A nutrient-sensing pathway regulates leptin gene expression in muscle and fat

Jiali Wang, Rong Liu, Meredith Hawkins, Nir Barzilai and Luciano Rossetti ()
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Jiali Wang: Diabetes Research and Training Center, Albert Einstein College of Medicine
Rong Liu: Diabetes Research and Training Center, Albert Einstein College of Medicine
Meredith Hawkins: Diabetes Research and Training Center, Albert Einstein College of Medicine
Nir Barzilai: Diabetes Research and Training Center, Albert Einstein College of Medicine
Luciano Rossetti: Diabetes Research and Training Center, Albert Einstein College of Medicine

Nature, 1998, vol. 393, issue 6686, 684-688

Abstract: Abstract Leptin, the protein encoded by the obese (ob) gene, is synthesized and released in response to increased energy storage in adipose tissue1,2,3,4. However, it is still not known how incoming energy is sensed and transduced into increased expression of the ob gene. The hexosamine biosynthetic pathway is a cellular ‘sensor’ of energy availability5,6,7,8 and mediates the effects of glucose on the expression of several gene products9,10,11,12. Here we provide evidence for rapid activation of ob gene expression in skeletal muscle by glucosamine. Increased tissue concentrations of the end product of the hexosamine biosynthetic pathway, UDP-N-acetylglucosamine (UDP-GlcNAc), result in rapid and marked increases in leptin messenger RNA and protein levels (although these levels were much lower than those in fat). Plasma leptin levels and leptin mRNA and protein levels in adipose tissue also increase. Most important, stimulation of leptin synthesis is reproduced by either hyperglycaemia or hyperlipidaemia, which also increase tissue levels of UDP-N-acetylglucosamine in conscious rodents7. Finally, incubation of 3T3-L1 pre-adipocytes and L6 myocytes with glucosamine rapidly induces ob gene expression. Our findings are the first evidence of inducible leptin expression in skeletal muscle and unveil an important biochemical link between increased availability of nutrients and leptin expression.

Date: 1998
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DOI: 10.1038/31474

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