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Regulation of Adipocyte and Macrophage Functions by mTORC1 and 2 in Metabolic Diseases
Author(s) -
Festuccia William T.
Publication year - 2021
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201900768
Subject(s) - mtorc1 , mechanistic target of rapamycin , adipocyte , pi3k/akt/mtor pathway , macrophage polarization , lipogenesis , mtorc2 , biology , adipose tissue , rheb , insulin resistance , inflammation , microbiology and biotechnology , endocrinology , cancer research , macrophage , medicine , signal transduction , insulin , immunology , biochemistry , in vitro
Scope Evidence gathered in the last decades suggests that lipotoxicity and inflammation are the main factors connecting adipose tissue dysfunction to the development of metabolic diseases such as insulin resistance, nonalcoholic fatty liver disease (NAFLD), cardiovascular disease, and certain types of cancer, among others. The mechanistic target of rapamycin (mTOR) is a serine threonine kinase that functions as the catalytic entity of two multiprotein complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). These complexes are important components of signaling pathways activated by nutrients, growth factors, and inflammatory mediators and are therefore directly involved in the regulation of adipocyte and macrophage metabolism and function. Methods and Results In this article, studies that evaluate the involvement of mTORC1 and 2 in the regulation of macrophage and adipocyte function and their implication in the development of metabolic‐disease‐associated adipose tissue dysfunction are reviewed. Conclusion In adipocytes, optimal levels of mTORC1 activity are required for its pro‐lipogenic actions, while in macrophages, mTORC1 regulates features of both M1 and M2 polarization. mTORC2, on the other hand, promotes glucose uptake and de novo lipogenesis in adipocytes and counteracts macrophage inflammatory response.