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Diabetes Publish Ahead of Print published online ahead of print April 17, 2007
DOI: 10.2337/db06-1699
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Original Research

CD36-facilitated fatty acid uptake inhibits leptin production and signaling in adipose tissue

Tahar Hajri1, Angela M Hall2, Dalan R Jensen3, Terri A Pietka2, Victor A Drover4, Huan Tao1, Robert Eckel3, and Nada A Abumrad2

1Department of Surgery, Vanderbilt University, Nashville, TN 37232
2Department of Medicine, Nutritional Science, Washington University, St Louis MO 63110
3Division of Endocrinology, University of Colorado Health Sciences Center, Aurora, CO 80010
4Department of Pharmacology, Stony Brook University, NY, 11794

Key Words: leptin • secretion • signaling • adipose tissue • CD36 null • fatty acid • glucose

Leptin plays an important role in regulating energy expenditure in response to food intake but nutrient regulation of leptin is incompletely understood. In this study using in vivo and in vitro approaches we examined the role of fatty acid (FA) uptake in modulating leptin expression and production. Leptin levels are doubled in the CD36 null mouse which has impaired cellular FA uptake despite a 40% decrease in fat mass. The CD36 null mouse is protected from diet-induced weight gain but not from that consequent to leptin deficiency. Leptin secretion in the CD36 null mouse is strongly responsive to glucose intake while a blunted response is observed in the wild type mouse. This indicates that leptin regulation integrates opposing influences from glucose and FA and loss of FA inhibition allows unsuppressed stimulation by glucose/insulin. FA inhibition of basal and insulin stimulated leptin release is linked to CD36-facilitated FA flux which is important for FA activation of PPAR{gamma} and likely contributes to the nutrient sensing function of adipocytes. FA uptake also may modulate adipocyte leptin signaling. The ratio of phosphorylated to unphosphorylated STAT3, an index of leptin activity, is increased in CD36 null fat tissue disproportionately to leptin levels. In addition expression of leptin sensitive FA oxidative enzymes is enhanced. Targeting adipocyte CD36 may offer a way to uncouple leptin production and adiposity.


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 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
A. Sclafani, K. Ackroff, and N. A. Abumrad
CD36 gene deletion reduces fat preference and intake but not post-oral fat conditioning in mice
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2007; 293(5): R1823 - R1832.
[Abstract] [Full Text] [PDF]


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