Gallbladder disease The risk of gallbladder disease, particularly gallstone formation, is increased in obesity and occurs with greater frequency in women. The prevalence of gallbladder disease in obese individuals increases with age, body weight, and parity. The etiology of increased gallstones is unclear, but genetic factors play a role. Increased cholesterol production, which leads to increased excretion of cholesterol in bile, is known to occur in obesity and correlates with increases in body weight. Many obese people skip meals and the reduced number of meals may result in less frequent emptying of the gallbladder. The resulting bile stasis may contribute to gallstone formation. Although long-term weight loss and maintenance may reduce the occurrence of gallbladder disease, the risk of gallstone formation actually increases during the active weight loss phase. The etiology of this increase is thought to be the mobilization of cholesterol from adipose tissue during rapid weight loss. This increased load of cholesterol in the circulation produces supersaturation of the bile, leading to gallbladder sludge in approximately 25% of patients and to symptomatic disease in approximately 1-3%. Treatment with ursodeoxycholic acid reduces or eliminates the risk of gallstone formation during weight loss.
Hepatic disease Abnormalities in hepatic function are commonly reported in obese people. Fatty liver, due to increased concentrations of fatty acids, digly-cerides, and triglycerides in hepatocytes, is reported in obese people. The frequency of fatty liver has been reported to be as high as 94% in very obese subjects. A small number of very obese subjects will develop micronodular cirrhosis. Abnormal liver enzymes on laboratory screening are very common in obese people and do not require further evaluation unless they are markedly elevated. Weight loss results in disappearance of the excess fat and normalization of the liver function tests.
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