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Effects of short‐term leptin exposure on triglyceride deposition in rat liver
Author(s) -
Roden Michael,
Anderwald Christian,
Fürnsinn Clemens,
Waldhäusl Werner,
Lohninger Alfred
Publication year - 2000
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1053/jhep.2000.18712
Subject(s) - leptin , medicine , endocrinology , triglyceride , insulin , chemistry , steatosis , glucagon , cholesterol , obesity
Leptin has recently been suggested to play a role in the pathogenesis of hepatic steatosis. Consequently, this study was designed to examine the direct effects of portal leptin on the intrahepatic lipid contents in the postabsorptive state. Rat livers (n = 6 per group) were perfused in a recirculating system and portally infused with leptin (0.5 nmol/L, 5 nmol/L, and 25 nmol/L), insulin (10 nmol/L), leptin (5 nmol/L) plus insulin (10 nmol/L), glucagon (1 nmol/L), or vehicle (control). Intrahepatic contents of triglycerides, free cholesterol, cholesteryl esters, and free fatty acids were determined from the lipid extract of frozen livers by capillary gas chromatography. Short‐term leptin infusion increased total triglycerides in a concentration‐dependent (0.5 nmol/L: 2.8 ± 0.4 mg/g, 5 nmol/L: 7.0 ± 0.5 mg/g, 25 nmol/L: 8.3 ± 1.0 mg/g) and time‐dependent manner. Total triglycerides also rose during exposure to insulin plus leptin (7.2 ± 0.6 mg/g) but fell during glucagon infusion (2.6 ± 0.2 mg/g; control: 4.3 ± 0.3 mg/g; P < .05). Leptin, insulin, and glucagon increased intrahepatic free cholesterol ( P < .05). Free fatty acids were also higher during leptin exposure (0.5 nmol/L: 1.28 ± 0.08 mg/g, 5 nmol/L: 0.47 ± 0.01 mg/g, 25 nmol/L: 0.48 ± 0.04 mg/g, control: 0.38 ± 0.03 mg/g; P < .05). In conclusion, hyperleptinemia increases hepatic triglyceride content and may therefore contribute to hepatic steatosis in hyperleptinemic obese patients.