Triglyceride-lowering Effect of Respiratory Uncoupling in White Adipose Tissue
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OBJECTIVE: Hypolipidemic drugs such as bezafibrate and thiazolidinediones are known to induce the expression of mitochondrial uncoupling proteins (UCPs) in white adipose tissue. To analyze the potential triglyceride (TG)-lowering effect of respiratory uncoupling in white fat, we evaluated systemic lipid metabolism in aP2-Ucp1 transgenic mice with ectopic expression of UCP1 in adipose tissue. RESEARCH METHODS AND PROCEDURES: Hemizygous and homozygous transgenic mice and their nontransgenic littermates were fed chow or a high-fat diet for up to 3 months. Total TGs, nonesterified fatty acids, and the composition of plasma lipoproteins were analyzed. Hepatic TG production was measured in mice injected with Triton WR1339. Uptake and the use of fatty acids were estimated by measuring adipose tissue lipoprotein lipase activity and fatty acid oxidation, respectively. Adipose tissue gene expression was assessed by quantitative reverse transcriptase-polymerase chain reaction. RESULTS: Transgene dosage and the high-fat diet interacted to markedly reduce plasma TGs. This was reflected by decreased concentrations of very-low-density lipoprotein particles in the transgenic mice. Despite normal hepatic TG secretion, the activity of lipoprotein lipase in epididymal fat was enhanced by the high-fat diet in the transgenic mice in a setting of decreased re-esterification and increased in situ fatty acid oxidation. DISCUSSION: Respiratory uncoupling in white fat may lower plasma lipids by enhancing their in situ clearance and catabolism.
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By acting on white adipocyte mass, mitochondrial uncouplers could protect against diabetes.
“By acting on white adipocyte mass, mitochondrial uncouplers could protect against diabetes, as limiting hyperaccumulation of triacyglycerol (TAG) in these cells might limit organelle stress [91,273,274,275] and modifications in the expression pattern of genes encoding adipokines, which are known to communicate the level of adiposity to other organs [221,276].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [275]
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Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases
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Self-citation
- Authors
- Rossmeisl, M., Kovar, J., Syrovy, I., Flachs, P., Bobkova, D., Kolar, F., Poledne, R., & Kopecky, J.
- Affiliations
- Czech Academy of Sciences (CZ)
- Institute of Clinical and Experimental Medicine (CZ)
- Venue
- Obesity Research
- Publisher
- Wiley
- Published
- 2005-05
- Volume
- 13
- Issue
- 5
- Pages
- 835-844
- ISSN
- 1071-7323 (ISSN-L)
- 1550-8528
- OpenAlex
- W2061027163
- Cited by
- 23
- References
- 53
- Citations by year
- 2025: 1 · 2023: 2 · 2022: 1 · 2019: 1 · 2017: 1 · 2015: 2 · 2014: 2 · 2013: 2 · 2012: 1
- FWCI
- 1.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Obesity Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Grantová Agentura České Republiky (AVOZ 5011922, GA303/02/1220, GP303/03/P127)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- respiratory uncoupling, UCP1, white adipose tissue, triglyceride lowering, high-fat diet, lipoprotein lipase, fatty acid oxidation, hepatic triglyceride secretion, VLDL, free fatty acids, lipid metabolism, bezafibrate, thiazolidinediones
- MeSH terms
- Uncoupling Protein 1, Adipose Tissue, Animals, Carrier Proteins, Dietary Fats, DNA-Binding Proteins, Epididymis, Fatty Acids, Fatty Acids, Nonesterified, Homozygote, Ion Channels, Ketone Bodies, Lipoprotein Lipase, Lipoproteins, Liver, Male, Membrane Proteins, Mice, Transgenic, Mitochondria, Oxidation-Reduction, Phosphoenolpyruvate Carboxykinase (GTP), Transcription Factors, Triglycerides, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, Mitochondrial Proteins, Transcription Factor AP-2, Mice
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