Adipose tissue includes multiple anatomical depots that serve as an energy reserve that can expand or contract to maintain metabolic homeostasis. During normal growth and in response to overnutrition, adipose tissue expands by increasing the volume of preexisting adipocytes (hypertrophy) and/or by generating new adipocytes (hyperplasia) via recruitment and differentiation of adipose progenitors. This so-called healthy expansion through hyperplasia is thought to be beneficial in that it protects against obesity associated metabolic disorders by allowing for the "safe" storage of excess energy. Remodeling adipose tissue to replace dysfunctional adipocytes that accumulate with obesity and age also requires new fat cell formation and is necessary to maintain metabolic health. Adipogenesis is the process by which adipose progenitors become committed to an adipogenic lineage and differentiate into mature adipocytes. This transition is regulated by complex array of transcriptional factors and numerous autocrine, paracrine, and endocrine signals. We will focus on hormonal factors that regulate adipocyte differentiation and their molecular mechanisms of actions on adipogenesis as studied in vitro and in vivo. Accumulating evidence indicates that adipose progenitors isolated from different adipose tissues exhibit intrinsic differences in adipogenic potential that may contribute to the depot and sex differences in adipose expansion and remodeling capacity. We will put special emphasis on the hormonal factors that are known to depot-dependently affect body fat accumulation and adipocyte development. © 2017 American Physiological Society. Compr Physiol 7:1151-1195, 2017.
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