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Updated: Jun 29, 2026
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Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
Published on: February 27, 2016
Sirtuin gene expression in human mononuclear cells is modulated by caloric restriction
A B Crujeiras1, D Parra, E Goyenechea
1Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, Pamplona, Spain.
European Journal of Clinical Investigation
|October 8, 2008
Summary
Caloric restriction up-regulates sirtuin (SIRT1 and SIRT2) gene expression in obese patients, improving antioxidant status and mitochondrial function. Peripheral blood mononuclear cells (PBMC) show potential as a model for studying sirtuin responses in obesity therapy.
Area of Science:
- Nutrigenomics
- Obesity research
- Oxidative stress and metabolism
Background:
- Sirtuins are potential therapeutic targets for diseases linked to oxidative stress, including obesity.
- Limited in vivo human studies exist on sirtuins in obese individuals undergoing caloric restriction.
- This study investigates sirtuin gene expression modulation by a hypocaloric diet in obese humans.
Purpose of the Study:
- To assess the impact of a hypocaloric diet on sirtuin (SIRT1 and SIRT2) gene expression in peripheral blood mononuclear cells (PBMC) of obese individuals.
- To evaluate the relationship between sirtuin expression and markers of antioxidant status and mitochondrial function.
- To explore the potential of PBMC as a model for obesity and sirtuin response research.
Main Methods:
- Investigated SIRT1 and SIRT2 gene expression in PBMC from obese subjects before and after an 8-week hypocaloric diet.
- Measured gene expression of NDUFS2 and COX15, plasma antioxidant power, and nitric oxide.
- Utilized quantitative real-time PCR for nutrigenomics analysis and a 2-keto[1-(13)C]isocaproate breath test (KICA-BT) for in vivo mitochondrial oxidation.
Main Results:
- The hypocaloric diet up-regulated the expression of both SIRT1 and SIRT2.
- Sirtuin expression was inversely associated with total antioxidant capacity.
- Sirtuin expression was directly related to nitric oxide, KICA-BT-assessed mitochondrial oxidation, and expression of mitochondrial proteins COX15 and NDUFS2.
Conclusions:
- SIRT1 and SIRT2 may be key regulators in obesity comorbidities associated with antioxidant status.
- PBMC serve as a viable model for studying sirtuin responses in obesity therapy.
- Hypocaloric diet intervention positively influences sirtuin expression and related metabolic markers in obese individuals.
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