteins but remains metabolically inactive. After 18 days in culture, the number (mean +/- SEM, n = 7) of HUVEC grown in 28.0 mmol/l D-glucose (435.7 +/- 59.1 x 10(3)) was lower than in 5.6 mmol/l D-glucose (818.3 +/- 75.2 x 10(3)), p < 0.0001. The addition of L-tyrosine 1.7 mmol/l corrected such growth inhibition (623.3 +/- 81.7 x 10(3)), p < 0.0001 vs. D-glucose 28.0 mmol/l, but the cells recovered were less numerous than in physiological glucose alone (p = 0.016). The addition of L-tyrosine to D-glucose 5.6 mmol/l (731.0 +/- 63.2 x 10(3)) did not modify the cell number significantly. HUVEC in extra L-glucose (687.4 +/- 72.0 x 10(3)) were less numerous than in 5.6 mmol/l D-glucose, p = 0.028, but more than in D-glucose 28 mmol/l, p < 0.0001, and were not modified by the addition of L-tyrosine (729.4 +/- 67.1 x 10(3)). HUVEC grown in physiologic and high glucose exhibited specific immunofluorescence for acetylated tubulin and MAPs.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1992 Feb
PMID:Delayed replication of human umbilical vein endothelial cells in high glucose is corrected by L-tyrosine. 128 44

The significance of 3HOH generation by cells exposed to D-[2-3H]glucose is reevaluated. It is proposed that such a metabolic variable, rather than being taken as an index of D-glucose phosphorylation, may provide information on the extent of D-glucose 6-phosphate and D-fructose 6-phosphate interconversion in the reaction catalyzed by phosphoglucoisomerase. In order to reach such an information, the total production of 3HOH from D-[2-3H]glucose needs to be corrected for that attributable to either the catabolism of D-[1-3H]fructose 1,6-bisphosphate or the circulation of D-[2-3H]glucose 6-phosphate in the pentose phosphate pathway. A method is introduced which allows for such a correction.
Diabetes Res 1992 Mar
PMID:Significance of 3HOH generation from D-[2-3H]glucose. 128 49

Patients with diabetes often develop complications involving collagen-containing connective tissues. Previous in vitro studies have demonstrated that glucose inhibits collagen fibril formation and subsequent cross-linking. Collagen with diminished cross-linking is more susceptible to collagenolytic degradation. This may underlie the decreased collagen levels. To test this hypothesis, D-glucose and its two analogs, L-glucose and 2-deoxy-D-glucose, were used in chick calvaria organ cultures to examine parameters of collagen metabolism. L-Glucose is not used by the cell and functions as an extracellular glucose-like molecule, while 2-deoxy-D-glucose inhibits normal D-glucose uptake by blockading the glucose transport mechanism. Each of these three sugars had the ability to inhibit collagen fibril formation. D-Glucose stimulated collagen synthesis; L-glucose had no effect; and deoxyglucose inhibited collagen synthesis. D-Glucose was able to reverse the inhibitory effect of deoxyglucose. D-Glucose did not change levels of degradation of newly synthesized collagen while both L-glucose and deoxyglucose stimulated collagen degradation. When glucose transport was inhibited by deoxyglucose, collagen degradation was further enhanced. We suggest that decreased collagen levels in the connective tissues of diabetics may result from a combination of inhibition of collagen fibril formation and subsequent cross-linking, as well as increased collagen degradation.
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PMID:Glucose and glucose analogs modulate collagen metabolism. 128 72


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