Sydney Spanbauer
Pronouns:
Research Mentor(s): Nadejda Bozadjieva Kramer
Research Mentor School/College/Department: Surgery / Medicine
Program: UROP
Session: Session 5 (2:40pm – 3:30pm)
Authors: Sydney Spanbauer, Ava Freimark, Nadejda Bozadjieva-Kramer
Abstract
Obesity is a growing epidemic posing major healthcare challenges worldwide. Ketogenic diets have proven useful for weight loss and metabolic improvements in people with obesity. The liver acts as the major contributor for ketone bodies during ketogenesis. However, the intestine also expresses the molecular machinery required to perform ketogenesis. The goal of this study is to identify the relative contributions of intestinal gut ketogenesis as a mediator of body composition and glucose tolerance during nutrient lipid overload. We used control (wild type) and mice deficient in gut-derived Hmgcs2, a key enzyme required for ketogenesis (Hmgcs2GUT-KO). We fed control and Hmgcs2GUT-KO mice three diets, low fat (LFD), high fat (HFD) and ketogenic diet (KD) for 14 weeks. Body weight, fat mass, and lean mass were measured biweekly for 14 weeks. An oral glucose tolerance test (OGTT) was performed at 6 weeks, intraperitoneal glucose test (IPGTT) was performed at 8 and 12 weeks, and a mixed meal tolerance test (MMTT) was performed at 11 weeks. The results showed no difference in body weight. The Hmgcs2GUT-KO mice fed LFD had improved IP glucose tolerance compared to controls. The Hmgcs2GUT-KO mice fed KD had improved glucose tolerance when challenged with a mixed meal compared to controls. These data suggests that decreased gut ketogenesis is beneficial in glucose metabolism.
