Journal
ADIPOCYTE
Volume 2, Issue 2, Pages 74-79Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/adip.23320
Keywords
metabolic disease; sex differences; obesity; food intake; fatty liver; circadian rhythm
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Funding
- National Institute of Diabetes and Digestive and Kidney Diseases (National Public Health Service) [R01 DK83561]
- Ruth L. Kirschstein National Research Service Award [GM007185]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK083561] Funding Source: NIH RePORTER
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Obesity and associated metabolic diseases are sexually dimorphic. To provide better diagnosis and treatment for both sexes, it is of interest to identify the factors that underlie male/female differences in obesity. Traditionally, sexual dimorphism has been attributed to effects of gonadal hormones, which influence numerous metabolic processes. However, the XX/XY sex chromosome complement is an additional factor that may play a role. Recent data using the four core genotypes mouse model have revealed that sex chromosome complement-independently from gonadal sex-plays a role in adiposity, feeding behavior, fatty liver and glucose homeostasis. Potential mechanisms for the effects of sex chromosome complement include differential gene dosage from X chromosome genes that escape inactivation, and distinct genomic imprints on X chromosomes inherited from maternal or paternal parents. Here we review recent data in mice and humans concerning the potential impact of sex chromosome complement on obesity and metabolic disease.
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