Cited by 138Circadian rhythm and melatoninAdipokines, Inflammation, and Metabolic DiseasesDietary Effects on Health

High-fat diet delays and fasting advances the circadian expression of adiponectin signaling components in mouse liver

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Barnea, Maayan, Madar, Zecharia, Froy, Oren·2009·Endocrinology

Abstract

The circadian clock controls energy homeostasis by regulating circadian expression and/or activity of enzymes involved in metabolism. Disruption of circadian rhythms may lead to obesity and metabolic disorders. We tested whether the biological clock controls adiponectin signaling pathway in the liver and whether fasting and/or high-fat (HF) diet affects this control. Mice were fed low-fat or HF diet and fasted on the last day. The circadian expression of clock genes and components of adiponectin metabolic pathway in the liver was tested at the RNA, protein, or enzyme activity level. In addition, serum levels of glucose, adiponectin, and insulin were measured. Under low-fat diet, adiponectin signaling pathway components exhibited circadian rhythmicity. However, fasting and HF diet altered this circadian expression; fasting resulted in a phase advance, and HF diet caused a phase delay. In addition, adenosine monophosphate-activated protein kinase levels were high during fasting and low during HF diet. Changes in the phase and daily rhythm of clock genes and components of adiponectin signaling pathway as a result of HF diet may lead to obesity and may explain the disruption of other clock-controlled output systems, such as blood pressure and sleep/wake cycle, usually associated with metabolic disorders.

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Crossref · 10.1210/en.2008-0944

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  • A high-fat diet may alter the function of the circadian clock, with an altered period of the locomotor activity rhythm and changes in the rhythms of core clock genes in adipose and liver tissue.

    “Even a high-fat diet may alter the function of the circadian clock, with an altered period of the locomotor activity rhythm and changes in the rhythms of the core clock genes in adipose and liver tissue [35–40,49].”

    From Circadian control of glucose metabolism (2014) · cites this paper as [36]

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Authors
Barnea, M., Madar, Z., & Froy, O.
Affiliations
Hebrew University of Jerusalem (IL)
Corresponding author
Froy, Oren
Venue
Endocrinology
Published
2008-09-18
Volume
150
Issue
1
Pages
161-168
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
OpenAlex
W2028181099
Cited by
138
References
50
Citations by year
2026: 5 · 2025: 4 · 2024: 6 · 2023: 8 · 2022: 4 · 2021: 5 · 2020: 7 · 2019: 8 · 2018: 11 · 2017: 5 · 2016: 4 · 2015: 9 · 2014: 10 · 2013: 12 · 2012: 9
FWCI
4.57
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Endocrinology (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • Toyota Research Institute, North America
  • Nutricia Research Foundation
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Dietary Effects on Health
Keywords
circadian clock, adiponectin signaling, high-fat diet, fasting, clock genes, AMPK, liver, obesity, metabolic disorders, insulin, glucose
MeSH terms
Acclimatization, Animals, Circadian Rhythm, Dietary Fats, Fasting, Liver, Male, Mice, Inbred C57BL, Signal Transduction, Diet, Fat-Restricted, Mice, Adiponectin

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