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Journal of Biological Sciences

Year: 2008 | Volume: 8 | Issue: 2 | Page No.: 421-425
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Authors

Wei Zhou

Katsunori Sato

Keywords

Research Article

Physiological Vulnerability to Diet Induced Obesity in Inbred Alloxan-Induced Diabetes-Susceptible Mice

Wei Zhou and Katsunori Sato
The effects of high fat diet on obesity and susceptibility to diabetics in Alloxan-induced diabetes-susceptible mice were studied. A total of 40 mice were divided equally (n = 10 per group) into four groups: (i) male high fat (40%) diet group (ii) female high fat (40% fat) diet group (iii) male control (7% fat) diet group and (iv) female control (7% fat) diet group. The body weight and blood glucose level of high fat male diet group were significantly (p<0.01; p<0.001) higher than those of other groups at 5 to 20 weeks of age. The high fat male and female mice produced significantly higher (p<0.05; p<0.001) perinephrium fat and mesenteric fat than those for corresponding control groups. However, the high fat female mice produced significantly (p<0.001) higher epididymal and high fat male mice produced significantly (p<0.001) lower epididymal fat than those for corresponding control groups. The high fat female mice produced significantly (p<0.01) higher retroperitoneal fat than that for control female group. The percentages of pancreas and genital organ trended to decrease and percentage of liver tended to increase for high fat male mice and percentage of pancreas and liver tended to decrease in high fat female mice than those for corresponding control group. However, the difference between two dietary groups in female mice for genital organ was insignificant. Only the male group fed with high fat diet developed diabetes (rate of incidence of glycosuria) with the earliest onset in strains occurred at the age of 10 weeks, followed by increasing to 100% disease at the age of 18 weeks and the phenomenon had been kept till the 20 weeks of age. Results of this study have shown that high fat diet male mice developed diabetics and dysfunction of glucose metabolism.
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