Physical Activity Modulating Lipid Metabolism in Gallbladder Diseases

Abstract

Physical activity encompasses a series of overall benefits on cardiovascular health and metabolic disorders. Research has recently focused on the hepatobiliary tract, as an additional target of the health-related outcomes of different types of physical exercise. Here, we focus on the global features of physical activity with respect to exercise modality and intensity, and on studies linking physical activity to lipid metabolism, gallbladder diseases (gallstones, symptoms, complications and health-related quality of life), gallbladder motor-function, enterohepatic circulation of bile acids, and systemic metabolic inflammation. Additional studies need to unravel the pathophysiological mechanisms involved in both beneficial and harmful effects of physical activity in populations with different metabolic conditions.

Fig. 1.

Pathogenetic factors involved in the formation of cholesterol gallstones. Current research is focusing on several overlapping pathways, and the preeminent role of cholesterol across such pathways is depicted by the chemical formula: - genetic factors (i.e., polygenic predisposition or role of specific lithogenic genes); - hepatic factors (i.e., mainly hypersecretion of biliary cholesterol); - biliary factors (i.e., supersaturated gallbladder bile due to re-absorption of water from the gallbladder epithelium, propensity to transition of liquid micellar cholesterol to concentrated vesicular cholesterol, precipitation of excess cholesterol into solid anhydrous/monohydrate crystals which aggregate and form the first nucleus of cholesterol gallstones); - gallbladder factors (i.e., hypomotile viscus predisposing to stasis of supersaturated, mucin-enriched bile in a chronically inflamed gallbladder); intestinal factors (i.e., sluggish intestine predisposing to increased absorption of dietary and re-circulating biliary cholesterol, decreased bile acid reabsorption and effect of intestinal, mainly colonic microbiota, on biotransformation of primary bile acids into secondary –more lithogenic- bile acids). Adapted from [, , , , , , , –157].

Fig. 2.

A. Structure, chemical formula, molecular weight, elemental analysis and 3D formula of human bile acids. Primary bile acids are cholic acid (CA) and chenodeoxycholic acid (CDCA). Secondary bile acids are deoxycholic acid (DCA) and lithocholic acid (LCA). Tertiary bile acid is ursodeoxycholic acid (UDCA). B. Structure, chemical formula, molecular weight, elemental analysis and 3D formula of taurine and glycine which upon conjugation with bile acids increase their solubilization in bile.

Fig. 3.

Summary of the effects of physical activity on the gallbladder, and outside the gallbladder. With respect to cholelithiasis, beneficial effects can therefore activate either direct and/or indirect pathways. Abbreviations: BA: bile acids; GLP-1/2: glucagon-like peptide 1/2; GPBAR-1: G protein bile acid receptor 1; PYY: peptide YY; ↑: increased; ↓: decreased. Image found on https://wallpapersafari.com/w/0O9mLa.