Abstract
Objectives
High glycemic index diet has been demonstrated to induce obesity and insulin resistance. The role of gut microbiota, as a key mediator of several metabolic syndromes, has not been elucidated. The objective of this project is to understand the effect of gut microbiota in a high-glycemic diet-induced obesity and associated metabolic complications.
Methods
Male C57Bl6/J mice aged 8–9 weeks were fed with a high-glycemic diet (HG, amylopectin-based) or low-glycemic diet (LG, amylose-based) ad libitum for 8 weeks. Body composition was determined by MRIs. Intraperitoneal glucose tolerance tests were performed after 6 weeks on diet. Mice were euthanized after 8 weeks on diet.
Results
After two weeks on diet, the HG group (n = 12) mice had a significantly higher body fat mass by MRI analysis, as compared to the LG group (n = 12) despite having similar body weight and equal food consumption. After 6 weeks, mice in the HG group had a significantly higher fasting glucose level compared to the LG group. There was no difference in fasting triglyceride level. Gonadal, subcutaneous and brown fat adipose tissue weight were significantly higher in the HG group after 8 weeks on diet. 16S rDNA sequencing on feces showed that the HG mice have a significantly higher Shannon diversity and different overall microbiome structure compared to the LG mice. The microbial community in the LG group was predominated by Bacteroidetes, particularly by Bacteroides thetaiotaomicron (Relative abundance 48.65 ± 12.88% versus HG 14.69 ± 0.07%), while the HG group was predominated by Firmicutes. Ongoing analysis will investigate the relative role of key microbial taxa on obesity and glucose homeostasis.
Conclusions
Consuming two weeks of a high-glycemic index diet induced adiposity and hyperglycemia along with a shift of the overall gut microbiota composition compared to a low-glycemic index diet.
Funding Sources
NIH, USDA, Robert C and Veronica Atkins Foundation