Key result
t10c12 CLA markedly increases oxidative stress by ~578% compared to placebo in metabolic syndrome.
Why the study?
The isomer-specific effects of conjugated linoleic acid on oxidative stress, inflammatory biomarkers, and their relationship to insulin resistance were unknown.
Does conjugated linoleic acid supplementation increase oxidative stress and inflammatory biomarkers in men with metabolic syndrome?
RCT (n=60)
Double-blind
randomized to one of 3 groups
Does conjugated linoleic acid supplementation increase oxidative stress and inflammatory biomarkers in men with metabolic syndrome?
Supplementation with the t10c12 isomer of conjugated linoleic acid significantly increases oxidative stress and inflammation, which correlates with induced insulin resistance in men with metabolic syndrome.
Answers are grounded in this paper and cite their sources.
t10c12 CLA supplementation induces oxidative stress and CRP elevation linked to worsened insulin resistance; confirms isomer-specific mechanisms in abdominally obese men.
BACKGROUND: Conjugated linoleic acids (CLAs), a group of fatty acids shown to have beneficial effects in animals, are also used as weight loss supplements. Recently, we reported that the t10c12 CLA-isomer caused insulin resistance in abdominally obese men via unknown mechanisms. The aim of the present study was to examine whether CLA has isomer-specific effects on oxidative stress or inflammatory biomarkers and to investigate the relationship between these factors and induced insulin resistance. METHODS AND RESULTS: In a double-blind placebo-controlled trial, 60 men with metabolic syndrome were randomized to one of 3 groups receiving t10c12 CLA, a CLA mixture, or placebo for 12 weeks. Insulin sensitivity (euglycemic clamp), serum lipids, in vivo lipid peroxidation (determined as urinary 8-iso-PGF(2alpha) [F2-isoprostanes]), 15-ketodihydro PGF(2alpha), plasma vitamin E, plasma C-reactive protein, tumor necrosis factor-alpha, and interleukin-6 were assessed before and after treatment. Supplementation with t10c12 CLA markedly increased 8-iso-PGF(2alpha) (578%) and C-reactive protein (110%) compared with placebo (P<0.0001 and P<0.01, respectively) and independent of changes in hyperglycemia or dyslipidemia. The increases in 8-iso-PGF(2alpha), but not in C-reactive protein, were significantly and independently related to aggravated insulin resistance. Oxidative stress was related to increased vitamin E levels, suggesting a compensatory mechanism. CONCLUSIONS: t10c12 CLA supplementation increases oxidative stress and inflammatory biomarkers in obese men. The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance. These unfavorable effects of t10c12 CLA might be of clinical importance with regard to cardiovascular disease, in consideration of the widespread use of dietary supplements containing this fatty acid.
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Risérus et al. (2002) conducted an RCT in metabolic syndrome (n=60). t10c12 CLA vs. Placebo was evaluated on 8-iso-PGF(2alpha) and C-reactive protein (p=P<0.0001). Supplementation with t10c12 CLA for 12 weeks markedly increased oxidative stress and C-reactive protein compared with placebo in men with metabolic syndrome.
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