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1 Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA; Department of Medicine, Stanford University, Stanford, CA, USA
2 Veterans Affairs Palo Alto Health Care System, Palo Alto, CA, USA
3 Department of Metabolic Diseases, University of Tokyo, Tokyo, Japan
4 Department of Internal Medicine, Jichi Medical School, Tochigi, Japan
* To whom correspondence should be addressed. E-mail: fbk{at}stanford.edu.
To elucidate the role of hormone-sensitive lipase (HSL) in diet-induced obesity, HSL deficient (HSL-/-) and wild-type mice were fed normal chow or high-fat diets. HSL-/- mice were resistant to diet-induced obesity showing higher core body temperatures. Weight and triacylglycerol contents were decreased in white adipose tissue (WAT) but increased in both brown adipose tissue (BAT) and liver of HSL-/- mice. Serum insulin levels in the fed state and tumor necrosis factor-
mRNA levels in adipose tissues were higher, while serum levels of ACRP30/adiponectin and leptin, as well as mRNA levels of
ACRP30/adiponectin, leptin, resistin and adipsin in WAT were lower in HSL-/- mice than in control. Expression of transcription factors associated with adipogenesis (peroxisome proliferator-activated receptor-
, CAAT/enhancer binding protein-) and lipogenesis (carbohydrate response element binding protein, adipocyte determination- and differentiation-dependent factor-1/sterol regulatory element binding protein-1c), as well as adipose differentiation markers (adipocyte lipid binding protein, perilipin, lipoprotein lipase),
lipogenic enzymes (glycerol-3-phosphate acyltransferase, acyl-CoA:diacylglycerol acyltransferase-1and -2, fatty acid synthase, ATP citrate lyase) and insulin signaling proteins
(insulin receptor, insulin receptor substrate-1, glucose transporter-4), was suppressed in WAT but not in BAT of HSL-/- mice. In contrast, expression of genes associated with cholesterol metabolism (sterol regulatory element binding protein-2, 3-hydroxy-3-methylglutaryl-
CoA reductase, acyl-CoA:cholesterol acyltransferase-1) and thermogenesis (uncoupling protein-2) were up-regulated in both WAT and BAT of HSL-/- mice. Our results suggest that impaired lipolysis in HSL-deficiency affects lipid metabolism through alterations of adipose differentiation and adipose-derived hormone levels.
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