glycogen and Diabetic-Angiopathies

The edematogenic properties of insulin have long been documented, although they have been underestimated despite current trends toward intensive insulin therapy. Insulin treatment has been associated with weight gain, mild or moderate edema, and, rarely, generalized edema and cardiopulmonary congestion. In addition, the use in recent years of thiazolidinediones, which improve insulin sensitivity, has been associated with weight gain and peripheral edema, which can progress to pulmonary edema, particularly when thiazolidinediones are used in combination with insulin. This article attempts to raise awareness about the overlooked edematogenic action of insulin. In addition, the potential role of edema-provoking properties of insulin in the development of vascular complications in patients with diabetes is discussed.

Topics: Capillary Permeability; Diabetic Angiopathies; Drug Interactions; Edema; Glycogen; Humans; Hyperinsulinism; Hypoglycemic Agents; Insulin; Mitochondria; Sodium; Thiazolidinediones; Water-Electrolyte Balance; Weight Gain

The use of beta-blockers in diabetes mellitus has largely been restricted because of the reported adverse effects. Clinical investigations aimed at elucidating the possible reactions associated with the use of beta-blockers have disclosed no evidence of masking or signs or insulin-induced hypoglycaemia or potentiation of the insulin effect. Prolonged hypoglycaemia may develop, however, as a result of physical effort. There is no proof that during insulin-induced hypoglycaemia the concentrations of counter-regulatory hormones are depressed, but that of glycerol, a gluconeogenic precursor, is slightly diminished. Intensification of the hypertensive reaction during hypoglycaemia is less likely to occur during treatment with beta-selective blockers. In insulin-dependent diabetics receiving beta 1-blockers there is no evidence of any change - either deterioration or improvement - in metabolic control. In one small controlled trial there was no sign of impairment of the peripheral arterial circulation over a short period of administration of a non-selective beta-blocker. In general, for patients suffering from insulin-dependent diabetes, cardioselective agents are preferable. Since cardioselectivity is a dose-dependent property, reasonable caution should also be observed when using this type of drug in diabetes.

Topics: Adrenergic beta-Antagonists; Alprenolol; Blood Glucose; Catecholamines; Diabetes Mellitus, Type 1; Diabetic Angiopathies; Drug Synergism; Fatty Acids, Nonesterified; Gluconeogenesis; Glucose Tolerance Test; Glycerol; Glycogen; Humans; Hypertension; Hypoglycemia; Insulin; Lactates; Lactic Acid; Metoprolol; Oxprenolol; Propranolol

Diabetic metabolism is reflected in the fetal blood and gives rise to diabetic angiopathy in the placenta. Capillary proliferation takes place with small newly formed vessels penetrating deeply into the trophoblast. Also signs of accelerated aging are found with thickening of the capillary basement membrane. Glycogen deposit/storage seems typical of diabetic placenta together with increased fibrosis. Uncertainty exists as to the degree of maturation of the trophoblast.

Topics: Basement Membrane; Blood Glucose; Capillaries; Chorionic Villi; Diabetic Angiopathies; Endothelium; Female; Fetal Blood; Fetus; Glycogen; Humans; Maternal-Fetal Exchange; Placenta; Pregnancy; Pregnancy in Diabetics

The metabolic effects of beta-adrenoceptor blocking agents during hypoglycaemia in patients prone to hypoglycaemia are of interest as diabetics are often treated with these drugs because of hypertension or angina pectoris. Compared with non-diabetics these patients also have impaired glucose compensation after hypoglycaemia, partly secondary to deficient release of glucagon. This makes the diabetics more dependent on adrenergic mechanisms to recover from low blood glucose concentrations. Non-selective beta-adrenoceptor blockade (propranolol) significantly impairs the glucose recovery rate after hypoglycaemia in insulin dependent diabetics, whereas selective beta-adrenoceptor blockade (metoprolol) does not have this side effect. The mechanism of the effect of propranolol is probably an attenuation of the gluconeogenesis secondary to deficient release of the important gluconeogenic substrates lactate and glycerol.

Topics: Adrenergic beta-Antagonists; Blood Glucose; Diabetes Mellitus, Type 1; Diabetic Angiopathies; Glucagon; Gluconeogenesis; Glycerol; Glycogen; Humans; Hypertension; Hypoglycemia; Insulin; Lactates; Lactic Acid; Liver; Metoprolol; Propranolol

The pathologies of diabetic micro- and macroangiopathy are different, suggesting that diabetes affects these two types of vascular tissue in a dissimilar manner. We have compared insulin receptors and the effects of insulin on cultured endothelium from calf retinal capillaries and aorta, and the vascular supporting cells, retinal pericytes, and aortic smooth muscle cells. 125I-insulin binds to high affinity insulin receptors on all four cell types. Receptor concentrations were similar except for aortic smooth muscle cells, which have 10-fold fewer receptors than the other cell types. Insulin at a concentration of 10 ng/ml stimulated [14C]glucose incorporation into glycogen in retinal endothelial cells and pericytes and aortic smooth muscle cells, but had no effect on aortic endothelium. Insulin over a concentration range of 10 ng/ml-10 microgram/ml, stimulated [3H]thymidine incorporation into the DNA of retinal pericytes, and endothelial cells and aortic smooth muscle cells but had no effect on aortic endothelial cells. These data suggested that a differential response to insulin may exist between endothelium of micro- and macrovasculature, and suggest that retinal capillary endothelium and retinal pericytes are both very insulin-sensitive tissues.

Topics: Animals; Aorta; Cattle; Diabetes Mellitus, Experimental; Diabetic Angiopathies; Diabetic Retinopathy; DNA; Endothelium; Glucose; Glycogen; Humans; Insulin; Muscle, Smooth, Vascular; Receptor, Insulin; Thymidine

Investigations on carbonhydrates were carried out with special regard to acid mucopolysaccharides and glycogen. The fluorescence-microscopical proof of acid micropolysaccharides with acridinorange (pH=3,3) and by means of the pseudoisocyanin-reaction (proof of-SO3H-groups) gave positive results on elastic membranes of blood vessels. These results were correlating to the increase of the diabetes mellitus. Healthy Wistar-rats did not show metachromasia with toluidinblue in the walls of the blood vessels, whereas in streptozotocin-diabetes there was strong metachromasia shown by these structures. The stages of diabetes in man were also correlated to an increase of metachromasia. The PAS-reaction, the staining with Best's carmine and the reaction with alizarinblue S for the proof of glycogen were positive in all blood vessels investigated.

Topics: Animals; Arteries; Carbohydrates; Diabetes Mellitus; Diabetic Angiopathies; Elastic Tissue; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Rats; Streptozocin

Topics: Basement Membrane; Capillaries; Cytoplasm; Diabetes Mellitus; Diabetic Angiopathies; Glycogen; Histocytochemistry; Humans; Lymphocytes; Staining and Labeling

Topics: Blood Cell Count; Carbohydrate Metabolism; Diabetes Mellitus; Diabetic Angiopathies; Female; Glycogen; Histocytochemistry; Humans; Lymphocytes; Methods