Biomaterial Database

Dietary excess regulates absorption and surface of gut epithelium through intestinal PPARα. 2021

Ozren Stojanović, and Jordi Altirriba, and Dorothée Rigo, and Martina Spiljar, and Emilien Evrard, and Benedek Roska, and Salvatore Fabbiano, and Nicola Zamboni, and Pierre Maechler, and Françoise Rohner-Jeanrenaud, and Mirko Trajkovski

Department of Cell Physiology and Metabolism, Centre Medical Universitaire (CMU), Faculty of Medicine, University of Geneva, Geneva, Switzerland.

Intestinal surface changes in size and function, but what propels these alterations and what are their metabolic consequences is unknown. Here we report that the food amount is a positive determinant of the gut surface area contributing to an increased absorptive function, reversible by reducing daily food. While several upregulated intestinal energetic pathways are dispensable, the intestinal PPARα is instead necessary for the genetic and environment overeating-induced increase of the gut absorptive capacity. In presence of dietary lipids, intestinal PPARα knock-out or its pharmacological antagonism suppress intestinal crypt expansion and shorten villi in mice and in human intestinal biopsies, diminishing the postprandial triglyceride transport and nutrient uptake. Intestinal PPARα ablation limits systemic lipid absorption and restricts lipid droplet expansion and PLIN2 levels, critical for droplet formation. This improves the lipid metabolism, and reduces body adiposity and liver steatosis, suggesting an alternative target for treating obesity.

UI	MeSH Term	Description	Entries
D007408	Intestinal Absorption	Uptake of substances through the lining of the INTESTINES.	Absorption, Intestinal
D007422	Intestines	The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.	Intestine
D008297	Male		Males
D008822	Mice, Transgenic	Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.	Transgenic Mice,Founder Mice, Transgenic,Mouse, Founder, Transgenic,Mouse, Transgenic,Mice, Transgenic Founder,Transgenic Founder Mice,Transgenic Mouse
D004032	Diet	Regular course of eating and drinking adopted by a person or animal.	Diets
D004435	Eating	The consumption of edible substances.	Dietary Intake,Feed Intake,Food Intake,Macronutrient Intake,Micronutrient Intake,Nutrient Intake,Nutritional Intake,Ingestion,Dietary Intakes,Feed Intakes,Intake, Dietary,Intake, Feed,Intake, Food,Intake, Macronutrient,Intake, Micronutrient,Intake, Nutrient,Intake, Nutritional,Macronutrient Intakes,Micronutrient Intakes,Nutrient Intakes,Nutritional Intakes
D005234	Fatty Liver	Lipid infiltration of the hepatic parenchymal cells resulting in a yellow-colored liver. The abnormal lipid accumulation is usually in the form of TRIGLYCERIDES, either as a single large droplet or multiple small droplets. Fatty liver is caused by an imbalance in the metabolism of FATTY ACIDS.	Liver Steatosis,Steatohepatitis,Steatosis of Liver,Visceral Steatosis,Liver Steatoses,Liver, Fatty,Steatohepatitides,Steatoses, Liver,Steatoses, Visceral,Steatosis, Liver,Steatosis, Visceral,Visceral Steatoses
D005786	Gene Expression Regulation	Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.	Gene Action Regulation,Regulation of Gene Expression,Expression Regulation, Gene,Regulation, Gene Action,Regulation, Gene Expression
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000070780	Perilipin-2	A perilipin that is expressed by many different cell types. It binds FATTY ACIDS and CHOLESTEROL, stabilizes TRIGLYCERIDES, and localizes to both the surface and hydrophobic core of LIPID DROPLETS, as well as the ENDOPLASMIC RECTICULUM and PLASMA MEMBRANE in MACROPHAGES. It also plays a central role in the biogenesis of lipid droplets and FOAM CELLS and is highly expressed by macrophages at atherosclerotic lesions in human arteries along with the INFLAMMATION markers TNF-ALPHA; MCP-1 RECEPTOR; and IL-6.	ADRP Protein,Adipophilin,Adipose Differentiation-Related Protein,PLIN2 Protein,Perilipin 2 Protein,Adipose Differentiation Related Protein,Perilipin 2,Protein, Adipose Differentiation-Related,Protein, PLIN2,Protein, Perilipin 2