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

We have examined the possibility that 125I-insulin binding by isolated rat hepatocytes is modulated by cellular ATP levels. To avoid complications due to ATP-dependent internalization of bound insulin, 125I-insulin binding was determined at 10 degrees C; at this temperature, equilibrium binding was achieved after incubation for 4-6 h. When hepatocytes were incubated at 37 degrees C under anaerobic conditions, ATP levels and 125I-insulin binding were both lowered by about 65%. Anoxia inhibited the association of 125I-insulin with the hepatocyte receptor; the dissociation of insulin from hepatocytes was not affected. Cellular ATP levels and 125I-insulin binding were both restored when anaerobic cells were incubated further at 37 degrees C under aerobic conditions. When anaerobic cells were incubated in air at 10 degrees C during the insulin binding assay, 125I-insulin binding recovered completely, but ATP levels were unaffected. The inhibitory effect of anoxia on 125I-insulin binding was not due to any effect on 125I-insulin degradation or on cell viability. We conclude (1) that the ability of hepatocytes to bind insulin can be modulated on a short-term basis in response to the metabolic status of the cell, and (2) that modulation of the liver cell insulin receptor is not a function of cellular ATP levels.
Diabetes Res Clin Pract 1986 Apr
PMID:Inhibitory effect of anoxia on 125I-insulin binding by rat hepatocytes. 352 46

An isolated perfused working rat heart preparation was used to assess the effect of alloxan-induced diabetes on myocardial performance. Ventricular performance was assessed under different aortic afterload, isoproterenol-stimulated and anoxic conditions. Basal left ventricular pressure development and rate of rise of ventricular pressure were depressed in hearts from diabetic animals. Neither coronary flow nor cardiac output were affected by diabetes. The dose and temporal responses to an infusion of isoproterenol were unaltered in diabetic hearts. Isoproterenol increased coronary flow by 50% and elevated ventricular pressure, dP/dt, and cardiac output by two- to threefold. Anoxia depressed ventricular pressure to below 20% of control within 5 min in both diabetic and normal hearts. Reoxygenation after 10 min of anoxia produced equivalent recovery in both groups working against a 52-mmHg aortic afterload, whereas recovery after 20 or 30 min of anoxia, was depressed in diabetic hearts. Elevating aortic afterload decreased performance of diabetic hearts and decreased their ability to recover from a 10-min anoxic exposure. Many of these observed differences in mechanical performance of diabetic hearts can be overcome by high glucose or insulin in the perfusion media.
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PMID:Performance of diabetic rat hearts: effects of anoxia and increased work. 700 27

Metabolism of ascorbic acid is deranged in Diabetes Mellitus (DM). One important reason of this derangement is its increased turnover in the process of handling an increased load of free radicals. Anoxia, the triggering factor in the pathogenesis of diabetic retinopathy generates free radicals in anoxia-reperfusion sequence. Any process like argon laser photocoagulation that destroys the anoxic sites and improves oxygenation in retina might hinder the process of generation of free radicals and thus expected to preserve ascorbic acid. In this study plasma total ascorbic acid concentration in matched groups of (I) diabetics with retinopathy with no history of photocoagulation (II) diabetics with retinopathy treated by laser and (III) diabetics without microvascular pathology were measured by 2-4 dinitrophenyl hydrazine method. Plasma total ascorbate concentration was significantly higher in group-II (0.47 +/- 0.09 mg/dl; X +/- SD) in comparison to group-I (0.19 +/- 0.07 mg/dl P < 0.001). The concentration was not significant between group-II and group-III (0.49 +/- 0.06 mg/dl; P = 0.40). Other clinical and metabolic parameters were not significantly different in between the groups. This observation leads to speculation that photocoagulation saves ascorbic acid from excessive turnover in anoxic retina in the process of handling free radicals.
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PMID:Comparison of plasma ascorbate status between diabetic retinopathy subjects with and without photo-coagulation therapy. 816 33

Fetal growth retardation is a result of a complex pathology caused by multiple factors of fetal, placental, and maternal origin. Hormones and growth factors released as a result of maternal-fetal physiological interactions play an importance role in fetal well being and fetal outcome. Intrauterine Growth Retardation (IUGR) is associated with significant perinatal and childhood morbidity. It is estimated that 13.7 million infants are born annually with IUGR, comprising 11% of all births in developing countries. Both maternal malnutrition and anemia are associated with various degrees of fetal growth retardation. The relationship between decreasing birth weight percentiles and increasing fetal morbidity and mortality has been demonstrated by several investigators and epidemiological studies suggest that IUGR is a significant risk factor for the subsequent development of chronic hypertension, ischemic heart disease, diabetes, and obstructive lung disease in adult life (Barker's Hypothesis). Maternal anemia and/or malnutrition are recognized to be the most frequent cause of IUGR and SGA birth in developing countries like India. In order to investigate adaptive mechanisms by the fetus to overcome the growth disadvantage caused due to maternal nutritional limitations, we examined the quantitative variations in hormonal and growth factor profiles in paired cord blood and maternal samples obtained from neonates born to malnourished and/or anemic mothers. The results of our study show that: 1) The percentage of small for gestational age (SGA) neonates born to malnourished and anemic mothers was significantly higher than those born to mothers who were either malnourished or anemic; 2) Significantly higher levels of GH, PRL, HPL and IGF-1 were observed in the cord blood of neonates born to malnourished and anemic mothers indicative of an adaptive response on part of the fetus to over come an in-utero growth disadvantage; 3) The anoxemia-related fetal perturbations may have unique features that make them distinct from nutrient deficiency-related IUGR. Thus, these novel observations are relevant to the context of the ongoing scientific debate on Barker's hypothesis.
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PMID:Effect of maternal malnutrition and anemia on the endocrine regulation of fetal growth. 1547 29