Abstract
Germ-free (GF) mice lacking intestinal microbiota are significantly leaner than normal (NORM) control mice despite consuming more calories. The contribution of microbiota on the recognition and intake of fats is not known. Thus, we investigated the preference for, and acceptance of, fat emulsions in GF and NORM mice, and associated changes in lingual and intestinal fatty acid receptors, intestinal peptide content, and plasma levels of gut peptides. GF and NORM C57Bl/6J mice were given 48-h two-bottle access to water and increasing concentrations of intralipid emulsions. Gene expression of the lingual fatty acid translocase CD36 and protein expression of intestinal satiety peptides and fatty-acid receptors from isolated intestinal epithelial cells were determined. Differences in intestinal enteroendocrine cells along the length of the GI tract were quantified. Circulating plasma satiety peptides reflecting adiposity and biochemical parameters of fat metabolism were also examined. GF mice had an increased preference and intake of intralipid relative to NORM mice. This was associated with increased lingual CD36 (P<0.05) and decreased intestinal expression of fatty acid receptors GPR40 (P<0.0001), GPR41 (P<0.0001), GPR43 (P<0.05), and GPR120 (P<0.0001) and satiety peptides CCK (P<0.0001), PYY (P<0.001), and GLP-1 (P<0.001). GF mice had fewer enteroendocrine cells in the ileum (P<0.05), and more in the colon (P<0.05), relative to NORM controls. Finally, GF mice had lower levels of circulating leptin and ghrelin (P<0.001), and altered plasma lipid metabolic markers indicative of energy deficits. Increased preference and caloric intake from fats in GF mice are associated with increased oral receptors for fats coupled with broad and marked decreases in expression of intestinal satiety peptides and fatty-acid receptors.
Highlights
By the year 2030, half of the American adult population is predicted to be obese, which is attributed primarily to increased caloric intake [1]
We have recently demonstrated that GF mice exhibit increased ‘‘sweet’’ nutrient receptors and, sodium glucose-like transporter 1 (SGLT1) expression in the proximal intestine which was associated with increased sucrose intake [10]
The contribution of nutrient receptors to increased caloric intake in GF animals is not known, activation of nutrient responsive receptors leads to release of intestinal satiety peptides, such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide YY (PYY) [11,12,13]
Summary
By the year 2030, half of the American adult population is predicted to be obese, which is attributed primarily to increased caloric intake [1]. Despite the strong link between dietary fat intake and obesity, the factors leading to the over consumption of, and preference for, fats are less clear, but may be due to oral, intestinal, and metabolic influences. Intestinal and metabolic factors are profoundly influenced and modulated by the presence of trillions of microbes residing in the intestinal tract, collectively referred to as the gut microbiota, which contribute to altered energy intake and increased adiposity. As well, increased systemic lipolysis through increased expression of fasting induced adipocyte factor (FIAF), an intestinal lipoprotein lipase (LPL) inhibitor which results predominantly from decreased extraction of energy from the diet [7], may play a role in the protection from obesity in GF mice, the role of FIAF in the relationship between gut colonization and adiposity has been recently disputed (see [9]). The contribution of nutrient receptors to increased caloric intake in GF animals is not known, activation of nutrient responsive receptors leads to release of intestinal satiety peptides, such as cholecystokinin (CCK), glucagon-like peptide-1
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
