OBJECTIVE: To determine how changes in lipids, liver enzymes, and inflammatory and glycemia markers intercorrelate during prolonged dietary intervention in obese participants with or without type 2 diabetes (T2D). METHODS: We examined the dynamics and intercorrelations among changes in biomarkers during the 2-y Dietary Intervention Randomized Controlled Trial (DIRECT) in 322 participants (including 46 with T2D; 52 y of age, body mass index 31 kg/m(2)) throughout rapid weight loss (0-6 mo) and weight-maintenance/regain (7-24 mo) phases. RESULTS: The 2-y increase of high-density lipoprotein cholesterol was greater in participants with T2D (+9.41 versus+6.57 mg/dL, P < 0.05), although they tended to have smaller waist circumferences (-2.1 versus -4.0 cm, P = 0.08). In models adjusted for age, sex, and weight loss, the 2-year decrease of triacylglycerols was associated with increases of low-density and high-density lipoprotein cholesterol. An increase of apolipoprotein A1 was associated with a decrease in high-sensitive C-reactive protein (P < 0.05 for all comparisons). Exclusively in participants with T2D, the 2-year decrease in triacylglycerols was further correlated with decreases in apolipoprotein B100 and liver enzymes, and a decrease in fasting glucose correlated with decreases in low-density lipoprotein cholesterol, apolipoprotein B100, and alanine aminotransferase (P < 0.05 for all comparisons). In the entire group, multivariate models adjusted for age, sex, intervention group, and 6-mo weight loss identified decreased high-sensitive C-reactive protein at 6 mo as an exclusive predictor of a greater decrease in triacylglycerols (β = 0.154, P = 0.008) and a greater increase in high-density lipoprotein cholesterol (β = -0.452, P = 0.005) during the subsequent 18 mo. CONCLUSIONS: Long-term dietary intervention induces a flow of changes within biomarkers and the cross-talk is likely to be stronger in T2D. A decrease in systemic inflammation during the weight-loss phase may predict greater long-term improvement in lipids (www.ClinicalTrials.gov, identifier NCT00160108).
RCT Entities:
OBJECTIVE: To determine how changes in lipids, liver enzymes, and inflammatory and glycemia markers intercorrelate during prolonged dietary intervention in obeseparticipants with or without type 2 diabetes (T2D). METHODS: We examined the dynamics and intercorrelations among changes in biomarkers during the 2-y Dietary Intervention Randomized Controlled Trial (DIRECT) in 322 participants (including 46 with T2D; 52 y of age, body mass index 31 kg/m(2)) throughout rapid weight loss (0-6 mo) and weight-maintenance/regain (7-24 mo) phases. RESULTS: The 2-y increase of high-density lipoprotein cholesterol was greater in participants with T2D (+9.41 versus+6.57 mg/dL, P < 0.05), although they tended to have smaller waist circumferences (-2.1 versus -4.0 cm, P = 0.08). In models adjusted for age, sex, and weight loss, the 2-year decrease of triacylglycerols was associated with increases of low-density and high-density lipoprotein cholesterol. An increase of apolipoprotein A1 was associated with a decrease in high-sensitive C-reactive protein (P < 0.05 for all comparisons). Exclusively in participants with T2D, the 2-year decrease in triacylglycerols was further correlated with decreases in apolipoprotein B100 and liver enzymes, and a decrease in fasting glucose correlated with decreases in low-density lipoprotein cholesterol, apolipoprotein B100, and alanine aminotransferase (P < 0.05 for all comparisons). In the entire group, multivariate models adjusted for age, sex, intervention group, and 6-mo weight loss identified decreased high-sensitive C-reactive protein at 6 mo as an exclusive predictor of a greater decrease in triacylglycerols (β = 0.154, P = 0.008) and a greater increase in high-density lipoprotein cholesterol (β = -0.452, P = 0.005) during the subsequent 18 mo. CONCLUSIONS: Long-term dietary intervention induces a flow of changes within biomarkers and the cross-talk is likely to be stronger in T2D. A decrease in systemic inflammation during the weight-loss phase may predict greater long-term improvement in lipids (www.ClinicalTrials.gov, identifier NCT00160108).
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