Circulating Betatrophin Levels Are Increased in Anorexia and Decreased in Morbidly Obese Women

Context: Betatrophin is produced primarily by liver and adipose tissue and has been recently reported as a novel hormone promoting β-cell proliferation and β-cell mass and improving glucose tolerance. Objective: Because it is markedly regulated by nutritional status, we hypothesized that circulating betatrophin levels might be affected by pathophysiological conditions altering body weight. Setting and Patients: We analyzed circulating betatrophin levels in 149 female patients, including 99 with extreme body mass index (30 anorexia nervosa, 24 obese, 45 morbid obese, and 50 healthy eating/weight controls). Outcome Measurements: Serum betatrophin levels and its correlations with different anthropometric and biochemical parameters were measured. Results: Plasma betatrophin levels were significantly elevated in anorexic patients, whereas its levels were reduced in morbidly obese women when compared with normal-weight women. Plasma betatrophin correlated negatively with weight, body mass index, fat percentage, glucose, insulin, and homeostatic model assessment index and positively correlated with high-density lipoprotein. Conclusions: These results suggest that metabolic status is an important regulator of circulating betatrophin levels. - See more at: http://press.endocrine.org/doi/full/10.1210/JC.2015-1595#sthash.xBpUlVWg.dpufThis work was supported by Grants BFU2011–29102 (to C.D.) and BFU2012–35255 (to R.N.) from the Ministerio de Economia y Competitividad; Xunta de Galicia Grants EM 2012/039 and 2012-CP069 (to R.N.); Fondo de Investigaciones Sanitarias Grants PI11/210, PI12/515, and PI14/290; and Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y Nutrición. Centro de Investigación Biomédica en Red de Fisiopatología de la Obesidad y Nutrición and Consorcio de Investigación Biomédica en Red Especializado en Epidemiología y Salud Pública are initiatives of the Instituto de Salud Carlos III of Spain, which is supported by Fondo Social Europeo of the European Community funds. The research leading to these results has also received funding from the European Community's Seventh Framework Programme under Grants FP7/2007–2013 (to C.D.) and 245009; NeuroFAST; and European Research Council Grant StG-2011-OBESITY53–281408 (to R.N.). S.-B.F. is supported by Xunta de Galicia and C.F. is supported by Instituto de Investigacion Sanitaria de Santiago. J.C.F.-G. is a recipient of a “Rio Hortega” contract from the Instituto de Salud Carlos III (Madrid, Spain) (Grant CM12/00059). - See more at: http://press.endocrine.org/doi/full/10.1210/JC.2015-1595#sthash.xBpUlVWg.dpu