P107 Deficiency Increases Energy Expenditure by Inducing Brown‐Fat Thermogenesis and Browning of White Adipose Tissue. Issue 2 (14th November 2018)

• Record Type: Journal Article
• Authors: Cunarro, Juan; Buque, Xabier; Casado, Sabela; Lugilde, Javier; Vidal, Anxo; Mora, Alfonso; Sabio, Guadalupe; Nogueiras, Rubén; Aspichueta, Patricia; Diéguez, Carlos; Tovar, Sulay
• Is Part Of: Molecular nutrition & food research. Volume 63:Issue 2(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2018-11-14
• Subjects: browning -- energy expenditure -- high‐fat diet -- homeostasis -- thermogenesis; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201801096
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Scope: The tumor suppressor p107, a pocket protein member of the retinoblastoma susceptibility protein family, plays an important role in the cell cycle and cellular adipocyte differentiation. Nonetheless, the mechanism by which it influences whole body Energy homeostasis is unknown. Methods and Results: The phenotype of p107 knockout (KO) mixed‐background C57BL6/129 mice phenotype is studied by focusing on the involvement of white and brown adipose tissue (WAT and BAT) in energy metabolism. It is shown that p107 KO mice are leaner and have high‐fat diet resistence. This phenomenon is explained by an increase of energy expenditure. The higher energy expenditure is caused by the activation of thermogenesis and may be mediated by both BAT and the browning of WAT. Consequently, it leads to the resistance of p107 KO mice to high‐fat diet effects, prevention of liver steatosis, and improvement of the lipid profile and glucose homeostasis. Conclusion: These data allowed the unmasking of a mechanism by which a KO of p107 prevents diet‐induced obesity by increasing energy expenditure via increased thermogenesis in BAT and browning of WAT, indicating the relevance of p107 as a modulator of metabolic activity of both brown and white adipocytes. Therefore, it can be targeted for the development of new therapies to ameliorate the metabolic syndrome. Abstract : The Rb family member p107 is widely recognized as a tumor suppressor, but it also implicated in cellular differentiation of adipocytes. p107‐null mice are leaner and resistant to diet‐induced metabolic disorders. This protection against high‐fat diets is explained by their stimulated brown fat thermogenic activity and browning of white adipose tissue, which ultimately trigger energy expenditure.