Abnormalities of lipid metabolism, gallstone disease and gallbladder function

Gallstone disease is highly prevalent with a complex and multifactorial pathogenesis. Gallstones are closely related to the metabolic syndrome associated disease conditions in which abnormal regulation of lipid metabolism secondary to insulin resistance plays a major pathogenic role. Insulin resistance increases biliary cholesterol secretion and affects gallbladder (GB) motility. Regulation of lipid metabolism and energy homeostasis is complex and the GB has been considered to have a minor regulatory role in both the intestinal absorption of lipids and metabolic homeostasis of the whole body. In fact, ablation of the GB does not affect nutrient absorption or the ability to lead a normal life. GB function regulates the cycling of bile salts through the enterohepatic circulation. Bile salts have important signaling effects that can affect whole body metabolic homeostasis. The GB and intestinal mucosa are rich in the hormone FGF15/19 and the receptor TGR5, which participate in metabolic regulation. Recent evidence supports the hypothesis that cholecystectomy may not be innocuous and that the GB has a significant role in the regulation of hepatic triglyceride metabolism. This article provides information regarding recent advances in the understanding of the interaction between regulation of lipid metabolism, insulin resistance, gallstone disease and GB function.