Stefano Paolacci
MAGI'S LAB
Giuseppe Pompucci
Department of Biotechnology, Chemistry and Pharmacy, University of Siena, Siena, Italy
Barbara Paolini
Department of Dietetics and Clinical Nutrition, Azienda Ospedaliera Universitaria Senese, Policlinico Santa Maria alle Scotte, Siena, Italy
Irene Del Ciondolo
Department of Dietetics and Clinical Nutrition, Azienda Ospedaliera Universitaria Senese, Policlinico Santa Maria alle Scotte, Siena, Italy
Giacinto Abele Donato Miggiano
UOC Nutrizione Clinica, Fondazione Policlinico Universitario A. Gemelli IRCCS; Centro di Ricerche in Nutrizione Umana, Università Cattolica S. Cuore, Rome, Italy
Barbara Aquilanti
UOC Nutrizione Clinica, Fondazione Policlinico Universitario A. Gemelli IRCCS
Andrea Scaramuzza
Department of Pediatrics, Ospedale Maggiore di Cremona, Cremona, Italy
Valeria Velluti
UOC Nutrizione Clinica, Fondazione Policlinico Universitario A. Gemelli IRCCS
Giuseppina Matera
UOC Nutrizione Clinica, Fondazione Policlinico Universitario A. Gemelli IRCCS
Lucilla Gagliardi
UOC Nutrizione Clinica, Fondazione Policlinico Universitario A. Gemelli IRCCS
Matteo Bertelli
MAGI Euregio, Bolzano, Italy
Keywords
Mendelian obesity, leptin/melanocortin pathway, adipogenesis
Abstract
Obesity is highly heritable and arises from the interplay of many genes and environmental factors. It can be defined as the result of prolonged imbalance between calorie intake and energy utilization. About 5% of cases of non-syndromic obesity are monogenic (Mendelian obesity). The amount of adipose tissue in the body is mainly regulated by leptin, a hormone produced by adipocytes, and Mendelian obesity is mainly caused by mutations that disrupt the leptin/melanocortin pathway. In this article, we summarize the genes involved in genetic obesity and the test we use for genetic analysis.