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Estrogen Reduced Blood Glucose in High Fat-Fed Mice: An Animal Model of Type 2 Diabetes

Suwattanee Kooptiwut, Namoiy Semprasert, Smarn Onreabroi

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Abstract

Objective: This study aims to produce a mouse model of type 2 diabetes by using high fat diet. The C57BL/6J mouse strain can develop type 2 diabetes by putting on high fat diet. Methods: A group of C57BL/6J male mice were fed with a high fat diet (53% energy by fat) while another group was fed with normal diet (4.5% energy by fat). Results: At the 16th week of feeding study, the high fat-fed mice developed type 2 diabetes and had higher fat-pad weight than the normal diet-fed mice. However, plasma triglyceride (TG) levels of the two groups were not different. High fat-induced diabetic mice were administered 0.2 μg/g body weight of 17-β estradiol for 2 weeks. Their fasting blood levels were reduced to become lesser than the levels in high-fat fed mice without estrogen. A trend of decrease in plasma TG level of 17-β estradiol treated mice was observed. Conclusion: This study demonstrated that high fat diet could induce type 2 diabetes in a mouse model and that estrogen could reduce the fasting blood glucose in these mice.

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What this paper is about

Objective: This study aims to produce a mouse model of type 2 diabetes by using high fat diet. The C57BL/6J mouse strain can develop type 2 diabetes by putting on high fat diet. Methods: A group of C57BL/6J male mice were fed with a high fat diet (53% energy by fat) while another group was fed with normal diet (4.5% energy by fat). Results: At the 16th week of feeding study, the high fat-fed mice developed type 2 diabetes and had higher fat-pad weight than the normal diet-fed mice. However, plasma triglyceride (TG) levels of the two groups were not different. High fat-induced diabetic mice were administered 0.2 μg/g body weight of 17-β estradiol for 2 weeks. Their fasting blood levels were reduced to become lesser than the levels in high-fat fed mice without estrogen. A trend of decrease in plasma TG level of 17-β estradiol treated mice was observed. Conclusion: This study demonstrated that high fat diet could induce type 2 diabetes in a mouse model and that estrogen could reduce the fasting blood glucose in these mice.

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Available abstract

Objective: This study aims to produce a mouse model of type 2 diabetes by using high fat diet. The C57BL/6J mouse strain can develop type 2 diabetes by putting on high fat diet. Methods: A group of C57BL/6J male mice were fed with a high fat diet (53% energy by fat) while another group was fed with normal diet (4.5% energy by fat). Results: At the 16th week of feeding study, the high fat-fed mice developed type 2 diabetes and had higher fat-pad weight than the normal diet-fed mice. However, plasma triglyceride (TG) levels of the two groups were not different. High fat-induced diabetic mice were administered 0.2 μg/g body weight of 17-β estradiol for 2 weeks. Their fasting blood levels were reduced to become lesser than the levels in high-fat fed mice without estrogen. A trend of decrease in plasma TG level of 17-β estradiol treated mice was observed. Conclusion: This study demonstrated that high fat diet could induce type 2 diabetes in a mouse model and that estrogen could reduce the fasting blood glucose in these mice.

Key concepts: Endocrinology, Internal medicine, Type 2 diabetes, Estrogen, Diabetes mellitus, Triglyceride, Obesity, Medicine

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