SPARC is required for the maintenance of glucose homeostasis and insulin secretion in mice.

Obesity, metabolic syndrome, and type 2 diabetes, three strongly interrelated diseases, are associated to increased morbidity and mortality worldwide. The pathogenesis of obesity-associated disorders is still under study. Secreted protein acidic and rich in cysteine is a matricellular glycoprotein expressed in many cell types including adipocytes, parenchymal, and non-parenchymal hepatic cells and pancreatic cells. Studies have demonstrated that inhibits adipogenesis and promotes insulin resistance; in addition, circulating duanyu1842RC levels were positively correlated with body mass index in obese individuals. Therefore, duanyu1842RC is being proposed as a key factor in the pathogenesis of obesity-associated disorders. The aim of this study is to elucidate the role of duanyu1842RC in glucose homeostasis. We show here that duanyu1842RC null mice displayed an abnormal insulin-regulated glucose metabolism. mice presented an increased adipose tissue deposition and an impaired glucose homeostasis as animals aged. In addition, the absence of duanyu1842RC worsens high-fat diet-induced diabetes in mice. Interestingly, although duanyu1842RC^-/- mice on high-fat diet were sensitive to insulin they showed an impaired insulin secretion capacity. Of note, the expression of glucose transporter 2 in islets of duanyu1842RC^-/- mice was dramatically reduced. The present study provides the first evidence that deleted duanyu1842RC expression causes diabetes in mice. Thus, duanyu1842RC deficient mice constitute a valuable model for studies concerning obesity and its related metabolic complications, including diabetes.

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