Evaluation of Anti-obesity Potentials of Phenolic-Rich Fraction of Solanum aethiopicum L. and Solanum macrocarpon L on Diet-induced Obesity in Wistar Rats

Obesity, one of the degenerative diseases, is a risk factor for chronical disease and an ultimate cause of metabolic syndrome which ismarked by the raising level of leptin on blood (hyperleptinemia). Metabolic syndrome is marked by the size of the waist is more than 40 inchfor man or 35 inch for woman, hypertension, hyperglycemia, high level of triglyceride, and the level of HDL (high-density lipoprotein) is low.This research is aimed to know the giving of quercetin (which has high anti oxide activities) on the declining level of leptin to the giving of DIO(Diet Induced Obesity). An experimental study using Post Test Control Group was done to the experimental wistar rats. Samples werechosen by using randomized complete block design. Rats were treated for 8 weeks. The dose of given quercetin were 2 mg/kgBB/day, 10mg/kgBB/day, and 50 mg/kgBB/day during the last 8 weeks of research. The variable measured in this research is the level of leptin onblood. Based on the experiment, quercetin is proven that gives influence to the level of leptin on obesity wistar rats’ serum compare to the givenlevel of leptin on controlled rats. There is different average on the level of leptin on wistar rats’ serum which being obesity on each grouptreatment. The giving of quercetin have significant correlation (p<0.05) with the level of leptin on wistar rats’ serum which being obesity (r = -0.704, p = 0.001). The conclusion from this research is the giving of quercetin to obesity rats for 8 weeks can decline the level of leptin onblood.Keywords: quercetin, leptin, high fat diet

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Broccoli extract improves high fat diet-induced obesity, hepatic steatosis and glucose intolerance in Wistar rats

Journal of Functional Foods ◽

10.1016/j.jff.2019.05.054 ◽

2019 ◽

Vol 59 ◽

pp. 319-328 ◽

Cited By ~ 4

Author(s):

Paula Aranaz ◽

David Navarro-Herrera ◽

Ana Romo-Hualde ◽

María Zabala ◽

Miguel López-Yoldi ◽

...

Keyword(s):

Hepatic Steatosis ◽

Glucose Intolerance ◽

High Fat Diet ◽

Wistar Rats ◽

High Fat ◽

Diet Induced Obesity

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Fatty acid composition of liver and adipose tissue lipids in Wistar rats with fat diet-induced obesity

Nahrung/Food ◽

10.1002/food.19850290608 ◽

1985 ◽

Vol 29 (6) ◽

pp. 577-583

Author(s):

C.-E. Völcker ◽

W. Haude

Keyword(s):

Adipose Tissue ◽

Fatty Acid Composition ◽

Fatty Acid ◽

Acid Composition ◽

Wistar Rats ◽

Diet Induced Obesity ◽

Tissue Lipids

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Diet-induced obesity and pancreatic islet blood flow in the rat: a preferential increase in islet blood perfusion persists after withdrawal of the diet and normalization of body weight

Journal of Endocrinology ◽

10.1677/joe.0.1510507 ◽

1996 ◽

Vol 151 (3) ◽

pp. 507-511 ◽

Cited By ~ 17

Author(s):

A M Svensson ◽

C Hellerström ◽

L Jansson

Keyword(s):

Blood Flow ◽

Body Weight ◽

Glucose Tolerance ◽

Pancreatic Islet ◽

Wistar Rats ◽

Blood Perfusion ◽

Cafeteria Diet ◽

Standard Diet ◽

Diet Induced Obesity ◽

Islet Blood Flow

Abstract The aim of the present study was to evaluate the effects of diet-induced obesity on pancreatic islet blood perfusion in normal Wistar rats. Furthermore, we investigated to what extent any obesity-associated changes in islet blood flow could be reversed after reversion to a normal diet with normalization of body weight. Young adult female Wistar rats were offered a palatable mixed high-caloric diet (cafeteria diet) in addition to standard pelleted chow. Age-matched control rats received standard pelleted chow only. After 4 weeks the diet-treated rats had a body weight of approximately 15% more than that of the controls. All diet-treated rats had decreased glucose tolerance and increased serum insulin concentrations, but basal blood glucose concentrations were similar in anesthetized diet-treated and control rats. Whole pancreatic and islet blood flow rates were measured with a microsphere technique. The islet blood flow as well as fractional islet blood flow were increased (P<0·01) in rats fed the cafeteria diet, while blood perfusion of the whole pancreas was similar to that of the control rats. In a second experiment, rats received the cafeteria diet for 4 weeks and were then fed standard pelleted food alone for another 3 weeks, while controls received standard diet for 7 weeks. After this period total body weight, retroperitoneal fat pad weight and glucose tolerance were similar to those of the controls. Whole pancreatic blood flow was unchanged as compared with that of control rats. However, both islet blood flow (P<0·01) and fractional blood flow (P<0·01) were increased. We conclude that diet-induced obesity in rats is associated with decreased glucose tolerance, hyperinsulinemia and a specific increase in absolute and fractional islet blood perfusion. This increase persists for at least 3 weeks after the diet is withdrawn despite normalization of body weight and glucose tolerance. Journal of Endocrinology (1996) 151, 507–511

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