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Biochemical, Molecular, and Genetic Mechanisms

-Synuclein Is an Adipocyte-Neuron Gene Coordinately Expressed with Leptin and Increased in Human Obesity^1–3,

⁴ USDA/Agricultural Research Service Western Human Nutrition Research Center, Davis, CA 95616; ⁵ Institute National de la Santé et de la Recherche Médicale U626, Marseille and Faculté de Médecine, Université de la Méditerranée, 13385 Marseille Cedex, France; ⁶ Assistance Publique/Hopitaux de Paris, Pitié-Saltéprière and Tenon Hospitals, 75013 Paris, France ⁷ University Pierre and Marie Curie, 75006 Paris, France; ⁸ Institute National de la Santé et de la Recherche Médicale U872, Cordelier Research Center, 75006 Paris, France; ⁹ School of Biosciences, Cardiff University, Cardiff CF10 3US UK; ¹⁰ Carl T. Hayden Veterans Affairs Medical Center, Phoenix, AZ 85012; ¹¹ Campbell Family Institute for Breast Cancer Research, Toronto M5G 1L7 Canada; and ¹² Department of Nutrition, University of California, Davis, CA 95616

^* To whom correspondence should be addressed. E-mail: sean.h.adams{at}ars.usda.gov.

Recently, we characterized tumor suppressor candidate 5 (Tusc5) as an adipocyte-neuron PPAR target gene. Our objective herein was to identify additional genes that display distinctly high expression in fat and neurons, because such a pattern could signal previously uncharacterized functional pathways shared in these disparate tissues. -Synuclein, a marker of peripheral and select central nervous system neurons, was strongly expressed in white adipose tissue (WAT) and peripheral nervous system ganglia using bioinformatics and quantitative PCR approaches. -Synuclein expression was determined during adipogenesis and in subcutaneous (SC) and visceral adipose tissue (VAT) from obese and nonobese humans. -Synuclein mRNA increased from trace levels in preadipocytes to high levels in mature 3T3-L1 adipocytes and decreased 50% following treatment with the PPAR agonist GW1929 (P < 0.01). Because -synuclein limits growth arrest and is implicated in cancer progression in nonadipocytes, we suspected that expression would be increased in situations where WAT plasticity/adipocyte turnover are engaged. Consistent with this postulate, human WAT -synuclein mRNA levels consistently increased in obesity and were higher in SC than in VAT; i.e. they increased 1.7-fold in obese Pima Indian adipocytes (P = 0.003) and 2-fold in SC and VAT of other obese cohorts relative to nonobese subjects. Expression correlated with leptin transcript levels in human SC and VAT (r = 0.887; P < 0.0001; n = 44). -Synuclein protein was observed in rodent and human WAT but not in negative control liver. These results are consistent with the hypothesis that -synuclein plays an important role in adipocyte physiology.

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