Title |
Microdialysis and proteomics of subcutaneous interstitial fluid reveals increased galectin-1 in type 2 diabetes patients
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Published in |
Metabolism: Clinical and Experimental, April 2016
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DOI | 10.1016/j.metabol.2016.04.003 |
Pubmed ID | |
Authors |
Emanuel Fryk, Jeanna Perman Sundelin, Lena Strindberg, Maria J. Pereira, Massimo Federici, Nikolaus Marx, Fredrik H. Nyström, Martin Schmelz, Per-Arne Svensson, Jan W. Eriksson, Jan Borén, Per-Anders Jansson |
Abstract |
To identify a potential therapeutic target for type 2 diabetes by comparing the subcutaneous interstitial fluid from type 2 diabetes patients and healthy men. Proteomics was performed on the interstitial fluid of subcutaneous adipose tissue obtained by microdialysis from 7 type 2 diabetes patients and 8 healthy participants. 851 proteins were detected, of which 36 (including galectin-1) showed significantly altered expression in type 2 diabetes. We also measured galectin-1 expression in: (1) adipocytes isolated from adipose tissue biopsies from these participants; (2) subcutaneous adipose tissue of 24 obese participants before, during and after 16weeks on a very low calorie diet (VLCD); and (3) adipocytes isolated from 6 healthy young participants after 4weeks on a diet and lifestyle intervention to promote weight gain. We also determined the effect of galectin-1 on glucose uptake in human adipose tissue. Galectin-1 protein levels were elevated in subcutaneous dialysates from type 2 diabetes compared with healthy controls (p<0.05). In agreement, galectin-1 mRNA expression was increased in adipocytes from the type 2 diabetes patients (p<0.05). Furthermore, galectin-1 mRNA expression was decreased in adipose tissue after VLCD (p<0.05) and increased by overfeeding (p<0.05). Co-incubation of isolated human adipocytes with galectin-1 reduced glucose uptake (p<0.05) but this was independent of the insulin signal. Proteomics of the interstitial fluid in subcutaneous adipose tissue in vivo identified a novel adipokine, galectin-1, with a potential role in the pathophysiology of type 2 diabetes. |
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