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Peroxisome proliferator‐activated receptor γ: the more the merrier?
Author(s) -
Argmann C. A.,
Cock T.A.,
Auwerx J.
Publication year - 2005
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2005.01456.x
Subject(s) - adipogenesis , peroxisome proliferator activated receptor , peroxisome , receptor , adipocyte , energy homeostasis , nuclear receptor , biology , endocrinology , medicine , microbiology and biotechnology , transcription factor , adipose tissue , gene , biochemistry
The consequence of activating the nuclear hormone receptor, peroxisome proliferator‐activated receptor gamma (PPARγ), which coordinates adipocyte differentiation, validates the concept, ‘you are what you eat’. Excessive caloric intake leads to fat formation if the energy from these nutrients is not expended. However, this evolutionary adaptation to store energy in fat, which can be released under the form of fatty acids, potent PPARγ agonists, has become a disadvantage in today's affluent society as it results in numerous metabolic imbalances, collectively known as the metabolic syndrome. With the surge of human and genetic studies on PPARγ function, the limitations to the benefits of PPARγ signalling have been realized. It is now evident that the most effective strategy for resetting the balance of this thrifty gene is through its modulation rather than full activation, with the goal to improve glucose homeostasis while preventing adipogenesis. Finally, as more PPARγ targeted pathways are revealed such as bone homeostasis, atherosclerosis and longevity, it is most certain that the PPARγ thrifty gene hypothesis will evolve to incorporate these.