Acylcarnitines Linked to MetS and Hypertension in Cohorts

Key Takeaways:
- Acylcarnitine profiles were associated with MetS features and blood pressure in women with obesity across two cohorts.
- MC and LC acylcarnitines, including specific species, were associated with hypertension, with LC acylcarnitines independently associated with SBP in adjusted models.
- Findings are observational and hypothesis-generating, with proposed links to mitochondrial metabolism and vascular function requiring further prospective and mechanistic study.
The study included 648 women with obesity: 428 from Cotonou, Benin, and 220 from the French Aldepi/Obesepi cohort. In the Benin cohort, MetS was associated with higher SC, MC, and LC acylcarnitines (p = 0.0001, p < 0.0001, and p = 0.0004, respectively). In the French cohort, MetS was associated with higher SC acylcarnitines (p < 0.0001), which were also linked to higher blood glucose (p < 0.001), lower HDL-cholesterol (p < 0.05), and higher triglycerides (p < 0.01). The authors also report baseline differences between cohorts (e.g., higher fasting glucose and insulin in the French cohort), and the cross-cohort contrasts in acylcarnitine patterns are descriptive and may reflect underlying population or contextual differences rather than directly comparable effects.
For blood pressure outcomes, both cohorts showed associations between MC and LC acylcarnitines—including mono-unsaturated species—and hypertension. Exploratory species-level analyses identified several acylcarnitines (e.g., C4, C8:1, C10:2, C12:1, C12, C12:1-OH, C12-OH, C16:1) as elevated in hypertensive participants. In multivariable models within the Benin cohort, LC acylcarnitines were independently associated with SBP after adjustment for age, BMI, glycemia, and lipid measures. These findings are presented as complementary signals at both grouped and species levels.
The authors also report higher total and free carnitine levels in participants with MetS in both cohorts. In discussion, they propose that acylcarnitine accumulation may reflect impaired fatty-acid β-oxidation and mitochondrial metabolism, with potential links to vascular function (e.g., nitric oxide pathways and endothelial dysfunction). However, they emphasize that directionality remains uncertain and that the observed associations may reflect either causal pathways or downstream metabolic consequences.