Bhumika Prajapati has completed her M.S. Pharma in Biotechnology from National Institute of Pharmaceutical Education and Research (NIPER). She is currently perusing her Ph.D from Institute of Science, Nirma University. She has been awarded with Jawaharlal Nehru Scholarship for Doctoral Studies sponsored by Department of Science and Technology, India. Her work is mainly focused on the Gut microflora alteration in diet induced obesity and diabetes. She has published three papers in international journals


Background: Gut microbiota modulation using antibiotics can prevent progression of high sucrose diet (HSD) mediated obesity and diabetes, through microbial metabolites, short chain fatty acids (SCFAs) and inflammatory mediators. Aim: Present investigation was aimed to study the effect of altering the microflora of small intestine and colon in HSD rats by oral administration of antibiotics in context with obesity and insulin sensitivity. Methods: Rats were fed HSD with or without antibiotics administration for 60 days. The fecal microbiota communities, metabolites, glucose tolerance, plasma and hepatic lipids profile, histological evaluation and gene expression were investigated. Results: Simultaneous administration of HSD and antibiotics has shown significant improvements in glucose tolerance and obesity associated parameters like hypercholesterolemia and hypertryglyceremia as compared to HSD. The qPCR study of fecal samples showed marked increase in Lactobacillus and decrease in Enterobacteriaceae and E.coli in treated group, which indicated the restoration of commensal microflora in direction to improvement in obesity and insulin sensitivity. Gas chromatographic study indicated altered levels of the SCFAs such as butyrate and acetate (major source of the energy for gut epithelial) in treated group as compared with HSD. Antibiotics co-administered group showed relatively less histopathological symptoms, compared to HSD group. Treatment had decreased the gut derived Lipopolysaccharide, which further reduced Immune Receptors expression along with reduced NF-kB activity to downregulate the expression of proinflammatory cytokines