Andreu Palou1, Catalina Picó, Maria Luisa Bonet. 1. Laboratory of Molecular Biology, Nutrition and Biotechnology (LBNB), Universitat de les Illes Balears (UIB), and CIBER de Fisiopatología de la Obesidad y Nutrición (CIBERobn), Campus de la UIB, Palma de Mallorca, Spain.
Abstract
PURPOSE OF REVIEW: Recent findings in animals suggest that diet-related factors can programme adipose tissue features in early life and remodel white adipose tissue (WAT) towards a brown adipose tissue (BAT)-like phenotype in adulthood, while impacting on body fat content and susceptibility to obesity. The purpose of this review is to address the significance of these results and their applicability in humans. RECENT FINDINGS: Nutritional conditions in the perinatal period influence sympathetic innervation to WAT and WAT cellularity in rodents. Leptin intake during the suckling period prevents obesity and other metabolic alterations in later life in rats through mechanisms that include increased sensitivity of adipose tissues to leptin. Recent data support the thermogenic functionality of inducible brown-like cells in rodent WAT and functional thermogenic beige adipogenesis from human progenitor cells. Diet-related factors and exercise can promote BAT activation and/or WAT-to-BAT remodelling (WAT browning) in animals. SUMMARY: Animal studies suggest that adipose tissue health and whole body adiposity might be influenced by early life nutrition and lifestyle factors in adulthood impacting energy metabolism in adipose tissues. For this knowledge to be translated to humans, biomarkers allowing early detection of the programming status of the individual and technologies allowing measuring of the thermogenic activity of adipose tissue depots in vivo are required.
PURPOSE OF REVIEW: Recent findings in animals suggest that diet-related factors can programme adipose tissue features in early life and remodel white adipose tissue (WAT) towards a brown adipose tissue (BAT)-like phenotype in adulthood, while impacting on body fat content and susceptibility to obesity. The purpose of this review is to address the significance of these results and their applicability in humans. RECENT FINDINGS: Nutritional conditions in the perinatal period influence sympathetic innervation to WAT and WAT cellularity in rodents. Leptin intake during the suckling period prevents obesity and other metabolic alterations in later life in rats through mechanisms that include increased sensitivity of adipose tissues to leptin. Recent data support the thermogenic functionality of inducible brown-like cells in rodent WAT and functional thermogenic beige adipogenesis from human progenitor cells. Diet-related factors and exercise can promote BAT activation and/or WAT-to-BAT remodelling (WAT browning) in animals. SUMMARY: Animal studies suggest that adipose tissue health and whole body adiposity might be influenced by early life nutrition and lifestyle factors in adulthood impacting energy metabolism in adipose tissues. For this knowledge to be translated to humans, biomarkers allowing early detection of the programming status of the individual and technologies allowing measuring of the thermogenic activity of adipose tissue depots in vivo are required.