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Cell Type-Specific Expression and Coregulation of Murine Resistin and Resistin-Like Molecule- in Adipose Tissue

Departments of Cell Biology (M.W.R., Y.L., P.E.S.), Biochemistry (M.R.), and Medicine (X.M.Y., N.B.), Albert Einstein College of Medicine, Bronx, New York 10461; Department of Research and Development (R.G., H.Q.), Linco Research, Inc., St. Charles, Missouri 63304; and Diabetes Research and Training Center (N.B., P.E.S.), Albert Einstein College of Medicine, Bronx, New York 10461

Address all correspondence and requests for reprints to: Dr. Phillip Scherer, Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. E-mail: scherer{at}aecom.yu.edu.

Adipocytes are the exclusive or predominant source of several secreted proteins that exert profound effects on systemic carbohydrate and lipid metabolism. Resistin, a 10-kDa adipose tissue specific secretory protein, has recently been implicated in exerting a negative effect on systemic insulin sensitivity. It is, however, not known how resistin mediates this insulin-desensitizing effect or what regulatory mechanisms control resistin expression. Resistin-like molecule- (RELM), a homolog of resistin originally identified by its upregulation in asthmatic lung, is another secreted protein expressed in adipose tissue. The regulation of RELM in adipose tissue and its relationship to resistin expression has not been addressed so far. Here, we demonstrate that the expression of resistin and RELM are similarly regulated in adipose tissue despite the fact that RELM is exclusively expressed in the stromal vascular fraction of adipose tissue and not in adipocytes. Interestingly, this coregulation is limited to adipose tissue as the expression of RELM in lung is independent of metabolic regulation. Additionally, we show that resistin and RELM levels are not subject to regulation by proinflammatory stimuli. Finally, acute hyperglycemia leads to up-regulation of resistin and RELM transcription in various adipose depots.

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