Diet Composition and Insulin Effect on Amylase to Lipase Ratio in Pancreas of Diabetic Rats

Digestion ◽  
1979 ◽  
Vol 19 (6) ◽  
pp. 386-391 ◽  
Author(s):  
R. Bazin ◽  
M. Lavau
Keyword(s):  
Diet Composition ◽  
Diabetic Rats ◽  
Insulin Effect

In vitro insulin effect on acetylcholine esterase of erythrocyte membranes of normal and diabetic rats

1985 ◽  
Vol 22 (4) ◽  
pp. 358-363 ◽  
Author(s):  
Veena R. Agarwal ◽  
Anil K. Rastogi ◽  
Maharaj K. Sahib ◽  
Prem Sagar
Keyword(s):  
Diabetic Rats ◽  
Acetylcholine Esterase ◽  
Erythrocyte Membranes ◽  
Insulin Effect

Glucocorticoids and insulin: complex interaction on brown adipose tissue

1995 ◽  
Vol 268 (5) ◽  
pp. R1209-R1216 ◽  
Author(s):  
A. M. Strack ◽  
C. J. Horsley ◽  
R. J. Sebastian ◽  
S. F. Akana ◽  
M. F. Dallman
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Uncoupling Protein ◽  
Diabetic Rats ◽  
Insulin Effect ◽  
Caloric Efficiency ◽  
Brown Adipose ◽  
System Input ◽  
Streptozotocin Induced Diabetes

Glucocorticoids and insulin effect long-term reciprocal changes in food intake and body weight. We tested the interactions of corticosterone and insulin on caloric efficiency, white adipose tissue (WAT) stores, and brown adipose tissue (BAT). Two experiments were performed: 1) adrenalectomized rats were treated with corticosterone with or without streptozotocin-induced diabetes and 2) adrenalectomized, corticosterone-treated, diabetic rats were treated with insulin. By 4-5 days later, > or = 50% of the variance in caloric efficiency, plasma triglycerides, and WAT stores was explained by regression of these variables on corticosterone (catabolic) and insulin (anabolic). When the ratio of the hormones was normal, but concentrations high, overall gain of energy stores decreased and energy was redistributed to fat. Both hormones were anabolic on BAT lipid storage; the hormones played a complex role in the regulation of uncoupling protein (UCP) in BAT. Although corticosterone inhibited and insulin stimulated UCP, these effects were only evident in diabetics and with normoglycemia, respectively. For BAT variables, < or = 50% of the variance was explained by regression on corticosterone and insulin, suggesting that the effects of these hormones are mediated through an intermediate such as sympathetic nervous system input to BAT.

Enhanced Sugar Uptake Fails to Simulate the Insulin Effect on Lipogenesis in the Isolated Perfused Rat Liver

1958 ◽  
Vol 193 (3) ◽  
pp. 469-475 ◽  
Author(s):  
David E. Haft ◽  
Leon L. Miller
Keyword(s):  
Metabolic Pathways ◽  
Ketone Body ◽  
Diabetic Rats ◽  
Sugar Uptake ◽  
Isolated Perfused Rat Liver ◽  
Primary Role ◽  
Perfused Rat Liver ◽  
Insulin Effect ◽  
Primary Action

Large quantities of glucose and fructose were infused without insulin into isolated livers of fasted normal and fed diabetic rats as a test of the widely accepted theory that the single primary role of insulin is to speed the entry of glucose into the cell. The liver disposed of large quantities of hexose in most cases without simultaneously increasing, as with insulin, the rate of incorporation of acetate-1-C14 into fatty acids. Much of the sugar was transformed to glycogen and CO2 without entering the pathways of fatty acid or ketone body synthesis, or influencing the conversion of acetate to these products. With livers of fasted normal rats, massive fructose infusion significantly inhibited urea formation and reduced the incorporation of acetate into glucose and plasma protein. The dissociation between carbohydrate balance and lipogenesis suggests that insulin has some primary action other than making more sugar available in metabolism. It is suggested that there is an anatomic separation of metabolic pathways in the liver, and that insulin serves to facilitate glucose transport between them.

Insulin binding and glucose transport activity in cardiomyocytes of a diabetic rat

1986 ◽  
Vol 250 (4) ◽  
pp. E402-E406 ◽  
Author(s):  
E. C. Almira ◽  
A. R. Garcia ◽  
B. R. Boshell
Keyword(s):  
Glucose Transport ◽  
Insulin Binding ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Heart Cells ◽  
Apparent Difference ◽  
Insulin Effect ◽  
Streptozotocin Induced Diabetes

We studied insulin binding and glucose transport in isolated adult cardiomyocytes from rats with 2-wk streptozotocin-induced diabetes. At 37 degrees C, cells from diabetic rats bound less 125I-insulin and exhibited lower rates of 3-O-methylglucose transport than cells from control rats. In contrast, the amount of 125I-insulin bound to myocytes at 4 degrees C was the same in both groups. Preincubation of cells from both groups with 10-10,000 ng/ml insulin significantly increased their basal rates of glucose transport by approximately 40%. However, the augmented rates in diabetics were still approximately 36% lower than the corresponding insulin-stimulated rates in the controls. When the glucose transport data were expressed as percent maximal insulin effect and plotted as a function of the amount of insulin bound, the curves obtained from both diabetic and nondiabetic controls were superimposable. These data demonstrate that 1) heart cells from diabetic rats bind less insulin than from control rats under conditions in which they exhibit impaired glucose transport rates, 2) there is no apparent difference in total receptor number between the two groups, but internalization of intact insulin appears to be diminished in diabetes, 3) coupling exists between insulin binding and glucose transport in both groups, and 4) these impaired processes are completely reversed by insulin treatment in vivo but not in vitro.

P 23: The possible contribution of thyroid hormones to insulin effect on beta adrenoceptor mediated cardiac responses in diabetic rats

2012 ◽  
Vol 38 ◽  
pp. S112-S113
Author(s):  
E. Arioglu-Inan ◽  
I. Ozakca ◽  
G. Kayki-Mutlu ◽  
A. Sepici-Dincel ◽  
V.M. Altan
Keyword(s):  
Thyroid Hormones ◽  
Diabetic Rats ◽  
Insulin Effect ◽  
Beta Adrenoceptor ◽  
Cardiac Responses

scholarly journals Insulin Within the Arcuate Nucleus Has Paradoxical Effects on Nociception in Healthy and Diabetic Rats

2020 ◽  
Vol 11 (6) ◽  
pp. 727-736
Author(s):  
Hossein Khaleghzadeh-Ahangar ◽  
◽  
Forouzan Sadeghimahalli ◽  
Shaghayegh Khandan ◽  
Sima Shahabi ◽  
...  
Keyword(s):  
Pain Perception ◽  
Arcuate Nucleus ◽  
Insulin Receptors ◽  
Regular Insulin ◽  
Diabetic Rats ◽  
Pain Tolerance ◽  
Tail Flick ◽  
Animal Group ◽  
Insulin Effect ◽  
Thermal Nociception

Introduction: Broad neural circuits originate from the hypothalamic arcuate nucleus and project to many parts of the brain which are related to pain perception. Insulin receptors are found in the arcuate nucleus. Since nociception may be affected in type 1 diabetes, the present study aimed to investigate the intra-arcuate nucleus insulin role in pain perception in streptozotocin (STZ)-induced diabetic and healthy rats. Methods: Regular insulin was microinjected within the arcuate nucleus and the pain tolerance was measured using the hot plate and the tail-flick apparatus in diabetic rats. Results: The results showed that the arcuate nucleus suppression with lidocaine could increase thermal nociception in non-diabetic animals. Also, insulin within the arcuate nucleus decreased the acute thermal pain perception in these animals. STZ-induced diabetes produced hypoalgesia which the latency of these tests, progressively increased over time after induction of diabetes. Also, in the same animal group, intra-arcuate injection of insulin reduced the latency of nociception. Conclusion: Intra-arcuate insulin has paradoxical and controversial effects in healthy and diabetic rats’ nociception. These effects seem to be due to the insulin effect on releasing pro-opiomelanocortin and its deriv

Sites of Insulin Action Using Ferritin Labeling

1971 ◽  
Vol 29 ◽  
pp. 540-541
Author(s):  
Burton B. Silver ◽  
Ronald S. Nelson
Keyword(s):  
Electron Microscopy ◽  
Binding Sites ◽  
Anterior Pituitary ◽  
Insulin Action ◽  
Diabetic Rats ◽  
Insulin Antibody ◽  
Fat Pad ◽  
Target Organs ◽  
Uranium Salts ◽  
Sugar Levels

Some investigators feel that insulin does not enter cells but exerts its influence in some manner on the cell surface. Ferritin labeling of insulin and insulin antibody was used to determine if binding sites of insulin to specific target organs could be seen with electron microscopy.Alloxanized rats were considered diabetic if blood sugar levels were in excess of 300 mg %. Test reagents included ferritin, ferritin labeled insulin, and ferritin labeled insulin antibody. Target organs examined were were diaphragm, kidney, gastrocnemius, fat pad, liver and anterior pituitary. Reagents were administered through the left common carotid. Survival time was at least one hour in test animals. Tissue incubation studies were also done in normal as well as diabetic rats. Specimens were fixed in gluteraldehyde and osmium followed by staining with lead and uranium salts. Some tissues were not stained.

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