‘Endocrine NAFLD’ a hormonocentric perspective of nonalcoholic fatty liver disease pathogenesis  Amedeo Lonardo, Cesare Carani, Nicola Carulli, Paola Loria  Journal of Hepatology  Volume 44, Issue 6, Pages 1196-1207 (June 2006) DOI: 10.1016/j.jhep.2006.03.005 Copyright © 2006 European Association for the Study of the Liver Terms and Conditions

Fig. 1 The ‘Endocrine NAFLD’. The figure illustrates the endocrine organs (left column) involved and respective major derangements (right column) consistently reported in NAFLD. GH, growth hormone; IGF-I, insulin-like growth factor-I; RAAS, renin angiotensin aldosterone system; ASP, acylation stimulating protein; SHBG, sex hormone binding globulin. Journal of Hepatology 2006 44, 1196-1207DOI: (10.1016/j.jhep.2006.03.005) Copyright © 2006 European Association for the Study of the Liver Terms and Conditions

Fig. 2 Estrogen replacement reverses steatosis in male mice and humans with estrogen-deficiency. Liver biopsy in male ArKO (aromatase knockout) mouse (left panels) and in a male patient with congenital aromatase deficiency (right panels) before and after estrogen replacement. Modified from Hewitt KN, et al. [94] and Maffei L, et al. [103], with permission. Journal of Hepatology 2006 44, 1196-1207DOI: (10.1016/j.jhep.2006.03.005) Copyright © 2006 European Association for the Study of the Liver Terms and Conditions

Fig. 3 Putative relationship between derangements of hormones/cytokines (visceral) obesity and NAFLD. Hormonal derangements can be primarily responsible for the development of NAFLD via anthropometric changes and/or alterations in the homeostasis of energy and metabolism of glucose and lipids. Journal of Hepatology 2006 44, 1196-1207DOI: (10.1016/j.jhep.2006.03.005) Copyright © 2006 European Association for the Study of the Liver Terms and Conditions