Lipoprotein Lipase Expression in Livers of Morbidly Obese Patients Could be Responsible for Liver Steatosis
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Most patients with morbid obesity develop non-alcoholic fatty liver disease (NAFLD). The origins of lipid deposition in the liver and the effects of bariatric surgery in the obese with NAFLD are controversial.
We analyzed lipids and lipoprotein lipase (LPL) in both plasma and liver biopsies performed before and 12–18 months after Roux-en-Y gastric bypass surgery in 26 patients.
In the livers of morbidly obese patients, the levels of LPL messenger RNA (mRNA) were higher (4.5-fold) before surgery than afterwards than control livers. In these patients, LPL activity was also significantly higher (91 ± 7 mU/g) than in controls (51 ± 3 mU/g, p = 0.0026) and correlated with the severity of the liver damage. All hepatic lipids were significantly increased in obese patients; however, after bariatric surgery, these lipids, with the exception of NEFA, tended to recover to normal levels.
The liver of obese patients presented higher LPL activity than controls, and unlike the controls, this enzyme could be synthesized in the liver because it also present LPL mRNA. The presence of the LPL activity could enable the liver to capture circulating triacylglycerides, thus favoring the typical steatosis observed in these patients.
KeywordsMetabolic syndrome Hepatic steatosis NAFLD NASH LPL
non-alcoholic fatty liver disease
free fatty acids
homeostasis model assessment of insulin resistance
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