Adiponectin stimulates AMP-activated protein kinase in the hypothalamus and increases food intake.

By N. Kubota, Wataru Yano, Tetsuya Kubota, Toshimasa Yamauchi, S. Itoh, Hiroki Kumagai, H. Kozono, Iseki Takamoto, S. Okamoto, T. Shiuchi and 17 more. Cell Metabolism, 2007

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Adiponectin has been shown to stimulate fatty acid oxidation and enhance insulin sensitivity through the activation of AMP-activated protein kinase (AMPK) in the peripheral tissues. The effects of adiponectin in the central nervous system, however, are still poorly understood. Here, we show that adiponectin enhances AMPK activity in the arcuate hypothalamus (ARH) via its receptor AdipoR1 to stimulate food intake; this stimulation of food intake by adiponectin was attenuated by dominant-negative AMPK expression in the ARH. Moreover, adiponectin also decreased energy expenditure. Adiponectin-deficient mice showed decreased AMPK phosphorylation in the ARH, decreased food intake, and increased energy expenditure, exhibiting resistance to high-fat-diet-induced obesity. Serum and cerebrospinal fluid levels of adiponectin and expression of AdipoR1 in the ARH were increased during fasting and decreased after refeeding. We conclude that adiponectin stimulates food intake and decreases energy expenditure during fasting through its effects in the central nervous system.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/90004755ed865a3136170ca583300afbf95534a2

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Citations in the corpus

AMPK: an emerging drug target for diabetes and the metabolic syndrome. (2009, background): “Agents that decrease the activity of AMPK in hypothalamus reduce food intake (Minokoshi et al., 2008), while agents that increase the activity of AMPK in hypothalamus may increase food intake as well as hepatic glucose output in rodents (Kubota et al., 2007; McCrimmon et al., 2008).”
AMPK and PPARd Agonists Are Exercise Mimetics (2008, positive): “In mammals, AMPK has been shown to contribute to glucose homeostasis, appetite, and exercise physiology (Andersson et al., 2004; Hardie, 2007; Kubota et al., 2007; Mu et al., 2001; Minokoshi et al., 2004; Thomson et al., 2007).”
AMPK in Health and Disease. (2009, background): “Since the constitutively active AMPK fragment 1 (1-312) is not activated by the PT1 compound, it is proposed that PT1 acts by reversing the autoinhibition of the AIS (313-335).”
Biochemistry of adipose tissue: an endocrine organ (2013, background): “It has been demonstrated that adiponectin stimulated appetite and reduced energy expenditure and that these effects were eliminated following the ablation of AdipoR1 (siRNA) or AMPK signaling (AMPK dominant negative) [26].”
What We Talk About When We Talk About Fat (2014, neutral): “This may be due partly to increased insulin sensitivity and partly to direct actions of adiponectin on the hypothalamus to increase food intake (Kubota et al., 2007).”
AMPK - a nutrient and energy sensor that maintains energy homeostasis (2012, neutral): “, whereas those that promote it, such as the hormone ghrelin from the stomach, the adipokine adiponectin or cannabinoids, activate AMPK (the specific isoform was not determined”
Adipose tissue as an endocrine organ. (2010, background): “Kubota et al. (2007) have shown that adiponectin regulates nergy expenditure through activation of AMPK in the hypothaamus.”