High-fat feeding alters the clock synchronization to light
Open accessAbstract
High-fat feeding in rodents leads to metabolic abnormalities mimicking the human metabolic syndrome, including obesity and insulin resistance. These metabolic diseases are associated with altered temporal organization of many physiological functions. The master circadian clock located in the suprachiasmatic nuclei controls most physiological functions and metabolic processes. Furthermore, under certain conditions of feeding (hypocaloric diet), metabolic cues are capable of altering the suprachiasmatic clock's responses to light. To determine whether high-fat feeding (hypercaloric diet) can also affect resetting properties of the suprachiasmatic clock, we investigated photic synchronization in mice fed a high-fat or chow (low-fat) diet for 3 months, using wheel-running activity and body temperature rhythms as daily phase markers (i.e. suprachiasmatic clock's hands). Compared with the control diet, mice fed with the high-fat diet exhibited increased body mass index, hyperleptinaemia, higher blood glucose, and increased insulinaemia. Concomitantly, high-fat feeding led to impaired adjustment to local time by photic resetting. At the behavioural and physiological levels, these alterations include slower rate of re-entrainment of behavioural and body temperature rhythms after 'jet-lag' test (6 h advanced light-dark cycle) and reduced phase-advancing responses to light. At a molecular level, light-induced phase shifts have been correlated, within suprachiasmatic cells, with a high induction of c-FOS, the protein product of immediate early gene c-fos, and phosphorylation of the extracellular signal-regulated kinases I/II (P-ERK). In mice fed a high-fat diet, photic induction of both c-FOS and P-ERK in the suprachiasmatic nuclei was markedly reduced. Taken together, the present data demonstrate that high-fat feeding modifies circadian synchronization to light.
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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 [38]
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- Authors
- Mendoza, J., Pévet, P., & Challet, E.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2008-12-12
- Volume
- 586
- Issue
- 24
- Pages
- 5901-5910
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC2655413
- OpenAlex
- W1566953244
- Cited by
- 213
- References
- 48
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 11 · 2023: 13 · 2022: 9 · 2021: 11 · 2020: 14 · 2019: 9 · 2018: 12 · 2017: 14 · 2016: 14 · 2015: 14 · 2014: 19 · 2013: 14 · 2012: 15
- FWCI
- 5.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Fondation pour la Recherche Médicale
- Centre National de la Recherche Scientifique
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- high-fat diet, circadian clock, suprachiasmatic nucleus, light entrainment, light-induced phase shift, body temperature rhythm, wheel running, c-fos, ERK1/2 phosphorylation, metabolic syndrome, insulin resistance, obesity, leptin, hyperleptinemia
- MeSH terms
- Administration, Oral, Animals, Biological Clocks, Blood Glucose, Body Temperature, Body Weight, Circadian Rhythm, Corticosterone, Dietary Fats, Insulin, Light, Male, Mice, Inbred C57BL, Motor Activity, Phosphorylation, Photic Stimulation, Suprachiasmatic Nucleus, Telemetry, Proto-Oncogene Proteins c-fos, Leptin, Extracellular Signal-Regulated MAP Kinases, Abdominal Fat, Mice
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