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

The relationship between metabolic control and glycogen lymphocyte content in diabetes mellitus, was studied. 30 insulin-treated and 30 type II diabetic subjects were evaluated with 40 age and sex matched normal controls. Glycaemic control was evaluated by a fasting and 2 h post-prandial plasma glucose and by glycosylated hemoglobin (GHb). Glycogen lymphocyte content was determined by calculation of the PAS-positive Index of the lymphocytes (PIL) according to Skrabalo. While fasting and post-prandial plasma glucose values were significantly higher in insulin-treated than in type II diabetes (p less than 0.001), no differences in GHb values were observed between the two groups (10.31 +/- 0.23% vs 9.80 +/- 0.36%). The mean PIL values were not different in these two groups (0.11 +/- 0.01 vs 0.12 +/- 0.02), but they were significantly higher when compared with control values (0.03 +/- 0.004, p less than 0.001), PIL was positively correlated with GHb in both insulin-treated (r = 0.76, p less than 0.001) and type II diabetes (r = 0.55, p less than 0.001). A correlation between PIL and plasma glucose values was observed only in the insulin-treated group and was weaker (p less than 0.005). No correlation was observed between glycogen lymphocyte content and glucose tolerance in the control group. These data confirm that diabetes mellitus is characterized by a significant increase of PAS-positive lymphocyte content and that it correlates well with glycaemic control.
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PMID:P.A.S. positive index of lymphocytes and metabolic control in insulin-treated and type II diabetes mellitus. 665 56

A radioimmunoassay specific for liver pyruvate kinase was used to determine the mechanism(s) involved in the insulin stimulation of this enzyme activity in chronically diabetic rats. Rats, made diabetic with alloxan, were fed on a high-carbohydrate (50%-sucrose) fat-free diet and treated with insulin for 12, 36 or 60 h. Livers were removed at the various times, a piece was kept for determination of glycogen, and the remainder was homogenized. The 100000 g supernatant was prepared and used for determination of pyruvate kinase activity and quantity. Glycogen increased to a maximum of approx. 7% by 12 h after insulin treatment, and was maintained at this elevated value for 60 h. Liver pyruvate kinase activity, which is depressed in diabetes, did not respond to insulin until 36 h of treatment, with a more substantial increase occurring by 60 h. Radioimmunoassay data indicated that the increase in activity was concomitant with a substantial increase in the quantity of the enzyme and a moderate increase in its specific activity. These results demonstrate that a dual mechanism, i.e. an increase in both the quantity and specific activity of the enzyme, regulates the insulin-mediated stimulation of liver pyruvate kinase in the diabetic rat.
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PMID:Insulin mediates the stimulation of pyruvate kinase by a dual mechanism. 676 Aug 59

In the islets of the rat pancreas, steroid diabetes induced by triamcinolon-acetonid leads to degranulation of the B cells and glycogen infiltration. The glycogen cannot be satisfactorily detected using methods like the chromic acid technique according to Bauer, staining with Best's carmine, or the usually applied periodic acid-Schiff (PAS) reaction. Glycogen detection is improved, however, when lead tetraacetate is used in place of periodic acid as oxidizing agent. When combining the carbohydrate detection method with the peroxidase--antiperoxidase (PAP) method used for immunocytochemical detection of the various pancreatic islet hormones, paraffin sections reveal that glycogen is primarily localized in granulated B cells; the degranulated B cells also contain glycogen, though in smaller amounts. In contrast, the islet cells containing somatostatin, glucagon and pancreatic polypeptide are nearly free of glycogen.
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PMID:Glycogen in pancreatic islets of steroid diabetic rats. Carbohydrate histochemical detection and localization using an immunocytochemical technique. 703 7

Electron microscopy of streptozotocin diabetic rat eyes showed increased intracellular levels of tonofilaments and glycogen, thickenings and infoldings of subepithelial basement membrane and basal cell degeneration after 8 months. Glycogen, glucose, sorbitol, and fructose were measured in corneal epithelium from short- and long-term diabetic rats. The small increase in sorbitol pathway products which were found after 8 months of diabetes (less than 1.0 mosm/1 tissue water) confirmed similar findings in rabbits and humans. Thus, the morphologic changes occur in the absence of significant accumulation of sorbitol pathway products. Osmotic damage secondary to corneal epithelial cell accumulation of sorbitol is probably not a significant factor in corneal epithelial diabetic disease.
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PMID:Corneal epithelial changes in diabetic rats. 713 21

Tibial nerves of streptozotocin-diabetic, alloxan-diabetic, and age-matched control rats were examined at 2 weeks and 2, 4, 8, and 12 months following the induction of diabetes. Glycogen-like granules accumulated within perineurial and Schwann cells of only the diabetic animals. This accumulation may reflect a metabolic abnormality in these cells which could account for the reduced conduction velocities seen in the peripheral nerves of these same diabetic rats (Moore et al. 1980a). Glycogen-like granules were also present and increased with age in myelinated axons of both diabetic and control rats. Quantitative data suggest that axonal accumulation of glycogen-like granules is related to aging or injury related phenomena to which diabetic axons may be more susceptible.
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PMID:Glycogen accumulation in tibial nerves of experimentally diabetic and aging control rats. 731 Apr 36

The levels of isometric developed tension (IDT) in portal veins from starved and diabetic rats in glucose medium were of the same magnitude but significantly reduced compared with veins from normal rats. Glucose removal led to contractile depression, more marked in starved veins (-74%; p < 0.001 vs. diabetics and normals). Addition of glucose, pyruvate, acetate, lactate, or butyrate counteracted this depression in all groups but in diabetics butyrate significantly stimulated IDT over controls whereas in starved veins lactate overcame IDT reduction only partially. Added insulin significantly enhanced contractile recovery with glucose in normal and diabetic preparations but was ineffective in starved veins. Glycogen content was significantly lower in diabetics; however, in no group did changes occur in incubated veins as compared with unincubated ones. Glycerol production was significantly higher in diabetic veins. It would appear that, although experimental diabetes induces a shift to fatty acid utilization, aerobic glycolysis and mitochondrial respiration are somehow preserved as reflected by the IDT recovery with pyruvate or lactate.
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PMID:Alterations induced by alloxan-diabetes and starvation on functional activity of the rat portal vein perfused in vitro. 742 91

Glycogen metabolism is a complex process which depends on the metabolic circumstances and the hormonal milieu. In this overview an intriguing new possibility has been emphasized--the possible central role of lactate in coordinating, with glucose, the net synthesis of glycogen. Since lactate changes acutely under many physiological circumstances, it would be a logical candidate for a signal which communicates to the liver the metabolic states of the periphery. It would then acutely determine the synthetic rate of glycogen synthesis within the range determined by the glucose concentrations which in turn could be said to reflect the nutritional state of the system. Interestingly, after oral glucose loading, portal glucose levels would be about 25% higher (Radziuk et al., 1978) relative to arterial. As seen from Figs 8 and 9 however the glycogen synthetic rate appears very sensitive to glucose (at a given lactate uptake). Everything else being assumed equal therefore, more glycogen would be synthesized than during intravenous loading with an equivalent peripheral concentration. This is indeed the case (Shulman and Rossetti, 1989). On the other hand, during equivalent loads, peripheral glucose levels are higher and the same quantity of glycogen is synthesized (Radziuk, 1989a, 1989b). If lactate is typical of other glucogenic substrates, then it is also logical that mixed meals with higher levels of portal substrate would maximize glycogen synthetic rates. Similarly, in diabetes where hyperglycemia and hyperlactatemia prevail, gluconeogenesis plays a predominant role in glycogen synthesis (Giaccari and Rossetti, 1992).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substrates and the regulation of hepatic glycogen metabolism. 824 86

Seven non-insulin-dependent diabetes mellitus (NIDDM) patients participated in three clamp studies performed with [3-3H]- and [U-14C]glucose and indirect calorimetry: study I, euglycemic (5.2 +/- 0.1 mM) insulin (269 +/- 39 pM) clamp; study II, hyperglycemic (14.9 +/- 1.2 mM) insulin (259 +/- 19 pM) clamp; study III, euglycemic (5.5 +/- 0.3 mM) hyperinsulinemic (1650 +/- 529 pM) clamp. Seven control subjects received a euglycemic (5.1 +/- 0.2 mM) insulin (258 +/- 24 pM) clamp. Glycolysis and glucose oxidation were quantitated from the rate of appearance of 3H2O and 14CO2; glycogen synthesis was calculated as the difference between body glucose disposal and glycolysis. In study I, glucose uptake was decreased by 54% in NIDDM vs. controls. Glycolysis, glycogen synthesis, and glucose oxidation were reduced in NIDDM patients (P < 0.05-0.001). Nonoxidative glycolysis and lipid oxidation were higher. In studies II and III, glucose uptake in NIDDM was equal to controls (40.7 +/- 2.1 and 40.7 +/- 1.7 mumol/min.kg fat-free mass, respectively). In study II, glycolysis, but not glucose oxidation, was normal (P < 0.01 vs. controls). Nonoxidative glycolysis remained higher (P < 0.05). Glycogen deposition increased (P < 0.05 vs. study I), and lipid oxidation remained higher (P < 0.01). In study III, hyperinsulinemia normalized glycogen formation, glycolysis, and lipid oxidation but did not normalize the elevated nonoxidative glycolysis or the decreased glucose oxidation. Lipid oxidation and glycolysis (r = -0.65; P < 0.01), and glucose oxidation (r = -0.75; P < 0.01) were inversely correlated. In conclusion, in NIDDM: (a) insulin resistance involves glycolysis, glycogen synthesis, and glucose oxidation; (b) hyperglycemia and hyperinsulinemia can normalize total body glucose uptake; (c) marked hyperinsulinemia normalizes glycogen synthesis and total flux through glycolysis, but does not restore a normal distribution between oxidation and nonoxidative glycolysis; (d) hyperglycemia cannot overcome the defects in glucose oxidation and nonoxidative glycolysis; (e) lipid oxidation is elevated and is suppressed only with hyperinsulinemia.
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PMID:Characterization of cellular defects of insulin action in type 2 (non-insulin-dependent) diabetes mellitus. 843 57

Statistical studies repeatedly have shown an association between systemic insulin resistance and a preponderance of highly glycolytic, relatively insulin-insensitive muscle fibers as well as a low density of muscle capillaries. The nature of the relationship between these observations is, however, not clear. Female rats were made hyperinsulinemic for 7 days by implantation of osmotic minipumps. Elevated adrenergic activity and secretion of glucocorticoids were controlled by another minipump with propranolol and adrenalectomy was controlled with glucocorticoid substitution. This resulted in hyperinsulinemia and moderate hypoglycemia, the latter probably counteracted by overeating and increased glucagon secretion, as indicated by increased body weight and lower liver glycogen contents, respectively. Systemic insulin sensitivity was increased and measured with a hyperinsulinemic-euglycemic clamp technique. This was paralleled by an elevated glucose utilization estimated as uptake of 2-deoxyglucose in parametrial, retroperitoneal, and inguinal adipose tissues and the soleus and extensor digitorum longus muscles. Glycogen synthesis was also elevated in the soleus muscle. Muscle fiber composition changed with hyperinsulinemia and elevated 2-deoxyglucose uptake toward more fast-twitch, type II, particularly type IIb fibers, whereas the proportion of slow-twitch, type I fibers, diminished. Capillary density was elevated per unit muscle surface area as well as per muscle fiber. This was paralleled by increased insulin sensitivity systemically and in muscles. These results suggest that muscle fiber composition alterations may be a consequence rather than a cause of hyperinsulinemia and that capillarization rather than fiber composition is of importance for insulin sensitivity in muscle.
Diabetes 1993 Jul
PMID:Effects of hyperinsulinemia on muscle fiber composition and capitalization in rats. 851 74

Glycogen synthesis is impaired in first degree relatives of subjects with non-insulin-dependent diabetes mellitus and genes relevant to this metabolic pathway are considered reasonable candidates in the pathogenesis of the disease. In skeletal muscle the de novo synthesis of glycogen in primed by an enzyme named glycogenin. We have cloned the glycogenin cDNA from human skeletal muscle mRNA: human glucogenin is a 333 amino acid protein exhibiting 93% identity with rabbit glycogenin. A single transcript of about 2.4 kb, prominent in skeletal muscle, was detected by Northern blot analysis. In situ hybridization unequivocally located the human glycogenin gene to chromosome 3q25.1. Furthermore, we mapped two intronless glycogenin-related sequences to human chromosomes 12 and 13.
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PMID:The human skeletal muscle glycogenin gene: cDNA, tissue expression and chromosomal localization. 860 61


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