Tenomodulin promotes human adipocyte differentiation and beneficial visceral adipose tissue expansion

Ozlem Senol-Cosar, Rachel J. Roth Flach, Marina DiStefano, Anil Chawla, Sarah Nicoloro, Juerg Straubhaar, Olga T. Hardy, Hye Lim Noh, Jason K. Kim, Martin Wabitsch, Philipp E. Scherer and Michael P. Czech ()
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Ozlem Senol-Cosar: Program in Molecular Medicine, University of Massachusetts Medical School
Rachel J. Roth Flach: Program in Molecular Medicine, University of Massachusetts Medical School
Marina DiStefano: Program in Molecular Medicine, University of Massachusetts Medical School
Anil Chawla: Program in Molecular Medicine, University of Massachusetts Medical School
Sarah Nicoloro: Program in Molecular Medicine, University of Massachusetts Medical School
Juerg Straubhaar: Program in Molecular Medicine, University of Massachusetts Medical School
Olga T. Hardy: Touchstone Diabetes Center, The University of Texas Southwestern Medical Center
Hye Lim Noh: Program in Molecular Medicine, University of Massachusetts Medical School
Jason K. Kim: Program in Molecular Medicine, University of Massachusetts Medical School
Martin Wabitsch: University Medical Center Ulm
Philipp E. Scherer: Touchstone Diabetes Center, The University of Texas Southwestern Medical Center
Michael P. Czech: Program in Molecular Medicine, University of Massachusetts Medical School

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Proper regulation of energy storage in adipose tissue is crucial for maintaining insulin sensitivity and molecules contributing to this process have not been fully revealed. Here we show that type II transmembrane protein tenomodulin (TNMD) is upregulated in adipose tissue of insulin-resistant versus insulin-sensitive individuals, who were matched for body mass index (BMI). TNMD expression increases in human preadipocytes during differentiation, whereas silencing TNMD blocks adipogenesis. Upon high-fat diet feeding, transgenic mice overexpressing Tnmd develop increased epididymal white adipose tissue (eWAT) mass, and preadipocytes derived from Tnmd transgenic mice display greater proliferation, consistent with elevated adipogenesis. In Tnmd transgenic mice, lipogenic genes are upregulated in eWAT, as is Ucp1 in brown fat, while liver triglyceride accumulation is attenuated. Despite expanded eWAT, transgenic animals display improved systemic insulin sensitivity, decreased collagen deposition and inflammation in eWAT, and increased insulin stimulation of Akt phosphorylation. Our data suggest that TNMD acts as a protective factor in visceral adipose tissue to alleviate insulin resistance in obesity.

Date: 2016
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DOI: 10.1038/ncomms10686

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