ISSN: 2155-9600
+32 25889658
Kristina Martinez
University of Chicago, USA
Posters-Accepted Abstracts: J Nutr Food Sci
It is widely accepted that the gut microbiota plays a role in the development of obesity, exemplified by the finding that germ free (GF) mice are resistant to high fat (HF) diet-induced obesity (DIO).Herein, we aimed to determine the mechanisms underlying this phenomenon. Results from our studies suggest that GF mice have impaired fat digestion and absorption. For instance, GF mice gavaged with radio-labeled tri-olein show less accumulation in the blood over time compared to conventional (Conv.) mice. Additionally, GF mice fed a HF diet for four weeks display elevated triglycerides in their stool and have enlarged gallbladders compared to Conv. mice, suggesting a potential impairment in bile secretion. Thus, mRNA expression of entero-endocrine hormones that regulate gallbladder contraction (i.e., cholescystokinin; CCK) and pancreatic secretion of lipases (i.e., secretin) were measured in the small intestine. Interestingly, gene expression levels of cck and secretin were reduced in the small intestineof GF mice compared to Conv. mice and were restored in conventionalized (Conv. D) GF mice. Additionally, GF mice given a lipid challenge had less pancreatic lipase and amylase in the small intestine compared to Conv. mice. Taken together, these data suggest that due to impaired secretin and CCK signaling, less bile and pancreatic enzymes are released to properly emulsify and digest fats, respectively. This may lead to impaired lipid absorption and thus resistance to DIO in GF mice.
Email:
kmartinez@medicine.bsd.uchicago.edu