The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Adiponectin Stimulates AMP-Activated Protein Kinase in the Hypothalamus and Increases Food Intake
Open accessAbstract
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.
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“In the brain, adiponectin activates AMPK signaling in hypothalamic ARC, resulting in an increase in food intake and a reduction in energy expenditure, suggesting that in the hypothalamus adiponectin promotes feeding and inhibits the anorexigenic effects of leptin 55, 56.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [56]
In the citing paper
“In contrast to leptin, adiponectin levels increase in low glucose and low insulin conditions, at least in the cerebrospinal fluid (CSF) 55, 56.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [56]
In the citing paper
“In pathological conditions of obesity, the reduction in CSF levels of adiponectin that is accompanied by feeding is lost, thus maintaining a “high food intake behavior” even in conditions that are not of energy scarcity (high energy conditions) 56.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [56]
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Cites
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Self-citationmouse brain in stereotaxic coordinates
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A Novel Serum Protein Similar to C1q, Produced Exclusively in Adipocytes
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Cloning of adiponectin receptors that mediate antidiabetic metabolic effects
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Adiponectin and adiponectin receptors in insulin resistance, diabetes, and the metabolic syndrome
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Self-citationThe adipocyte-secreted protein Acrp30 enhances hepatic insulin action
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Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase
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Narkar, V. A., Downes, M., Yu, R. T., Embler, E., Wang, Y.-X., Banayo, E., Mihaylova, M. M., Nelson, M. C., Zou, Y., Juguilon, H., et al. (2008) · Cell · doi:10.1016/j.cell.2008.06.051 · Cited by 1,222
Metadata
- Authors
- Kubota, N., Yano, W., Kubota, T., Yamauchi, T., Itoh, S., Kumagai, H., Kozono, H., Takamoto, I., Okamoto, S., Shiuchi, T., Suzuki, R., Satoh, H., Tsuchida, A., Moroi, M., Sugi, K., Noda, T., Ebinuma, H., Ueta, Y., Kondo, T., Araki, E., Ezaki, O., Nagai, R., Tobe, K., Terauchi, Y., Ueki, K., Minokoshi, Y., & Kadowaki, T.
- Affiliations
- Japan Science and Technology Agency (JP)
- The University of Tokyo (JP)
- Toho University (JP)
- National Institute for Physiological Sciences (JP)
- Tohoku University (JP)
- University of Occupational and Environmental Health Japan (JP)
- Kumamoto University (JP)
- Yokohama City University (JP)
- Corresponding author
- Kadowaki, Takashi
- ORCID
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2007-07
- Volume
- 6
- Issue
- 1
- Pages
- 55-68
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2128485668
- Cited by
- 844
- References
- 37
- Citations by year
- 2026: 24 · 2025: 26 · 2024: 26 · 2023: 46 · 2022: 36 · 2021: 54 · 2020: 37 · 2019: 36 · 2018: 42 · 2017: 34 · 2016: 59 · 2015: 31 · 2014: 56 · 2013: 54 · 2012: 53
- FWCI
- 22.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- Ministry of Health and Welfare
- Juvenile Diabetes Research Foundation International (1-2003-746)
- Daiichi Sankyo Foundation of Life Science
- Astellas Foundation for Research on Metabolic Disorders
- Kanae Foundation for the Promotion of Medical Science
- Japan Society for the Promotion of Science (10NP0201)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- adiponectin, AMPK, arcuate nucleus, hypothalamus, dietary intake, energy expenditure, AdipoR1, fasting, refeeding, high-fat diet-induced obesity, central nervous system
- MeSH terms
- Adenoviridae, Animals, Arcuate Nucleus of Hypothalamus, Eating, Energy Metabolism, Female, Hypothalamus, Immunoenzyme Techniques, Male, Mice, Inbred C57BL, Multienzyme Complexes, Phosphorylation, Receptors, Cell Surface, RNA Probes, Protein Serine-Threonine Kinases, In Situ Hybridization, Mice, Knockout, Leptin, Mice, Adiponectin, Adipose Tissue, White, Receptors, Leptin, Receptors, Adiponectin, AMP-Activated Protein Kinases
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