Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 24, Issue 9, Pages -Publisher
MDPI
DOI: 10.3390/ijms24097987
Keywords
U0126; MEK inhibition; adipose tissue; obesity; adipogenesis; thermogenesis; AMPK
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In recent years, thermogenic differentiation and activation in brown and white adipose tissues have been considered as a promising strategy for treating and improving obesity. However, the pharmacological approach to this process has been limited, posing a challenge for obesity treatment. This research examines the effects of U0126 compound on thermogenic differentiation during adipogenesis and suggests it as a potential pharmacological option to enhance thermogenic adipocyte formation and energy expenditure.
In recent years, thermogenic differentiation and activation in brown and white adipose tissues have been regarded as one of the major innovative and promising strategies for the treatment and amelioration of obesity. However, the pharmacological approach towards this process has had limited and insufficient commitments, which presents a greater challenge for obesity treatment. This research evaluates the effects of U0126 compound on the activation of thermogenic differentiation during adipogenesis. The results show that U0126 pretreatment primes both white and brown preadipocytes to upregulate thermogenic and mitochondrial genes as well as enhance functions during the differentiation process. We establish that U0126-mediated thermogenic differentiation induction occurs partially via AMPK activation signaling. The findings of this research suggest U0126 as a promising alternative ligand in pursuit of a pharmacological option to increase thermogenic adipocyte formation and improve energy expenditure. Thus it could pave the way for the discovery of therapeutic drugs for the treatment of obesity and its related complications.
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