BACKGROUND: Although evidence from cohort studies has suggested that trans fatty acid (TFA) consumption may be associated with insulin resistance and diabetes, randomized placebo-controlled trials (RCTs) have yielded conflicting results. OBJECTIVE: In a meta-analysis, we combined all available RCTs that examined the role of TFA intake on glucose homeostasis. DESIGN: A systematic review of PubMed was performed, and a total of 7 RCTs were included in the meta-analysis. Primary outcomes were glucose and insulin concentrations. Secondary outcomes were total, LDL-, and HDL-cholesterol and triglyceride concentrations. The pooled effect size (ES) was calculated through fixed- and random-effects meta-analyses. The potential existence of publication bias was evaluated by using funnel-plot analysis. Metaregression analysis was performed to evaluate for potential dose-response relations between the ES of outcomes and TFA intake. RESULTS: Increased TFA intake did not result in significant changes in glucose or insulin concentrations. Increased TFA intake led to a significant increase in total and LDL-cholesterol [ES (95% CI): 0.28 (0.04, 0.51) and 0.36 (0.13, 0.60), respectively] and a significant decrease in HDL-cholesterol concentrations [ES (95% CI): -0.25 (-0.48, -0.01)]. Our analysis also showed the absence of publication bias and any dose-response relations between the ES and TFA intake. CONCLUSIONS: Increased TFA intake does not result in changes in glucose, insulin, or triglyceride concentrations but leads to an increase in total and LDL-cholesterol and a decrease in HDL-cholesterol concentrations. There is no evidence to support a potential benefit of the reduction of dietary TFA intake on glucose homeostasis.
BACKGROUND: Although evidence from cohort studies has suggested that trans fatty acid (TFA) consumption may be associated with insulin resistance and diabetes, randomized placebo-controlled trials (RCTs) have yielded conflicting results. OBJECTIVE: In a meta-analysis, we combined all available RCTs that examined the role of TFA intake on glucose homeostasis. DESIGN: A systematic review of PubMed was performed, and a total of 7 RCTs were included in the meta-analysis. Primary outcomes were glucose and insulin concentrations. Secondary outcomes were total, LDL-, and HDL-cholesterol and triglyceride concentrations. The pooled effect size (ES) was calculated through fixed- and random-effects meta-analyses. The potential existence of publication bias was evaluated by using funnel-plot analysis. Metaregression analysis was performed to evaluate for potential dose-response relations between the ES of outcomes and TFA intake. RESULTS: Increased TFA intake did not result in significant changes in glucose or insulin concentrations. Increased TFA intake led to a significant increase in total and LDL-cholesterol [ES (95% CI): 0.28 (0.04, 0.51) and 0.36 (0.13, 0.60), respectively] and a significant decrease in HDL-cholesterol concentrations [ES (95% CI): -0.25 (-0.48, -0.01)]. Our analysis also showed the absence of publication bias and any dose-response relations between the ES and TFA intake. CONCLUSIONS: Increased TFA intake does not result in changes in glucose, insulin, or triglyceride concentrations but leads to an increase in total and LDL-cholesterol and a decrease in HDL-cholesterol concentrations. There is no evidence to support a potential benefit of the reduction of dietary TFA intake on glucose homeostasis.
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