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Biomedical subjects

A S Reddi

Publications and source records attributed to A S Reddi.

70 records · Page 4Linked to original sources
PubMed1978

Diabetic microangiopathy. I. Current status of the chemistry and metabolism of the glomerular basement membrane.

In recent years, the nature of the renal glomerular basement membrane has been the subject of numerous investigations. In diabetes mellitus, the renal glomerulus is characterized primarily by thickening of the basement membrane and excessive accumulation of basement membrane-like material in the mesangial region. Compositional analyses have shown that basement membranes are glycoprotein in nature. Studies of the glomerular basement membranes in diabetes have indicated a change from normal chemical composition. Furthermore, studies of the metabolism of diabetic kidneys in experimental animals, using cortical homogenates and isolated glomeruli, have demonstrated higher anabolic and lower catabolic enzyme activities. However, contradictory data have been reported with regard to both the chemical composition and metabolism of the kidney in human and experimental diabetes. This review attempts to examine these reports in detail and discuss the possible causes for these discrepancies.

Amino Acids↗
PubMed1976

Elevated kidney glucosyltransferase activity in genetic prediabetic mice.

Glucosyltransferase activity in the renal cortex of genetic diabetic KK mice was significantly increased at 40 days of age when compared to that of Swiss albino and F1 hybrid mice. This increase in enzyme activity in the absence of glucose intolerance can be regarded as an earlier genetic marker for the diagnosis of diabetic microangiopathy.

Age Factors↗
PubMed1976

Effect of pregnancy on serum alanine concentration in normal and genetically diabetic mice.

Serum alanine concentration was determined in nonpregnant and pregnant normal control Swiss albino (SA) and genetically diabetic KK mice. The serum alanine levels were significantly lower in nonpregnant KK than in nonpregnant SA mice. Fasting elicited hypoglycemia, hypoinsulinemia and hypoalaninemia in both groups of pregnant mice. Oral administration of alanine in nonpregnant and pregnant mice resulted in a significant rise in blood sugar levels within 15 min in both groups. However, the initial blood sugar response to oral alanine was greater in pregnant than in nonpregnant mice. This increase in blood sugar response to exogenous alanine appears to be mediated by glucagon. The data suggest that pregnancy elicits hypoglycemia, hypoinsulinemia and hypoalaninemia in both nondiabetic and diabetic mice.

Alanine↗
PubMed1975

Pre- and postnatal distribution of lipids in the liver of genetic diabetic mice.

Triglycerides, phospholipids, cholesterol and cholesterol esters were determined by thin layer chromatography in the fetal and neonate livers of normal (Swiss albino) and genetic diabetic (KK) mice. In general, the lipids were elevated in the fetal liver of the KK mice. Despite this elevation in liver lipids, no increase in the weight of the newborn was observed.

Age Factors↗
PubMed1975

Prolonged fasting in mice: a more sensitive approach to genetic diabetes.

Effects of two different periods of fasting were studied on glucose tolerance and insulin response to glucose in genetically diabetic KK and nondiabetic C57BL/6J mice. Blood sugar levels of the KK mice did not differ markedly from those of the C57BL/6J mice at the fed state or after 8 h fasting. They were, however, significantly higher in the KK mice when fasted for 18 h. The serum IRI levels, which were at least twice as high in the KK mice, decreased more markedly after 18 h fasting. The KK mice showed impaired glucose tolerance after 8 h fasting, which became more pronounced after 18 h fasting. The insulin response to glucose in the KK mice was not altered after an 8-hour fast; it was, however, diminished greatly after an 18-hour fast. These data suggest that prolonged fasting is necessary to detect the diabetic traits in the KK mice. The C57BL/6J mice showed neither impaired glucose tolerance nor diminished insulin response to glucose at both periods of fasting. Studies with the F1 hybrids (KK male X C57BL/6J female), which carry half of the diabetic genes, suggest that the mode of inheritance of diabetes in the KK mice might be polygenic.

Animals↗
PubMedDate not supplied

Long-term effects of antihypertensive treatment and good glycemic control on plasma lipids in diabetic rats.

The long-term effects of angiotensin-converting enzyme inhibitors (captopril and enalapril), calcium-entry blockers (diltiazem and nicardipine), and good glycemic control on plasma lipids and lipoproteins were studied in streptozotocin diabetic rats. Diabetic rats had increased plasma cholesterol, tryiglycerides, very-low-density lipoprotein (VLDL), and low-density lipoprotein (LDL) cholesterol, and decreased levels of high-density lipoprotein (HDL) cholesterol than in normal rats. Compared to other antihypertensives, nicardipine seems to have a less beneficial effect on lipids and lipoproteins. However, it is only the good glycemic control that normalized these plasma lipids and lipoproteins in diabetic rats. This suggests that good glycemic control prevents dyslipidemia in diabetic rats. The observed beneficial effects of antihypertensives were unrelated to either food or water intake.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Effect of insulin-glipizide combination on skeletal muscle capillary basement membrane width in diabetic patients.

This study investigated the long-term effect of insulin or the combination of insulin and an oral hypoglycemic compound (glipizide) on the skeletal muscle capillary basement membrane width in insulin-requiring diabetic patients. Seventy diabetic patients were randomized to treatment with either insulin-placebo or insulin-glipizide (5 mg/d) for 3 years. Of these, only 61 patients completed the study; 27 patients received insulin-placebo and 34 patients received insulin-glipizide. Three skeletal muscle (quadriceps femoris) biopsies were performed in all patients over a 3-year period. Glycosylated hemoglobin A1 was determined every 100 +/- 20 days, including plasma glucose levels. Muscle capillary basement membrane width was quantitated by a previously described method. After approximately 16 months, glycosylated hemoglobin A1 decreased significantly in each group from its baseline (P < 0.001 insulin-glipizide group and P < 0.025 insulin-placebo), although no statistically significant difference was seen between the two groups. After 3 years this decrease was statistically significant (P < 0.001) only in the insulin-glipizide group. At baseline, no statistically significant difference was found in the muscle capillary basement membrane width between the two groups. In spite of the significant decrease in glycosylated hemoglobin A1 in both groups after 14 to 16 months, only muscle capillary basement membrane width in the insulin-glipizide group decreased significantly compared with baseline. Patients receiving insulin-placebo showed a gradual increase in the muscle capillary basement membrane width, which after 3 years was significantly higher than baseline (P < 0.02). Although the mechanisms by which the addition of glipizide to insulin treatment reduced the thickening of the muscle capillary basement membrane are not clearly understood, the current findings suggest that diabetic microangiopathy is not necessarily progressive and that prophylaxis may be attained.

Adult↗
PubMedDate not supplied

Aldose reductase inhibition by ponalrestat (statil) does not prevent proteinuria in long-term diabetic rats.

The aldose reductase pathway has been implicated in the development of chronic complications of diabetes. In this study, we investigated the effect of an aldose reductase inhibitor, statil, on glomerular synthesis of heparan sulfate and albuminuria in male Wistar rats made diabetic with streptozotocin. Heparan sulfate is the predominant glycosaminoglycan (GAG) proteoglycan in the glomerular basement membrane (GBM). It confers a negative charge on the GBM, and its loss has been related to the presence of albumin in the urine. Diabetic rats synthesized less glomerular heparan sulfate and excreted more albumin than normal rats. Glomerular sorbitol concentration was significantly higher in diabetic than in normal rats. Chronic treatment of diabetic rats with statil did not improve either heparan sulfate synthesis or albuminuria despite normalization of glomerular sorbitol content. The present study does not support the role of excess sorbitol in the development of glomerular abnormalities in this rat model of streptozotocin diabetes.

Aldehyde Reductase↗
PubMedDate not supplied

Effect of metformin treatment on glucose tolerance and glomerulosclerosis in KK mice.

Non-obese KK mice, aged 90-100 days, demonstrating an abnormal tolerance to glucose, hyperinsulinaemia with insulin resistance and glomerulosclerosis were treated with either water (control N = 10) or metformin (N = 15), a biguanide, orally at a concentration of 50 mg/kg twice daily for 16 weeks. Oral glucose tolerance was performed at 7 weeks. Only 10 of 15 metformin-treated mice (responders) improved their oral glucose tolerance. The remaining 5 mice (non-responders) did not improve their tolerance to the oral glucose load. A repeated oral glucose tolerance test at 16 weeks showed similar results. Blood lactate and insulin levels were similar in all 3 groups of mice. At sacrifice, responders had significantly less glomerulosclerosis compared to control mice. No difference in the incidence of glomerulosclerosis was found between control mice and non-responders. The data suggest that chronic metformin treatment improves glucose tolerance in 70% of KK mice without increasing blood lactate or insulin levels. This improvement in glycaemic control is associated with a lesser incidence of glomerulosclerosis in KK mice.

Animals↗