Review: low caloric intake and gall-bladder motor function

Cholelithiasis is the primary expression of obesity in the hepatobiliary sy stem. In obese subjects the risk of developing gallstones is increased due to a higher cholesterol saturation of gall-bladder bile. During weight redu ction with very low calorie diets (VLCD) the incidence of gallstones increa ses, but the mechanism for gallstone formation is not completely understood and several pathogenetic mechanisms have been suggested: increased saturat ion of bile, increased gall-bladder secretion of mucin and calcium, increas ed presence of prostaglandins and arachidonic acid. Alterations in gall-bla dder motility may contribute to gallstone formation, but few studies have a ddressed the issue of gall-bladder motility during rapid weight loss and it s possible role in gallstone formation. VLCD have been associated with a ga ll-bladder stasis, as consequence of reduced gall-bladder stimulation by lo w fat content: of the diets. A threshold quantity of fat (10 g) has been do cumented to obtain efficient gallbladder emptying. Ursodeoxycholic acid adm inistered during VLCD seems to have a protective role in developing a bilia ry cholesterol crystals. Gall-bladder emptying was lower in response to low fat meals with respect to relative higher fat meals, before as well as dur ing the VLCD. This may account the possibility of an adaptative response of the gall-bladder motility to a given diet regimen. Adequate fat content of the VLCD may prevent gallstone formation, maintaining adequate gall-bladde r motility and may be more economic and physiologically acceptable than adm inistration of a pharmacological agent.