Effect of Simvastatin Treatment on Mitochondrial Function and Inflammatory Status of Human White Adipose Tissue

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BACKGROUND: Statin therapy has shown pleiotropic effects affecting both mitochondrial function and inflammatory status. However, few studies have investigated the concurrent effects of statin exposure on mitochondrial function and inflammatory status in human subcutaneous white adipose tissue.

OBJECTIVES: In a cross-sectional study, we investigated the effects of simvastatin on mitochondrial function and inflammatory status in subcutaneous white adipose tissue of 55 human participants: 38 patients (19 female/19 male) in primary prevention with simvastatin (> 40 mg/day,  > 3 mo) and 17 controls (9 female/8 male) with elevated plasma cholesterol. The two groups were matched on age, BMI and VO2max.

METHODS: Anthropometrics and fasting biochemical characteristics were measured. Mitochondrial respiratory capacity was assessed in white adipose tissue by high-resolution respirometry. Subcutaneous white adipose tissue expression of the inflammatory markers IL-6, CCL-2, CCL-5, TNFα, IL-10 and IL-4 was analysed by qPCR.

RESULTS: Simvastatin-treated patients showed lower plasma cholesterol (p < 0.0001), LDL (p < 0.0001) and triglyceride levels (p = 0.0116) than controls. Simvastatin-treated patients had a lower oxidative phosphorylation capacity of mitochondrial complex II (p = 0.0001 when normalised to wet weight, p < 0.0001 when normalised to citrate synthase activity (intrinsic)) and a lower intrinsic mitochondrial electron transport system capacity (p = 0.0004). Simvastatin-treated patients showed higher IL-6 expression than controls (p = 0.0202).

CONCLUSION: Simvastatin treatment was linked to mitochondrial respiratory capacity in human subcutaneous white adipose tissue, but no clear link was found between statin exposure, respiratory changes and inflammatory status of adipose tissue.

Original languageEnglish
JournalJournal of Clinical Endocrinology and Metabolism
Issue number10
Pages (from-to)e916-e922
Number of pages7
Publication statusPublished - 2023

Bibliographical note

© The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

ID: 348166779