Cited by 176Metabolism, Diabetes, and CancerRegulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic Diseases

AMPK β1 Deletion Reduces Appetite, Preventing Obesity and Hepatic Insulin Resistance

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Dzamko, Nicolas, van Denderen, Bryce J.W., Hevener, Andrea L., Jørgensen, Sebastian Beck, Honeyman, Jane, Galic, Sandra, Chen, Zhi-Ping, Watt, Matthew J. +3 more·2010·Journal of Biological Chemistry

Abstract

The AMP-activated protein kinase (AMPK) is an alphabetagamma heterotrimer that regulates appetite and fuel metabolism. We have generated AMPK beta1(-/-) mice on a C57Bl/6 background that are viable, fertile, survived greater than 2 years, and display no visible brain developmental defects. These mice have a 90% reduction in hepatic AMPK activity due to loss of the catalytic alpha subunits, with modest reductions of activity detected in the hypothalamus and white adipose tissue and no change in skeletal muscle or heart. On a low fat or an obesity-inducing high fat diet, beta1(-/-) mice had reduced food intake, reduced adiposity, and reduced total body mass. Metabolic rate, physical activity, adipose tissue lipolysis, and lipogenesis were similar to wild type littermates. The reduced appetite and body mass of beta1(-/-) mice were associated with protection from high fat diet-induced hyperinsulinemia, hepatic steatosis, and insulin resistance. We demonstrate that the loss of beta1 reduces food intake and protects against the deleterious effects of an obesity-inducing diet.

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Crossref · 10.1074/jbc.m109.056762

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  • AMPK β1 KO mice have reduced AMPK activity in liver but not skeletal muscle.

    “AMPK β1 KO mice have reduced AMPK activity in liver but not skeletal muscle, are hyperphagic and as a result have lower body weight, adiposity and hepatic lipid accumulation, and are protected from high-fat diet induced insulin resistance [27].”

    From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [27]

  • AMPK β1 KO mice are protected from high-fat diet induced insulin resistance.

    “AMPK β1 KO mice have reduced AMPK activity in liver but not skeletal muscle, are hyperphagic and as a result have lower body weight, adiposity and hepatic lipid accumulation, and are protected from high-fat diet induced insulin resistance [27].”

    From AMPK and Exercise: Glucose Uptake and Insulin Sensitivity (2013) · cites this paper as [27]

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Authors
Dzamko, N., van Denderen, B. J. W., Hevener, A. L., Jørgensen, S. B., Honeyman, J., Galic, S., Chen, Z.-P., Watt, M. J., Campbell, D. J., Steinberg, G. R., & Kemp, B. E.
Affiliations
  • The University of Melbourne (AU)
  • University of California, Los Angeles (US)
  • University of Copenhagen (DK)
  • Monash University (AU)
Corresponding author
  • Steinberg, Gregory R.
  • Kemp, Bruce E.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2010-01
Volume
285
Issue
1
Pages
115-122
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2028308875
Cited by
175
References
43
Citations by year
2026: 3 · 2025: 5 · 2024: 6 · 2023: 7 · 2022: 12 · 2021: 11 · 2020: 13 · 2019: 8 · 2018: 10 · 2017: 9 · 2016: 16 · 2015: 9 · 2014: 14 · 2013: 15 · 2012: 15
FWCI
4.70
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
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
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
AMPK, appetite regulation, dietary intake, obesity, hepatic insulin resistance, hyperinsulinemia, hepatic steatosis, high-fat diet, knockout mice, adipose tissue lipolysis, lipogenesis, metabolic rate
MeSH terms
AMP-Activated Protein Kinase Kinases, Animals, Appetite, Body Weight, Carbon Dioxide, Darkness, Dietary Fats, Fasting, Feeding Behavior, Gene Expression Regulation, Gluconeogenesis, Insulin, Insulin Resistance, Liver, Mice, Inbred C57BL, Obesity, Organ Specificity, Oxidation-Reduction, Oxygen, Protein Kinases, Respiration, Gene Deletion, Protein Subunits, Hepatocytes, Mice

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