4.7 Review

Adipose Tissue Hyperplasia and Hypertrophy in Common and Syndromic Obesity-The Case of BBS Obesity

Journal

NUTRIENTS
Volume 15, Issue 15, Pages -

Publisher

MDPI
DOI: 10.3390/nu15153445

Keywords

obesity; Bardet-Biedl syndrome (BBS); hyperplasia; hypertrophy; adipogenesis

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Obesity is a metabolic state characterized by the expansion of adipose tissue, which is regulated by genetics and excess energy intake. While the genetic regulation of adipose tissue expansion is not fully understood, studies on both monogenic and syndromic obesity have identified several genes related to obesity. Syndromic obesity, such as Bardet-Biedl syndrome (BBS), involves additional features and provides insights into peripheral adipocyte regulation in obesity. This review summarizes current knowledge on adipocyte hyperplasia and hypertrophy in common obesity and highlights the importance of studying syndromic obesity models like BBS.
Obesity is a metabolic state generated by the expansion of adipose tissue. Adipose tissue expansion depends on the interplay between hyperplasia and hypertrophy, and is mainly regulated by a complex interaction between genetics and excess energy intake. However, the genetic regulation of adipose tissue expansion is yet to be fully understood. Obesity can be divided into common multifactorial/polygenic obesity and monogenic obesity, non-syndromic and syndromic. Several genes related to obesity were found through studies of monogenic non-syndromic obesity models. However, syndromic obesity, characterized by additional features other than obesity, suggesting a more global role of the mutant genes related to the syndrome and, thus, an additional peripheral influence on the development of obesity, were hardly studied to date in this regard. This review summarizes present knowledge regarding the hyperplasia and hypertrophy of adipocytes in common obesity. Additionally, we highlight the scarce research on syndromic obesity as a model for studying adipocyte hyperplasia and hypertrophy, focusing on Bardet-Biedl syndrome (BBS). BBS obesity involves central and peripheral mechanisms, with molecular and mechanistic alternation in adipocyte hyperplasia and hypertrophy. Thus, we argue that using syndromic obesity models, such as BBS, can further advance our knowledge regarding peripheral adipocyte regulation in obesity.

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