AMP‐activated protein kinase is a key regulator of obesity‐associated factors

An imbalance between caloric intake and energy expenditure leads to obesity. Obesity is an important risk factor for the development of several metabolic diseases including insulin resistance, metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. So, controlling obesity could be...

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Veröffentlicht in:Cell biochemistry and function 2023-01, Vol.41 (1), p.20-32
Hauptverfasser: Mohseni, Roohollah, Teimouri, Maryam, Safaei, Mohsen, Arab Sadeghabadi, Zahra
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Sprache:eng
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Zusammenfassung:An imbalance between caloric intake and energy expenditure leads to obesity. Obesity is an important risk factor for the development of several metabolic diseases including insulin resistance, metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease. So, controlling obesity could be effective in the improvement of obesity‐related diseases. Various factors are involved in obesity, such as AMP‐activated protein kinases (AMPK), silent information regulators, inflammatory mediators, oxidative stress parameters, gastrointestinal hormones, adipokines, angiopoietin‐like proteins, and microRNAs. These factors play an important role in obesity by controlling fat metabolism, energy homeostasis, food intake, and insulin sensitivity. AMPK is a heterotrimeric serine/threonine protein kinase known as a fuel‐sensing enzyme. The central role of AMPK in obesity makes it an attractive molecule to target obesity and related metabolic diseases. In this review, the critical role of AMPK in obesity and the interplay between AMPK and obesity‐associated factors were elaborated. Significance statement 1. Obesity is an important risk factor for metabolic syndrome, type 2 diabetes mellitus, insulin resistance, and cardiovascular disease. 2. AMP‐activated protein kinase (AMPK) is an enzyme that known as a cellular energy sensor. 3. AMPK acts as a central regulator of obesity‐associated factors. So, targeting AMPK could improve obesity.
ISSN:0263-6484
1099-0844
DOI:10.1002/cbf.3767