Is retinol binding protein 4 a link between adiposity and cancer?
نویسندگان
چکیده
منابع مشابه
Serum retinol-binding protein: a link between obesity, insulin resistance, and type 2 diabetes.
Insulin resistance occurs under conditions of obesity, metabolic syndrome, and type 2 diabetes. It was found to be accompanied by down-regulation of the insulin-responsive glucose transporter GLUT4. Decreased adipocyte GLUT4 caused secretion by adipocytes of the serum retinol-binding protein RBP4. Enhanced levels of serum RBP4 appeared to be the signal for the development of systemic insulin re...
متن کاملRetinol-Binding Protein 4 in Twins
OBJECTIVE Retinol-binding protein (RBP) 4 is an adipokine of which plasma levels are elevated in obesity and type 2 diabetes. The aims of the study were to identify determinants of plasma RBP4 and RBP4 mRNA expression in subcutaneous adipose tissue (SAT) and skeletal muscle and to investigate the association between RBP4 and in vivo measures of glucose metabolism. RESEARCH DESIGN AND METHODS ...
متن کاملRetinol-binding protein 4 in human obesity.
Studies in mice suggest that adipocytes serve as glucose sensors and regulate systemic glucose metabolism through release of serum retinol-binding protein 4 (RBP4). This model has not been validated in humans. RBP4 was highly expressed in isolated mature human adipocytes and secreted by differentiating human adipocytes. In contrast to the animal data, RBP4 mRNA was downregulated in subcutaneous...
متن کاملRetinol-binding protein 4 and insulin resistance in preeclampsia.
Preeclampsia is characterized by the onset of high blood pressure and proteinuria during pregnancy, which results in substantial maternal and neonatal morbidity and mortality. Insulin resistance has been observed before the onset of preeclampsia, and is implicated in its pathophysiology. Recently, retinol-binding protein 4 (RBP4), which carries retinol in circulation, has been shown to be a pot...
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ژورنال
عنوان ژورنال: Hormone Molecular Biology and Clinical Investigation
سال: 2015
ISSN: 1868-1891,1868-1883
DOI: 10.1515/hmbci-2015-0019