cytosolic malic enzyme 1 (me1) mediates high fat diet-induced adiposity, endocrine profile, and gastrointestinal tract proliferation-associated biomarkers in male mice胞质苹果酸脱氢酶1(组织)介导高脂肪食源性肥胖,内分泌,并在雄性小鼠胃肠道proliferation-associated生物标记.pdf

Cytosolic Malic Enzyme 1 (ME1) Mediates High Fat Diet- Induced Adiposity, Endocrine Profile, and Gastrointestinal Tract Proliferation-Associated Biomarkers in Male Mice 1 1,3 1,2,3 1,2 Ahmed Al-Dwairi , John Mark P. Pabona , Rosalia C. M. Simmen , Frank A. Simmen * 1 Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America, 2 Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America, 3 Arkansas Children’s Nutrition Center, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America Abstract Background: Obesity and associated hormonal disturbances are risk factors for colon cancer. Cytosolic Malic Enzyme (ME1) generates NADPH used for lipogenesis in gastrointestinal (GI), liver and adipose tissues. We have reported that inclusion of soy protein isolate (SPI) in the diet lowered body fat content and colon tumor incidence of rats fed AIN-93G diet, while others have demonstrated SPI inhibition of rat hepatic ME1 expression. The present study examined the individual and combined effects of dietary SPI and absence of ME1 on: 1) serum concentrations of hormones implicated in colon cancer development, 2) expression of lipogenic and proliferation-associated genes in the mouse colon and small intestine, and 3) liver and adipose expression of lipogenic and adipocytokine genes that may contribute to colon cancer predisposition. Methods: Weanling wild type (WT) and ME1 null (MOD-1) male mice were fed high-fat (HF), iso-caloric diets containing either casein (CAS) or SPI as sole protein source for 5 wks. Somatic gr