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Biomedical subjects

A S Reddi

Publications and source records attributed to A S Reddi.

At least 37 records · Page 2Linked to original sources
PubMed1992

Erythrocyte Ca, Na/K-ATPase in long-term streptozotocin diabetic rats. Effect of good glycemic control and a Ca antagonist.

This study evaluated the effect of chronic hyperglycemia on erythrocyte membrane Ca and Na/K-ATPase activities in streptozotocin-induced diabetic rats. The activity of Ca-ATPase was significantly lower in diabetic than in normal rats. Good glycemic control by insulin restored the Ca-ATPase activity to normal. By contrast, diltiazem, a calcium entry blocker, had no effect on the enzyme activity. Calmodulin stimulated Ca-ATPase activity in all groups of rats. Na/K-ATPase activity was not altered in diabetic rats, and no effects of either insulin or diltiazem treatments were observed. The results suggest that erythrocyte Ca-ATPase activity is decreased in diabetic rats and is normalized by good glycemic control.

Animals↗
PubMed1992

In vivo glycogen and lipid synthesis by various tissues from normal and metformin-treated KK mice.

The incorporation of [14C] U-glucose into glycogen by liver, kidney and skeletal muscle and that into total lipid by adipose tissue was studied in noninsulin-dependent genetically diabetic KK mice treated either with metformin (50 mg/kg) or water for 10 weeks. Results show that glycogen synthesis was increased in the skeletal muscle from metformin-treated mice. Liver and kidney glycogen synthesis was not affected by metformin. Glucose incorporation was significantly increased into lipid in metformin-treated mice. Insulin administration stimulated lipid synthesis in adipose tissue, but had no effect on muscle glycogen synthesis in metformin-treated mice. These data suggest that chronic metformin treatment potentiates the endogenous insulin action on glucose in skeletal muscle and adipose tissue, and thus confirm our previous results of increased glycogen synthesis by skeletal muscle in metformin-treated KK mice.

Animals↗
PubMed1991

Vitamin and micronutrient concentrations in cyclosporine-induced renal tumor from diabetic rats.

Concentrations of vitamins, biopterin, free inositol and acid-soluble carnitine were determined in cyclosporine A induced renal adenocarcinoma and uninvaded renal tissue from streptozotocin diabetic rats. Vitamin B6, thiamin, riboflavin, nicotinate, free inositol and acid-soluble carnitine were significantly decreased in tumor than nontumor tissue. Concentrations of folic acid, B12, biotin, pantothenate and biopterin were similar in both tissues. These studies suggest that renal adenocarcinoma affects concentrations of only certain vitamins and micronutrients.

Adenocarcinoma↗
PubMed1991

Effect of short- and long-term diabetes on carnitine and myo-inositol in rats.

1. The effect of short- (2 wk) and long-term (20 wk) streptozotocin diabetes was studied on urine, blood, liver, heart, brain, skeletal muscle, pancreas and kidney concentrations of acid-soluble carnitine and free myo-inositol. 2. Short-term diabetic rats excreted significantly higher concentrations of carnitine as well as myoinositol than normal rats. Blood carnitine and myo-inositol were not different between normal and diabetic rats. Diabetes caused a decrease in liver, brain and pancreatic carnitine, but not in heart, skeletal muscle and kidney. Myo-inositol concentration was decreased in liver, heart and kidney but not in brain, pancreas and skeletal muscle. 3. Long-term diabetic rats had higher urinary excretions of both carnitine and myo-inositol. Blood carnitine did not change; however, myo-inositol was higher in diabetic than in normal rats. Diabetes caused a significant increase in liver and a decrease in heart, brain, skeletal muscle and pancreatic content of carnitine; no difference in kidney carnitine was noted. Myo-inositol content was elevated only in liver of diabetic rats. 4. We suggest that carnitine and myo-inositol concentrations are influenced both by short- and long-term diabetes through changes in tissue metabolism.

Acute Disease↗
PubMed1991

Potentiation of renal tumorigenicity by cyclosporine A in streptozotocin diabetic rats.

Male Wistar rats with streptozotocin induced diabetes were treated every third day with 10 mg/kg (13 rats) of cyclosporine A (CyA) for 20 weeks. At sacrifice, 7 of 13 rats (53.8%) demonstrated renal tumors. By contrast, only 2 of 16 streptozotocin diabetic rats (12.5%) without CyA demonstrated renal tumors. No tumors were noted in 10 non-diabetic control rats. These studies suggest that CyA potentiates renal tumorigenicity in streptozotocin diabetic rats.

Animals↗
PubMed1991

Prevention of albuminuria by captopril in diabetic rats.

1. Streptozotocin diabetic rats were treated with captopril (50 mg l), an angiotensin converting enzyme-inhibitor, in drinking water for 20 weeks. 2. Systolic blood pressure and 24-hr urinary excretions of heparan sulfate and albumin were done at 2, 8, 16 and 20 weeks. 3. At the end of 20 weeks, all rats were killed, kidneys removed and glomeruli isolated. 4. Total glycosaminoglycan and heparan sulfate synthesis were determined by incubating glomeruli in the presence of 35S-sulfate. 5. Captopril significantly lowered blood pressure in diabetic rats 8 weeks after treatment. 6. Diabetic glomeruli synthesized less total glycosaminoglycan and heparan sulfate than glomeruli from nondiabetic rats. 7. Further characterization of heparan sulfate by ion-exchange chromatography showed that the fraction eluted with 1 M NaCl was significantly lower and the fraction eluted with 1.25 M NaCl significantly higher in diabetic than in normal rats. 8. Therapy with captopril normalized not only glomerular synthesis and content but also various fractions of heparan sulfate in diabetic rats. 9. Excretions of heparan sulfate and albumin were significantly higher in diabetic than in nondiabetic rats. 10. Captopril therapy did significantly lower but not normalize both these excretions in diabetic rats. 11. The data suggest that catopril therapy improves albuminuria through preservation of glomerular heparan sulfate and prevention of its urinary loss in diabetic rats.

Albuminuria↗
PubMed1991

Enalapril improves albuminuria by preventing glomerular loss of heparan sulfate in diabetic rats.

Angiotensin converting enzyme (ACE) inhibitors, particularly enalapril and captopril, have been shown to decrease proteinuria in diabetic animals and human subjects. Since heparan sulfate proteoglycan confers a negative charge on the glomerular basement membrane, and either decreased synthesis or loss of this charge causes albuminuria in diabetic animals, we examined the possibility that enalapril prevents albuminuria through glomerular preservation of heparan sulfate in long-term diabetic rats. A total of 22 male Wistar rats were used in the study. Diabetes was induced in 15 rats by a single intraperitoneal injection of streptozotocin (60 mg/kg). The remaining 7 rats received buffer. One week following induction of diabetes, 8 diabetic rats were allowed to drink tap water containing enalapril at a concentration of 50 mg/liter; the remaining 7 diabetic and 7 nondiabetic rats were given only tap water. The drug treatment was continued for 20 weeks. Systolic blood pressure and 24-hr urinary excretion of albumin were measured at 2, 8, 16, and 20 weeks. At the end of 20 weeks, all rats were killed, kidneys were removed, and glomeruli were isolated by differential sieving technique. Total glycosaminoglycan and heparan sulfate synthesis was determined by incubating glomeruli in the presence of [35S]sulfate. Characterization of heparan sulfate was performed by ion-exchange chromatography. Systolic blood pressures were significantly lower in enalapril-treated diabetic rats compared to untreated diabetic rats. Diabetic glomeruli synthesized less heparan sulfate than glomeruli from nondiabetic rats. Also, glomerular heparan sulfate content of diabetics was significantly lower than that of nondiabetics. Further characterization of heparan sulfate showed that the fraction eluted with 1 M NaCl was significantly lower and the fraction eluted with 1.25 M NaCl significantly higher in diabetic than in normal rats. Enalapril treatment normalized not only glomerular synthesis and content but also various fractions of heparan sulfate in diabetic rats. Diabetic rats excreted increased quantities of heparan sulfate and albumin than nondiabetic rats. Enalapril therapy prevented both these increases in diabetic rats. These data suggest that enalapril treatment improves albuminuria through preservation of glomerular heparan sulfate and prevention of its urinary loss in diabetic rats.

Albuminuria↗
PubMed1991

Bioavailability of aspirin and salicylamide following oral co-administration in human volunteers.

BC powder (I) is a commercially available analgesic containing the active ingredients aspirin and salicylamide. The kinetics of I, BC powder minus aspirin (II), and BC powder minus salicylamide (III) were evaluated in 13 volunteers. Ten minutes after administration of I, aspirin reached a maximum concentration of 12.9 micrograms/mL, while salicylamide concentration reached a peak value of 3.4 micrograms/mL. However, when III was administered, aspirin was not detected at 10 min and only reached a concentration of 0.4 microgram/mL at 2 and 6 h. Furthermore, the area under the plasma concentration versus time curve for aspirin when III was administered was sixfold less compared with treatment with I. The area under the curve for aspirin metabolites was significantly different in I versus III. After treatment with II, a delay in salicylamide peak concentration was observed. Gentisamide was not detected throughout the study. This study demonstrates that salicylamide significantly enhances plasma levels of aspirin with potential therapeutic implications.

Adult↗
PubMed1990

Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis.

Twenty-three nonobese KK mice with abnormal tolerance to glucose, hyperinsulinemia with insulin resistance and human diabetic-like nephropathy were treated with either saline (12 mice) or glipizide, an oral hypoglycemic compound, 1 mg/kg, (11 mice) from 120 to 360 days of age. These mice develop significant increases in mesangial volume and matrix by 40 days of age. Oral glucose tolerance (OGTT), glucosyltransferase and N-acetyl-beta-glucosaminidase (enzymes involved in synthesis and degradation of kidney glycoproteins, respectively) in the kidney and serum, 24-hr proteinuria, and light microscopy studies of the kidney were performed. Glipizide-treated mice improved their OGTT. There was no difference in body weight; however, a 16% decrease (P less than 0.05) in kidney weight was observed in glipizide-treated mice. Both enzymes were significantly increased in the kidneys of mice treated with glipizide. No difference in serum enzymes was found between the two groups of mice. About 58% of the saline-treated mice had moderate glomerulosclerosis. By contrast, only 27% of glipizide-treated mice had moderate glomerulosclerosis. Also, a significant decrease in proteinuria was found in glipizide-treated mice. These data suggest that glipizide improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals.

Acetylglucosaminidase↗
PubMed1990

Effect of genetic diabetes and alcohol on tissue carnitine and inositol concentrations in mice.

Concentrations of acid-soluble L-carnitine and inositol were determined in heart, kidney, muscle, pancreas, liver, brain and blood of genetically diabetic obese db/db and their nondiabetic control C57BL/6J (CBL) mice. Results were compared to a group of diabetic and CBL mice fed ethanol (ETOH) 4 g/kg daily for 58-64 days. In CBL and db/db mice, heart muscle was found to have the greatest and brain the least content of carnitine. Diabetes caused a significant decrease in hepatic concentration of carnitine but did not affect carnitine concentration of heart, kidney, skeletal muscle, brain and pancreas. ETOH intake had no effect on carnitine content of any of the tissues studied. Free inositol content was highest in brain and lowest in skeletal muscle of CBL and db/db mice; diabetes or ETOH intake did not affect tissue inositol content. Except for liver, neither diabetes nor ETOH intake affects tissue carnitine or inositol concentration.

Alcohol Drinking↗
PubMed1990

Riboflavin excretion in normal and diabetic rats.

Twenty-four hour urinary excretion of riboflavin was determined in normal and short-term and long-term streptozotocin diabetic rats. Compared to non-diabetic rats (controls), short-term (1 week) diabetic rats had no increased urinary riboflavin. In contrast, long-term (20 week) diabetic rats excreted significantly elevated levels of urinary riboflavin. Results suggest that the reported riboflavin deficiency seen in chronic diabetes may be related to augmented urinary excretion of riboflavin.

Animals↗
PubMed1990

Effect of alcohol on urinary glycosaminoglycan and protein excretion in normal and diabetic mice.

The effect of alcohol on urinary glycosaminoglycan (GAG) and protein excretion was studied in one-month-old normal control C57BL/6J (CBL) and genetically diabetic (db/db) mice. Ethyl alcohol (4 g/kg) was given once a day by gavage for 58-64 days. Increased amounts of urinary total GAGs and protein were found in diabetic mice. Alcohol treatment increased urinary excretion of total GAGs, heparan sulfate and protein only in nondiabetic CBL but not in diabetic mice. Also, alcohol increased creatinine clearance only in CBL mice. The reason for the lack of effect of alcohol in diabetic mice is unknown. A significant positive linear relationship was found between urinary total GAG and protein concentrations. Possible significance of this relationship in diabetes is discussed.

Alcohol Drinking↗
PubMed1990

Diabetic nephropathy. An update.

Nephropathy is a serious microvascular complication in patients with insulin-dependent diabetes mellitus. In the United States, diabetes accounts for one fourth of new cases of end-stage renal disease each year. Complication rates and costs are much higher for diabetic than for nondiabetic patients with end-stage renal disease. Despite numerous studies, the pathophysiology of diabetic renal disease is not completely understood. We reviewed the current status of the structural, functional, biochemical, pathogenetic, and treatment modalities of diabetic renal disease and examined future therapeutic interventions.

Diabetes Mellitus, Type 1↗
PubMed1988

Hereditary diabetes in the KK mouse: an overview.

Table III compares metabolic and morphologic characteristics of different species of control and KK mice. The C57BL/6J demonstrates no significant metabolic, clinical or histologic abnormalities. Our two highly inbred Swiss albino groups I and II also do not show significant glomerular lesions, although we found striking intolerance to glucose, hyperinsulinism, and obesity among them. Thus a genetic predisposition may be necessary in addition to various environmental factors to produce microangiopathy in KK mice. The yellow AY mouse is included in this table, since it is strikingly hyperinsulinemic and obese without concomitant vasculopathy such as the other mentioned control strains have. In conclusion, the KK mice develop chemical diabetes preceded by a stage of prediabetes and also demonstrate renal, retinal and neurologic complications similar to those seen in human diabetes. Of particular interest is the development of mild to moderate glomerulosclerosis in the prediabetic stage; with progression to severe glomerulosclerosis and attendant proteinuria later in life. With proper back-crossing, both hyperglycemia and glomerulosclerosis can be transmitted to normal control mice, suggesting that a specific genetic background is necessary for the development of diabetes and diabetic-like microangiopathy. We therefore suggest that the KK mouse serves as an ideal genetic animal for the study of non-insulin-dependent diabetes mellitus and its complications for rational prevention and therapy.

Animals↗