Inositol polyphosphate multikinase: An emerging player for the central action of AMP-activated protein kinase

• Published in: Biochemical and biophysical research communications 2012-04, Vol.421 (1), p.1-3
• Main Authors: Dailey, Megan J., Kim, Seyun
• Format: Article
• Language: English
• Subjects: AMP-Activated Protein Kinases - metabolism; AMPK; Animals; Arcuate Nucleus of Hypothalamus - enzymology; Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism; Eating; Energy homeostasis; Energy Metabolism; Food intake; Glucose - metabolism; Humans; Inositol - metabolism; IPMK; Mice; Phosphotransferases (Alcohol Group Acceptor) - metabolism
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2012.04.010

► We review the role of IPMK-mediated regulation of AMPK in response to glucose. ► We discuss a novel role for the hypothalamic IPMK signaling in energy homeostasis. ► We found that IPMK deletion within the Arc affects AMPK signaling and food intake. ► We propose that IPMK–AMPK signaling may provide new therapeutic targets for obesity. AMP-activated protein kinase (AMPK) is an essential enzyme indispensable for energy sensing and metabolic homeostasis at both the cellular and whole-body levels. Phosphorylation of AMPK, a key step for its activation, is known to be regulated by upstream kinases such as liver kinase B1 (LKB1) and calmodulin-dependent protein kinase kinase-beta (CaMKKβ). Recent evidence shows that inositol polyphosphate multikinase (IPMK), which possesses both inositol phosphate kinase and lipid inositol kinase activities, can physiologically regulate AMPK signaling in cultured cells and in the arcuate nucleus. IPMK-mediated regulation of AMPK occurs through the dynamic protein interactions of IPMK with AMPK in response to glucose availability. Here we review and discuss a novel role for the hypothalamic IPMK signaling in the control of AMPK and central energy homeostasis.