GLP-1 is produced from the proglucagon gene in L-cells of the small intestine and is secreted in response to nutrients ( figure 1 ) [ 3 ]. GLP-1 binds to a specific GLP-1 receptor, which is expressed in various tissues, including pancreatic beta cells, pancreatic ducts, gastric mucosa, kidney, lung, heart, skin, immune cells, and the hypothalamus [ 2,4 ]. GLP-1 exerts its main effect by stimulating glucose-dependent insulin release from the pancreatic islets [ 2 ]. It has also been shown to slow gastric emptying [ 5 ], inhibit inappropriate post-meal glucagon release [ 3,6 ], and reduce food intake ( table 1 ) [ 3 ]. Owing in part to the effects of GLP-1 on slowed gastric emptying and appetite centers in the brain, therapy with GLP-1 and its receptor agonists is associated with weight loss, even among patients without significant nausea and vomiting. (See 'Weight loss' below.)
Poverty is a good indicator of the rate of infectious diarrhea in a population. This association does not stem from poverty itself, but rather from the conditions under which impoverished people live. The absence of certain resources compromises the ability of the poor to defend themselves against infectious diarrhea. "Poverty is associated with poor housing, crowding, dirt floors, lack of access to clean water or to sanitary disposal of fecal waste ( sanitation ), cohabitation with domestic animals that may carry human pathogens, and a lack of refrigerated storage for food, all of which increase the frequency of diarrhea... Poverty also restricts the ability to provide age-appropriate, nutritionally balanced diets or to modify diets when diarrhea develops so as to mitigate and repair nutrient losses. The impact is exacerbated by the lack of adequate, available, and affordable medical care."