Hnf4g invalidation prevents diet-induced obesity via intestinal lipid malabsorption.

Changes in dietary habits have occurred concomitantly with a rise of type 2 diabetes (T2D) and obesity. Intestine is the first organ facing nutrient ingestion and has to adapt its metabolism with these dietary changes. HNF-4γ, a transcription factor member of the nuclear receptor superfamily and mainly expressed in intestine, has been suggested to be involved in susceptibility to T2D.

Intestinal alteration of α-gustducin and sweet taste signaling pathway in metabolic diseases is partly rescued after weight loss and diabetes remission.

Carbohydrates and sweeteners are detected by the sweet taste receptor in enteroendocrine cells (EECs). This receptor is coupled to the gustducin G-protein, which α-subunit is encoded by gene. In intestine, the activation of sweet taste receptor triggers a signaling pathway leading to GLP-1 secretion, an incretin hormone.

Type 2 diabetes is associated with impaired jejunal enteroendocrine GLP-1 cell lineage in human obesity.

Objectives: Altered enteroendocrine cell (EEC) function in obesity and type 2 diabetes is not fully understood. Understanding the transcriptional program that controls EEC differentiation is important because some EEC types harbor significant therapeutic potential for type 2 diabetes.

Methods: EEC isolation from jejunum of obese individuals with (ObD) or without (Ob) type 2 diabetes was obtained with a new method of cell sorting.

Housing conditions and sacrifice protocol affect neural activity and vocal behavior in a songbird species, the zebra finch (Taeniopygia guttata).

Individual cages represent a widely used housing condition in laboratories. This isolation represents an impoverished physical and social environment in gregarious animals. It prevents animals from socializing, even when auditory and visual contact is maintained.