AMP-activated protein kinase (AMPK) is best known as a sensor of oxidative stress. AMPK is activated by increased intracellular AMP levels, which are a result of alterations in cellular metabolism from causes such as hypoxia, changes in ATP, senescence and more. In cell stress models, AMPK can protect cells from reduced ATP production by altering ATP biosynthetic pathways. Furthermore, AMPK has implications in reducing inflammatory reactions in apoptosis pathways. AMPK is also activated during exercise and other situations where lipolysis is enhanced. While this mechanism is not fully understood, research has shed light on the phosphorylation of the Thr-172 residue of the AMPK Alpha 1 subunit by upstream kinases. An AMPK Alpha 1 antibody has been used to further investigate how adipose tissue and energy regulation play into AMPK behavior and lipid metabolism. The following articles discuss the use of the AMPK Alpha 1 antibody in lipid metabolism.
AMPK alpha 1 Antibody (2B7) [NBP2-22127] - Western blot analysis using AMPK alpha 1 mouse mAb against Jurkat (1), Hela (2), HepG2 (3), MCF-7 (4), Cos7 (5), NIH/3T3 (6), K562 (7), HEK293 (8), and PC-12 (9) cell lysate.
Gauthier et al used an AMPK Alpha 1 antibody in their study of AMPK activation as a direct consequence of lipolysis in adipocyte cells. It was first established by Gauthier’s group that exercise in rodents increases AMPK activity in adipose tissue samples. In addition, beta-adrenergic agonists and factors that stimulate cyclic AMP production also activate lipolysis and AMPK activation. An AMPK Alpha 1 antibody was used in 3T3-L1 adipocytes in western blot for various experimental procedures. First, the AMPK Alpha 1 antibody helped to determine that agents that increase cAMP also stimulate AMPK activation in 3T3-L1 adipocyte cells. Subsequently, the AMPK Alpha 1 antibody showed a reduction in AMPK activation after introduction of the lipolysis inhibitor, Orlistat. Overall, an AMPK Alpha 1 antibody was vital to determining that increased AMPK activation in lipolysis is a secondary reaction to the AMP:ATP ratio, is not due to increases in cAMP or PKA, and is a result of acylation of fatty acids during lipid metabolism.
Another study by Hou et al used an AMPK Alpha 1 antibody to research the effects of SIRT1 on hepatocyte lipid metabolism through AMPK. Hou et al previously defined AMPK activation as a key player in how polyphenols can effect lipid accumulation and hyperlipidemia. First, an AMPK Alpha 1 antibody was used in western blot on HepG2 cells exposed to high glucose to show that activation of SIRT1 by the antioxidant compound resveratrol prevents a decrease in AMPK activity. Likewise, inhibition of SIRT1 rescues the polyphenol induced activated of AMPK. Furthermore, an AMPK Alpha 1 antibody was used to establish a direct role between SIRT1 and the regulation of AMPK by examining whether adenovirus mediated overexpression of wtSIRT1 would increase stimulation of APMK in HepG2 cells. The results showed a 2-fold increase in AMPK activation, strengthening the tie between the two.
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