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PubMed1984

Alloxan-induced diabetes in the rat - protective action of (-) epicatechin?

Administration of alloxan (150 mg/kg body weight, i.p.) to male Wistar rats induced a reproducible and persistent diabetes mellitus as evidenced by elevated serum glucose and low serum insulin concentrations. Administration of either (-)epicatechin or (+)catechin (250 mg/kg, i.p. on each occasion) at 36, 24, 12 and 1 hour before and at 12 and 24 hours after alloxan administration did not prevent the induction of the diabetes. Similarly, treatment of animals with (-)epicatechin or (+)catechin (125 mg/kg i.p. twice daily) for 21 days commencing 24 hours after alloxan administration did not reverse the persisting elevated serum glucose and low serum insulin concentrations. Moreover, administration of these compounds did not relieve any of the symptoms of the alloxan-induced diabetes such as poor weight gain, polyuria or polydipsia. Thus, this study does not confirm previous reports of prophylactic and curative effects of (-)epicatechin against alloxan-induced diabetes in rats, in spite of the high dosages of the compounds used in these experiments.

Animals↗

PubMed1987

Selected physical and biochemical parameters in the streptozotocin-treated guinea pig: insights into the diabetic guinea pig model.

Since evidence suggests that ascorbic acid deficits may provoke certain diabetic complications, it becomes necessary to develop a diabetic animal model which, like man, is unable to synthesize this vitamin. To this end, the present study monitored the diabetogenic effects of streptozotocin (STZ, 150 mg/kg) in the male guinea pig, a species rarely used in diabetes research. Over a 3-week period, body weight and relative food intake were lower in the STZ group compared to controls. The mean daily water intake and urine volume of the STZ group after 1 week were 175 and 270% of their initial pretreatment values, respectively, while control values were unchanged. The STZ group also exhibited a persistent glycosuria throughout the study. At the end of 3 weeks, aldehyde fuchsin staining of pancreatic beta cell granules (an index of stored insulin) was 58% lower in the STZ group compared to controls. Plasma C-peptide (indicator of insulin secretion) was expressed in human equivalents (mean +/- SEM). C-peptide was reduced in the STZ group (103 +/- 65 pg/ml) compared to controls (549 +/- 96 pg/ml); however, no change in plasma glucose was observed. Plasma ascorbic acid levels also were lower for STZ animals (150 +/- 26 micrograms%) versus controls (410 +/- 28 micrograms%). This study 1) demonstrates a diabetic syndrome in the STZ-treated guinea pig based on a reduced growth rate, beta cell dysfunction, polydipsia, polyuria and glycosuria, and 2) suggests the usefulness of this diabetic model in studies of pathologic mechanisms influenced by ascorbic acid.

Animals↗

PubMed1980

In vitro culture--a method of pancreatic islet preservation for transplantation.

Pancreatic islets from adult rats, accumulated daily for a period of 2 wk, were cultured in artificial capillary culture units that were perfused with nutrient medium. Viability and functional capacity of these islets in this in vitro culture system has been shown to be maintained. The therapeutic efficiency of cultured islets was comparable to freshly isolated islets when assessed by transplantation into streptozotocin-induced diabetic rats. Intraportal implantation of either freshly isolated or cultured islets into isogeneic diabetic rats resulted in normal weight gain as well as complete reversal of hyperglycemia, glycosuria, and polyuria in the diabetic rat recipient. The normoglycemic state was sustained for more than 12 mo. Plasma glucose clearance rate (KG) were significantly lower in both the transplanted fresh or cultured islet groups than in the normal controls; however, the cultured islets were not less effective than the fresh islets. The results of the present study indicate the feasibility of accumulation of large numbers of islets in the in vitro culture system without any loss of therapeutic efficiency when implanted in vivo. Further improvement of this in vitro culture system can thus be applied in islet preservation for islet transplantation.

Animals↗

PubMed1989

Satellite cells derived from streptozotocin-diabetic rats display altered fusion parameters in vitro.

Myogenic satellite cells were isolated from nondiabetic and streptozotocin-diabetic rats and studied in vitro. Streptozotocin (STZ) administration produced both hyperglycemia and glucosuria in adult rats when compared to controls. (P less than 0.01), with 12.5% mortality in untreated animals. Insulin therapy diminished blood glucose levels to those found in nondiabetic animals. Only STZ-diabetic rats displayed symptoms of Type I diabetes, including polydipsia, polyuria, and hyperphagia. STZ-treated rats possessed less leg muscle mass and less subcutaneous, intermuscular, and intramuscular fat. Conversely, nondiabetic rats had a greater mean body weight (P less than 0.01) at the end of the experiment than did diabetic rats. Primary cultures of diabetic-derived satellite cells displayed decreased overall ability (P less than 0.01) to fuse to form multinucleated myotubes in vitro than controls. In addition, secondary cultures of diabetic-derived satellite cells achieved maximal fusion one day later than secondary cultures of control-derived cells. Collectively, these data provide preliminary evidence to suggest that untreated insulin-dependent diabetes results in altered fusion characteristics of myogenic satellite cells. Additional studies utilizing satellite cells from diabetic animals will provide valuable definition of the satellite cell involvement in skeletal muscle autophagy which is a symptom of type I diabetes.

Animals↗

PubMed1990

Vascular filtration function in galactose-fed versus diabetic rats: the role of polyol pathway activity.

These studies were undertaken to assess the effects of increased galactose (v increased glucose) metabolism via the polyol pathway on vascular filtration function in the kidneys, eyes, nerves, and aorta. Quantitative radiolabeled tracer techniques were used to assess glomerular filtration rate (GFR) and regional tissue vascular clearance of plasma 131I-bovine serum albumin (BSA) in five groups of male Sprague-Dawley rats: nondiabetic controls, streptozotocin-diabetic rats, nondiabetic rats fed a 50% galactose diet, diabetic rats treated with sorbinil (an aldose reductase inhibitor), and galactose-fed rats treated with sorbinil. Sorbinil was added to the diet to provide a daily dose of approximately .2 mmol/kg body weight. After 2 months of diabetes or galactose ingestion, albumin clearance was increased twofold to fourfold in the eye (anterior uvea, choroid, and retina), sciatic nerve, aorta, and kidney; GFR was increased approximately twofold and urinary excretion of endogenous albumin and IgG were increased approximately 10-fold. Sorbinil treatment markedly reduced or completely prevented all of these changes in galactose-fed, as well as in diabetic rats. These observations support the hypothesis that increased metabolism of glucose via the sorbitol pathway is of central importance in mediating virtually all of the early changes in vascular filtration function associated with diabetes in the kidney, as well as in the eyes, nerves, and aorta. On the other hand, renal hypertrophy in diabetic rats and polyuria, hyperphagia, and impaired weight gain in galactose-fed and in diabetic rats were unaffected by sorbinil and therefore are unlikely to be mediated by increased polyol metabolism.

Animals↗

PubMed1991

Beneficial effects of dietary acarbose in the streptozotocin-induced diabetic rat.

Diabetes is characterized by hyperphagia, polydipsia, polyuria, and elevations in blood and urinary glucose. It has also been documented that beta-adrenergic responsiveness is reduced in diabetes. The intestinal glucosidase inhibitor, acarbose (BAY G 5421), decreases postprandial glycemia by delaying carbohydrate absorption. The purpose of this study was to evaluate the effects of chronic acarbose treatment (20 and 40 mg/100 g of diet) on the metabolic and adrenergic parameters altered in streptozotocin (STZ) (50 mg/kg, intravenously [IV] )-induced diabetes. Metabolic parameters were measured daily for 8 weeks. Diabetic rats were hyperphagic, polydipsic, and polyuric within 1 week of STZ treatment. Acarbose treatment did not consistently effect the food intake but did reduce water intake, urinary output, blood glucose, and the urinary loss of glucose associated with STZ-induced diabetes. Adrenergic responses were assessed by monitoring the increase in tail skin temperature (TST) associated with administration of isoproterenol. Diabetic rats were less responsive than controls and acarbose treatment restored responses toward that of the controls. Additionally, 3H-NE release from the tail artery was elevated in the diabetic rat and restored to normal in the acarbose-treated animals. Collectively these data suggest that acarbose treatment is effective in reducing the severity of metabolic and autonomic complications associated with STZ-induced diabetes.

Acarbose↗

PubMed1992

Metabolic abnormalities of the hyperglycemic obese Zucker rat.

In a cross-sectional study, we evaluated the metabolic profiles of lean (Fa/?) and obese (fa/fa) Zucker male rats at 4 to 8 months of age. Although all of the obese rats (N = 108) demonstrated glucose intolerance, most of the obese rats exhibited only mild elevations of fasted and fed plasma glucose. Only 14 of the obese rats were severely hyperglycemic, which resulted in substantial elevations of glycohemoglobin (GHb) levels. The nerve and lens levels of glucose, sorbitol, and fructose were elevated, and the myo-inositol was depleted in all hyperglycemic obese rats, but not in the euglycemic obese rats. With increasing duration of hyperglycemia, the neural myo-inositol level approached normal, while the lenses became cataractous. All obese rats had increased urinary albumin excretion (UAE), which was dependent on age (r = .45, P less than .02) and independent of hyperglycemia, glucosuria, and polyuria. In conclusion, although the euglycemic obese rats exhibited some diabetic abnormalities, the hyperglycemic obese Zucker rat more closely resembled the altered metabolic profile associated with type II diabetes mellitus.

Animals↗

PubMed1975

Dental fluorosis associated with hereditary diabetes insipidus.

Among the characteristics of hereditary pituitary diabetes insipidus are polydipsia and polyuria from early infancy. Drinking of large amounts of water, even with lower than accepted fluoride content, can produce fluorosis of the teeth. A mother and her four children affected by this disorder presented different degrees of fluorosis directly related to the stage at which hormonal therapy was introduced.

Adolescent↗

PubMed1985

Clinical efficacy of prednisone in the treatment of patients with oral inflammatory ulcerative diseases: a study of fifty-five patients.

An objective evaluation of 55 patients with chronic vesiculoerosive oral diseases was made to compare the beneficial and adverse effects of prednisone treatment. Patients were divided into groups of high, intermediate, and low drug dosages, as well as short and long periods of administration. Prednisone benefited 49 patients in spite of the fact that 55% had some adverse side effects. The duration of prednisone administration appeared to have a larger impact on side effects than the daily amount given. The most common side effects were gastrointestinal disturbances, mood alterations, polyuria and insomnia. There were no significant changes in blood pressure, blood sugar level, weight, or white blood cell counts. This study confirmed that systemic prednisone is a useful and beneficial treatment modality for patients with chronic oral inflammatory diseases.

Adolescent↗

PubMed1975

Renal deficiency associated with diabetes insipidus in the SWR/J mouse.

The age-dependent polydipsia and polyuria observed in SWR/J mice was found to be caused by relative inability of the kidneys to respond to antidiuretic hormone (ADH), resulting in a concentrating defect, which persisted even following Pitressin injection or water deprivation. Posterior pituitaries contained large amounts of ADH, which was also found in the urine and increased in output following water deprivation, indicating normal, or above normal synthesis and release of ADH. Kidneys of polydipsic SWR/J mice weighed more than those of normal strains and sometimes contained a lesion in the medullary area. No clear relationship was found between the size of the lesion and water intake.

Animals↗

PubMed1985

Effect of nicotine on drinking and diuresis in septal lesioned rats.

Lesions of septal nuclei in rats enhance water intake and urine outflow. The effects of nicotine tartrate (2.5 mg/kg) on drinking and diuresis were investigated in normal, sham and septal lesioned rats. Nicotine administration resulted in a surprising hyperdipsia and polyuria in lesioned animals, the mean output rose from 38 +/- 1.3 ml (before treatment) to 101.6 +/- 6.1 (during treatment) and water intake increased from 74.2 +/- 1.8 ml to 129.8 +/- 6.4 ml.

Acetylcholine↗

PubMed1993

Circadian rhythms of food and water intake and urine excretion in diabetic rats.

The light/dark (L/D) rhythms of food and water intake and urine output were studied in normal and diabetic rats for 7 consecutive days at 4-h intervals. The control rats showed the highest values of these parameters during the dark phase (83.68% food, 68.71% water, and 67.44% urine). The diabetic rats also maintained this nocturnal predominance, although the values were less marked (59.55% food, 55% water, and 56% urine). A circadian rhythm of food (phi = 3.31 h) and water (phi = 3.54 h) intake as well as of the volume of urine excreted (phi = 1.10) was detected in the control animals. The diabetic rats, inspite of presenting polyphagia, maintain the circadian rhythm of food intake, whereas a loss of the normal circadian variation of drinking intake was observed as well as the absence of circadian rhythm in urinary excretion. It was concluded that in streptozotocin-diabetic rats we have observed a loss of the normal patterns of water intake and urinary excretion, perhaps masked by the polydipsia and polyuria, whereas the circadian rhythm of food intake remains.

Animals↗

PubMed1993

Insulin and satiety from feeding in pancreatic-normal and diabetic rats.

Insulin's role in food ingestion and satiety was investigated in streptozotocin-diabetic and pancreatic-normal rats. Markedly diabetic rats (60-65 mg/kg b.wt. streptozotocin with mean glycemia of 380 mg/dl) were observed for daily food/water intake and body weight changes and meal pattern in a standard operant chamber. Diabetic animals showed an immediate hypophagia (days 1-4) by decreasing meal size (MS). As animals lost weight, a significant hyperphagia appeared, accomplished by an elevation in MS. Treatment with insulin infused via osmotic minipump at a stable rate (6.0 U/24 h) reduced polyuria and glycemia, eliminated glycosuria, and restored weight gain. MS did not, however, return to baseline immediately. In a second experiment with milder diabetes (20-22 mg/rat streptozotocin, which produced glycemia ranging from 148 to 304 mg/dl), significant hyperphagia appeared, again attributable to an increase in MS. Minipumps infusing 2.4-4.0 U insulin/24 h reversed this hyperphagia. In pancreatic-normal rats, pumps infusing insulin at 1.2 or 2.4 U/24 h produced a modest hypophagia accomplished by a primary decrease in nocturnal intake (11% suppression in dark feeding). Subdiaphragmatically vagotomized rats showed an attenuation of this suppression (no significant effects on food or water intake produced by insulin infused). Insulin appears to participate in satiety by limiting MS, without significantly shortening latency to take the next meal.

Animals↗

PubMed1994

The abnormal quinine drinking aversion in the Brattleboro rat with diabetes insipidus is reversed by the vasopressin agonist DDAVP: a possible role for vasopressin in the motivation to drink.

The Brattleboro rat with hypothalamic diabetes insipidus (BDI) has an abnormal aversion to drinking quinine-adulterated water compared with normal rats of the parent Long Evans (LE) strain. This BDI animal tolerates marked hypovolemia and decreased body weight in preference to drinking the quinine-adulterated fluid, indicative of a reduced motivation to drink. Acute or chronic treatment of BDI rats with desamino-8D arginine vasopressin (DDAVP) restored to normal their drinking response to quinine solution. Partial restoration of fluid turnover in BDI rats with hydrochlorothiazide, which has an antidiuretic effect in diabetes insipidus (when vasopressin is absent), failed to abolish the abnormal drinking response to quinine-adulterated solution in 8 out of 12 animals. In contrast, induction of diabetes mellitus in LE rats, which resulted in a marked polydipsia and polyuria even though vasopressin was still present, did not impair the drinking response to quinine solutions. These results suggest that the abnormal drinking response to quinine-adulterated fluid in BDI rats is reversed by treatment with the vasopressin V2-receptor agonist DDAVP but is unlikely to be a consequence of the restoration of fluid turnover to normal levels by a renal action. A possible central action involving vasopressin and the motivation to drink is discussed.

Animals↗

PubMed1985

Acute renal failure and glucosuria induced by ferric nitrilotriacetate in rats.

Nitrilotriacetate (NTA), an effective metal-chelating agent, has been used as a substitute for polyphosphates in household laundry detergents. Nephrotoxicity and renal tumorigenicity have been reported in experimental animals that received high doses of NTA po for 4 weeks to 2 years. Since NTA exists in water as a variety of NTA-metal complexes, it was important to investigate the biological effects of NTA in a complexed form. In this study, acute and subchronic toxicity of a ferric iron chelate of NTA (Fe-NTA) was investigated in rats. When Fe-NTA was given ip, acute tubular necrosis and renal failure occurred following a single injection of 15 mg iron/kg. Repeated injections of sublethal doses produced degeneration and necrosis of the proximal tubular epithelium and was associated with polyuria, glucosuria, aminoaciduria, and azotemia. After 9 days of treatment, regeneration of the tubular epithelium with atypical cells was observed. Except for a parenchymal iron deposit, no marked changes were observed in other organs. None of these effects were observed in animals given noncomplexed NTA. In conclusion, the toxicity observed following high doses of NTA given po may be the result of an absorbed metal-NTA chelate.

Acute Kidney Injury↗

PubMed1986

Comparative nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) and chlorozotocin: functional-structural correlations in the Fischer 344 rat.

1-(2-Chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) and chlorozotocin (CZ; 2-[3-(2-chloroethyl)-3-nitrosoureido]-D-glucopyranose) are structurally related anticancer agents which differ by virtue of the increased water solubility, and comparatively low carbamylating activity, of CZ relative to MeCCNU. In the present study, a single sc injection of either of these chloroethylnitrosoureas was nephrotoxic to male Fischer 344 rats. However, at equimolar doses, CZ was shown to be a much more potent nephrotoxicant. A lethal 40-mg/kg dose of CZ (127 microM) initially resulted in acute tubular necrosis of the proximal tubules of the cortex, followed later by a necrosis of papillary collecting ducts. In contrast, lethal doses of MeCCNU (100-180 mg/kg; 400-730 microM) produced only minimal proximal tubule injury. A 250-mg/kg (1 mM) dose of MeCCNU resulted in massive papillary necrosis within 7 days, with only limited necrosis to the proximal tubules. Sublethal doses of either drug, resulted in a similar, chronic, progressive nephropathy which was delayed in onset and was characterized by polyuria, enzymuria, a decrease in urine concentrating ability, and in renal slice organic ion accumulation. Alterations in less sensitive indicators of renal toxicity (i.e., proteinuria, glucosuria, and elevated blood urea nitrogen) were observed no earlier than 3 to 7 days after administration of only the highest tested doses of CZ (40 mg/kg) or MeCCNU (250 mg/kg). At sublethal doses, administration of either drug resulted in karyomegaly to the collecting ducts in the renal medulla within 2 to 4 weeks. These studies demonstrate that carbamylation-mediated reactions may not be necessary for nephrotoxicity to develop following administration of this class of antitumor agent.

Animals↗

PubMed1986

The progression of adriamycin-induced nephrotic syndrome in rats and the effect of captopril.

The progression of adriamycin-induced nephrotic syndrome in rats was studied over a 3-month period. The effect of an angiotensin-converting enzyme inhibitor, captopril, on this model of renal disease, was also studied. Two weeks following a single iv injection of adriamycin, rats were divided into two treatment groups: one received a daily po dose of captopril and the other received a placebo. Measurements of renal function were performed at 4, 8, and 11 weeks following the initiation of therapy. Necropsies and light microscopic evaluation of the kidneys were performed at the end of the treatment period. Functional and morphologic alterations in both groups of rats were compared to each other and to normal age/weight-matched control rats studied over the same time period. At 13 weeks following the administration of adriamycin, both treatment groups had significant renal dysfunction when compared to normal controls. In addition to severe proteinuria, rats receiving adriamycin exhibited polyuria, polydipsia, increased plasma urea nitrogen and plasma creatinine, and decreased endogenous creatinine clearance. They had severe generalized kidney lesions characterized by tubular dilation and atrophy, cast formation, interstitial fibrosis and lymphocytic infiltration, and focal, global glomerulosclerosis. The histopathologic ranking of the kidneys was correlated with some antemortem laboratory parameters but not with the degree of proteinuria. Captopril had no ameliorating effects on the progression of renal disease. Certain findings indicate that captopril may actually have promoted the deterioration of renal function. We conclude that adriamycin-induced nephrotic syndrome in the rat is a progressive disease resulting in generalized renal dysfunction, and that captopril, at the dose given in this experiment, is unable to slow the progression of the disease.

Animals↗

PubMed1990

Alteration of renal amino acid transport system in cadmium-intoxicated rats.

Effects of cadmium intoxication on renal transport systems for various amino acids were studied. Subcutaneous injections of CdCl2, at a dose of 2 mg Cd/kg.day for 2 weeks, resulted in polyuria, proteinuria, glycosuria, phosphaturia, and aminoaciduria, as observed in chronic cadmium-intoxicated humans and experimental animals. The nature of aminoaciduria was nonspecific, including iminoacid as well as almost all species of neutral, acidic, and basic amino acids. In renal cortical brush border membrane vesicles isolated from cadmium-intoxicated rats, Na(+)-dependent transport of L-proline, L-alanine, and L-lysine was markedly attenuated, whereas the amino acid transport in the basolateral membrane vesicle was not significantly affected. Similar results were obtained in the normal membrane vesicles directly exposed to inorganic cadmium. These results indicate that cadmium intoxication impairs various Na(+)-amino acid cotransport systems in the renal brush border membrane, which leads to panaminoaciduria.

Amino Acids↗