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The rate of overweight and obese adults continues to rise in the US and world. Obese women have higher risk and mortality rates from all types of cancers including breast cancer. The intestinal microbiota is composed of a diverse population of obligate and facultative anaerobic microorganisms, and these organisms carry out a broad range of metabolic activities. Previously, we reported that a soy protein diet containing high isoflavone levels promoted 7, 12 dimethylbenz [a]anthracene (DMBA) induced mammary tumor development compared to a casein-based diet and the plasma equol was significantly lower in obese soy-fed rats compared to lean soy-fed rats. Obesity has been linked to changes in the intestinal microbiota, but the effects of obesity and soy protein diet on the composition of the intestinal microbiota have not been studied. The objective of study was to determine the effects of obesity and diet containing soy protein isolate on gut microbiota. Lean and obese female Zucker rats (n = 34) were randomly assigned to 1) casein, or 2) soy protein diets for 8 weeks. Fecal samples, collected at the end of the experiment, were analyzed using 16S rRNA gene sequencing to determine the bacterial populations present. Bacterial DNA was isolated from the fecal samples using a commercial kit and the DNA prepared for sequencing using barcoded primers specific for the Illumina MiSeq platform. Following sequencing, the readings were de-multiplexed and the different taxa identified to characterize the total bacterial populations. Our results suggest that there are differences in gut microbiota associated with diet and the lean/ obese state. Further investigation will be needed to determine the effects of obesity and soy protein diet on gut microbiota in relation to DMBA-induced mammary tumor formation. Mg2+-Deficiency in Liver Cells: At the Cross-Road Between Inflammation and Dysmetabolism Andrea Romani*, Chesinta Voma and Lauren Keenan Case Western Reserve University, Department of Physiology and Biophysics, Cleveland, OH, USA Abstract A decrease in tissue and serum Mg2+ content has been observed in several endocrinopathies including metabolic syndrome and diabetes, but it is still undefined whether Mg2+ deficiency plays a role in the onset of these pathologies and/or their complications. Our experimental observation in animals and human liver cells indicate that Mg2+ deficiency increases G6P entry into the ER, and results in an increased oxidation by H6PD. The produced NADPH is then utilized by the 11β-HSD1 to convert inactive cortisone to active cortisol. Our data indicate that cortisol production is markedly increased in Mg2+ deficient hepatocytes and results in enhanced gluconeogenesis, hepatic fatty acid synthesis, and intrahepatic triglycerides deposition. Furthermore, Mg2+-deficient hepatocytes present decreased insulin responsiveness, which is further compromised by cortisol J of Obesity and Chronic DiseasesA decrease in tissue and serum Mg2+ content has been observed in several endocrinopathies including metabolic syndrome and diabetes, but it is still undefined whether Mg2+ deficiency plays a role in the onset of these pathologies and/or their complications. Our experimental observation in animals and human liver cells indicate that Mg2+ deficiency increases G6P entry into the ER, and results in an increased oxidation by H6PD. The produced NADPH is then utilized by the 11β-HSD1 to convert inactive cortisone to active cortisol. Our data indicate that cortisol production is markedly increased in Mg2+ deficient hepatocytes and results in enhanced gluconeogenesis, hepatic fatty acid synthesis, and intrahepatic triglycerides deposition. Furthermore, Mg2+-deficient hepatocytes present decreased insulin responsiveness, which is further compromised by cortisol J of Obesity and Chronic Diseases