Renal Hypertrophy in Streptozotocin-Diabetic Rats

1976 ◽  
Vol 51 (6) ◽  
pp. 551-555 ◽  
Author(s):  
K. Seyer-Hansen
Keyword(s):  
Weight Gain ◽  
Protein Content ◽  
Dna Content ◽  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Renal Hypertrophy ◽  
Kidney Weight ◽  
Streptozotocin Diabetic Rats ◽  
Rna And Dna

1. Kidney weight and content of protein, RNA and DNA were measured in rats with streptozotocin diabetes of varying duration. 2. Diabetic rats had larger kidneys than control rats: after 3 days of diabetes the weight increase was 15% and after 42 days of diabetes it was 90%. The protein content rose in parallel to the weight. 3. RNA content was already increased after 36 h of glycosuria, whereas DNA content was unchanged for the first 3 days of diabetes, and increased thereafter. The protein/DNA ratio increased rapidly during the first 3 days but remained constant thereafter. 4. Insulin treatment decreased the renal weight gain by about 67% during the first 8 days of diabetes, but did not prevent the increase in DNA. When insulin was started after 25 days of diabetes there was only a slight regression of kidney growth.

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

Kidney tissue insulin-like growth factor I and initial renal growth in diabetic rats: Relation to severity of diabetes

1990 ◽  
Vol 122 (3) ◽  
pp. 374-378 ◽  
Author(s):  
Allan Flyvbjerg ◽  
Hans Ørskov
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Experimental Diabetes ◽  
Diabetic Rats ◽  
Renal Hypertrophy ◽  
Kidney Weight ◽  
Factor I ◽  
Urinary Glucose ◽  
Igf I ◽  
Growth Factor I

Abstract The initial renal hypertrophy in experimental diabetes is dependent on the prevailing blood glucose level and is associated with renal accumulation of insulinlike growth factor I. To investigate the relationship of blood glucose to kidney IGF-I, a graded range of diabetic aberration was established in young rats by iv injection of increasing amounts of streptozotocin (25–80 mg/kg) at day 0. In 30 diabetic rats the mean of day 1 and day 2 blood glucose concentrations ranged from 6.2 to 32.0 mmol/l and 24-h urinary glucose excretion (24–48 h) from 0.04 to 43.3 mmol/24 h. The right kidneys were removed after 48 h, weighed and their IGF-I concentration analysed by radioimmunoassay. Kidney IGF-I was positively correlated to blood glucose (r = 0.66, p<0.0001) as well as to 24-h urinary glucose output (r = 0.54, p<0.005). At this early stage, kidney weight already correlated to blood glucose (r = 0.60, p<0.0005). No relationship between kidney IGF-I and kidney weight was found. However, if animals with severe diabetes were excluded, a significant correlation could be established (r = 0.51, p = 0.01, N = 24). The results support the hypothesis that IGF-I plays a causal role in the initial renal hypertrophy of experimental diabetes.

Dietary tyrosine supplementation enhances weight gain in streptozotocin-diabetic rats

1984 ◽  
Vol 62 (7) ◽  
pp. 781-786 ◽  
Author(s):  
N. Theresa Glanville ◽  
G. Harvey Anderson
Keyword(s):  
Weight Gain ◽  
Dietary Protein ◽  
Feed Efficiency ◽  
Protein Concentration ◽  
Proximate Analysis ◽  
Diabetic Rats ◽  
Specific Increase ◽  
Streptozotocin Diabetic Rats ◽  
Similar Body ◽  
Protein Diets

The effect of dietary protein concentration and tyrosine supplementation on growth in streptozotocin (65 mg/kg, ip) diabetic rats was evaluated. When rats were fed diets ranging from 15 to 60% protein, weight gain and feed efficiency were greatest in rats fed the 45% protein diet. Adding tyrosine to this diet (8%, incorporated as a percentage of protein) did not promote further weight gain relative to nonsupplemented diabetic animals. In contrast, rats choosing 45% of total calories as protein by selecting from 10 and 60% protein diets supplemented with either 0, 4, or 8% tyrosine demonstrated a 35% (4% tyrosine) to 45% (8% tyrosine) increase in weight gain. Proximate analysis indicated similar body composition in tyrosine supplemented and nonsupplemented diabetic animals. Including tryptophan (1.45%) with tyrosine in the self-selection diet was without effect. Thus, tyrosine supplementation promoted a modest but consistent and specific increase in weight gained by self-selecting diabetic rats.

Chondrosarcoma growth: influence of diabetes, caloric restriction, and insulin treatment

1981 ◽  
Vol 241 (2) ◽  
pp. E129-E135 ◽  
Author(s):  
W. D. McCumbee ◽  
H. E. Lebovitz
Keyword(s):  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Diet Restriction ◽  
Cartilage Growth ◽  
Serum Pool ◽  
In Vivo Growth

Diabetes and malnutrition result in decreased somatomedin production and cartilage growth in rats. The growth and metabolism of the Swarm rat chondrosarcoma are dramatically affected by somatomedins. Data presented here show that streptozotocin diabetes and diet restriction inhibit in vivo chondrosarcoma growth. Tumors grown in diabetic rats were significantly smaller than tumors grown in diet-restricted rats showing the same changes in body weight. Insulin treatment increased the rate of tumor growth in diabetic rats. Tumors grown in rigidly controlled diabetic rats were as large as tumors grown in nondiabetic controls. Diet restriction and diabetes reduced the capacity of the serum of the rat to stimulate alpha-amino[14C]isobutyrate uptake and [3H]uridine incorporation into RNA in chondrosarcoma pieces grown in nondiabetic rats. This somatomedin activity of the serum was restored by treating diabetic rats with insulin. There was a significant correlation between the in vitro stimulatory effect of a particular serum pool on chondrosarcoma metabolism and in vivo chondrosarcoma growth in the animals from whom the serum was obtained. These studies demonstrate that the in vivo growth of malignant chondrocytes is similar to that of normal chondrocytes with respect to the role of nutrition and insulin.

scholarly journals The metabolism of l-phenylalanine and l-tyrosine by liver cells isolated from adrenalectomized rats and from streptozotocin-diabetic rats

1985 ◽  
Vol 228 (1) ◽  
pp. 249-255 ◽  
Author(s):  
J C Stanley ◽  
M J Fisher ◽  
C I Pogson
Keyword(s):  
Insulin Treatment ◽  
Maximal Activity ◽  
Liver Cells ◽  
Diabetic Rats ◽  
Steroid Treatment ◽  
Phosphorylation State ◽  
Tyrosine Metabolism ◽  
Streptozotocin Diabetic Rats ◽  
Adrenalectomized Rats

Flux through, and maximal activities of, key enzymes of phenylalanine and tyrosine degradation were measured in liver cells prepared from adrenalectomized rats and from streptozotocin-diabetic rats. Adrenalectomy decreased the phenylalanine hydroxylase flux/activity ratio; this was restored by steroid treatment in vivo. Changes in the phosphorylation state of the hydroxylase may mediate these effects; there was no significant change in the maximal activity of the hydroxylase. Tyrosine metabolism was enhanced by adrenalectomy; this was not related to any change in maximal activity of the aminotransferase. Steroid treatment increased the maximal activity of the aminotransferase. Both acute (3 days) and chronic (10 days) diabetes were associated with increased metabolism of phenylalanine; insulin treatment in vivo did not reverse these changes. Although elevated hydroxylase protein concentration was a major factor, changes in the enzyme phosphorylation state may contribute to differences in phenylalanine degradation in the acute and chronic diabetic states. Tyrosine metabolism, increased by diabetes, was partially restored to normal by insulin treatment in vivo. These changes can, to a large extent, be interpreted in terms of changes in the maximal activity of the aminotransferase.

Epidermal Growth Factor in Renal Hypertrophy in Streptozotocin-Diabetic Rats

Nephron ◽  
1991 ◽  
Vol 59 (4) ◽  
pp. 641-647 ◽  
Author(s):  
Jinn-Yuh Guh ◽  
Yung-Hsiung Lai ◽  
Shyi-Jang Shin ◽  
Lea-Yea Chuang ◽  
Juei-Hsiung Tsai
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Diabetic Rats ◽  
Renal Hypertrophy ◽  
Epidermal Growth ◽  
Streptozotocin Diabetic Rats

scholarly journals Factors influencing the altered thermogenic response of rat brown adipose tissue in streptozotocin-diabetes

1988 ◽  
Vol 249 (2) ◽  
pp. 415-421 ◽  
Author(s):  
Z Jamal ◽  
E D Saggerson
Keyword(s):  
Blood Flow ◽  
Maximum Rate ◽  
Insulin Treatment ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Brown Fat ◽  
Male Rats ◽  
Maximum Effect ◽  
O2 Uptake ◽  
Flow Through

1. Adipocytes were isolated from the interscapular brown fat of male rats maintained at 21 degrees C. These animals were controls, streptozotocin-diabetics or 2-day insulin-treated diabetics. 2. With adipocytes from diabetic animals, maximum rates of noradrenaline-stimulated O2 uptake were decreased by 58%, and the Bmax. of [3H]GDP binding to mitochondria was decreased by 55%. Insulin administration reversed both of these changes. 3. Streptozotocin-diabetes increased basal lipolysis in adipocytes incubated with adenosine deaminase (1 unit/ml), decreased the EC50 (concn. giving 50% of maximum effect) for noradrenaline, but did not change the maximum rate of noradrenaline-stimulated lipolysis. Except for some small differences at very low concentrations (10-100 pM), diabetes or insulin treatment did not alter the sensitivity of noradrenaline-stimulated lipolysis or O2 uptake to the inhibitory effect of N6-phenylisopropyladenosine. It is therefore concluded that the lesion(s) in thermogenesis in diabetes are not attributable to any changes in lipolysis. 4. Blood flow through interscapular brown fat, measured by accumulation of [14C]DDT [14C-labelled 1,1,1-trichloro-2,2-bis-(p-chlorophenyl)ethane] was increased by 2.3-fold 70 min after a single administration of insulin to diabetic rats. This treatment decreased blood flow through epididymal white fat by 58%. 5. Propranolol treatment of diabetic rats muted the ability of insulin treatment to increase the maximum rate of noradrenaline-stimulated O2 uptake, suggesting that this action of insulin may be a secondary one rather than a direct effect of the hormone on the adipocytes.

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