AMPK integrates nutrient and hormonal signals to regulate food intake and energy balance through effects in the hypothalamus and peripheral tissues
Open accessAbstract
The evolutionarily conserved serine/threonine kinase, AMP‐activated protein kinase (AMPK), functions as a cellular fuel gauge that regulates metabolic pathways in glucose and fatty acid metabolism and protein synthesis. Recent data strongly implicate the AMPK–acetyl CoA carboxylase (ACC)–malonyl CoA pathway in the hypothalamus in the regulation of food intake, body weight and hepatic glucose production. Furthermore, data indicate that AMPK is a mediator of the effects of adipocyte‐derived and gut‐derived hormones and peptides on fatty acid oxidation and glucose uptake in peripheral tissues. Studies are now elucidating the potential role of kinases upstream of AMPK in these metabolic effects. In addition, recently, several novel downstream effectors of AMPK have been identified. The AMPK pathway in the hypothalamus and peripheral tissues coordinately integrates inputs from multiple hormones, peptides and nutrients to maintain energy homeostasis.
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Hypothalamic AMPK activity is inhibited by central administration of either insulin or leptin.
“In the hypothalamus, AMPK activity is sensitive not only to changes of nutrient (e.g., glucose) availability, but is inhibited by central administration of either insulin or leptin (115, 208).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [208]
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References 83 · Cited by 338
- Authors
- Xue, B., & Kahn, B. B.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2006-06-19
- Volume
- 574
- Issue
- 1
- Pages
- 73-83
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC1817809
- OpenAlex
- W2136980094
- Cited by
- 338
- References
- 83
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 10 · 2023: 11 · 2022: 8 · 2021: 16 · 2020: 14 · 2019: 9 · 2018: 10 · 2017: 12 · 2016: 14 · 2015: 17 · 2014: 17 · 2013: 16 · 2012: 35
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK56116, P01DK056116, R01 DK60839, R01DK060839)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- AMPK, food intake regulation, energy balance, hypothalamus, acetyl-CoA carboxylase, malonyl-CoA, hepatic glucose production, adipokines, gastrointestinal hormones, fatty acid oxidation, glucose uptake, energy homeostasis, nutrient signaling, upstream kinases, downstream effectors
- MeSH terms
- Animals, Body Weight, Eating, Energy Metabolism, Feedback, Glucose, Homeostasis, Hormones, Humans, Hypothalamus, Liver, Multienzyme Complexes, Signal Transduction, Protein Serine-Threonine Kinases, AMP-Activated Protein Kinases
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