The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
Circadian Regulation of Lipid Mobilization in White Adipose Tissues
Open accessAbstract
In mammals, a network of circadian clocks regulates 24-h rhythms of behavior and physiology. Circadian disruption promotes obesity and the development of obesity-associated disorders, but it remains unclear to which extent peripheral tissue clocks contribute to this effect. To reveal the impact of the circadian timing system on lipid metabolism, blood and adipose tissue samples from wild-type, ClockΔ19, and Bmal1(-/-) circadian mutant mice were subjected to biochemical assays and gene expression profiling. We show diurnal variations in lipolysis rates and release of free fatty acids (FFAs) and glycerol into the blood correlating with rhythmic regulation of two genes encoding the lipolysis pacemaker enzymes, adipose triglyceride (TG) lipase and hormone-sensitive lipase, by self-sustained adipocyte clocks. Circadian clock mutant mice show low and nonrhythmic FFA and glycerol blood content together with decreased lipolysis rates and increased sensitivity to fasting. Instead circadian clock disruption promotes the accumulation of TGs in white adipose tissue (WAT), leading to increased adiposity and adipocyte hypertrophy. In summary, circadian modulation of lipolysis rates regulates the availability of lipid-derived energy during the day, suggesting a role for WAT clocks in the regulation of energy homeostasis.
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“For example, the hepatic clock regulates fasting glycemic control and glucose clearance (8), the pancreatic clock regulates insulin secretion and its response to glucose (9-11), the adipose clock regulates lipid storage and mobilization (12,13), and the skeletal muscle clock regulates glucose uptake and metabolism (14).”
From Circadian rhythms, metabolism, and chrononutrition in rodents and humans (2016) · cites this paper as [13]
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Metadata
- Authors
- Shostak, A., Meyer-Kovac, J., & Oster, H.
- Affiliations
- Max Planck Institute for Biophysical Chemistry (DE)
- Circadian Rhythms Group, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
- Corresponding author
- Oster, Henrik
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2013-06-14
- Volume
- 62
- Issue
- 7
- Pages
- 2195-2203
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC3712056
- OpenAlex
- W2098360522
- Cited by
- 243
- References
- 54
- Citations by year
- 2026: 12 · 2025: 22 · 2024: 17 · 2023: 23 · 2022: 26 · 2021: 14 · 2020: 22 · 2019: 19 · 2018: 16 · 2017: 17 · 2016: 20 · 2015: 16 · 2014: 14 · 2013: 5
- FWCI
- 9.90
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- circadian clock, white adipose tissue, lipolysis, lipid mobilization, free fatty acids, glycerol, adipose triglyceride lipase, hormone-sensitive lipase, Clock mutant mice, Bmal1, adipocyte hypertrophy, adiposity, energy homeostasis, circadian rhythm disruption
- MeSH terms
- Animals, Sterol Esterase, Circadian Rhythm, Fatty Acids, Nonesterified, Glycerol, Mice, Knockout, Adiposity, Lipid Metabolism, Mice, Adipose Tissue, White, CLOCK Proteins
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