RESUMO
BACKGROUND & AIMS: Haptoglobin (Hp) is associated with risks of obesity and cardiometabolic dysfunction; however, the role of the Hp phenotype in diet-induced weight loss remains to be elucidated. This study investigated whether the Hp phenotype contributes to inter-individual variations in body weight reduction as well as changes in the metabolic profile. METHODS: Secondary data analysis from a randomized controlled trial. In total, 151 abdominally obese Taiwanese women with ≥2 metabolic components were randomized to each of four dietary programs [calorie restriction (CR), calorie restriction plus fish oil supplementation (CRF), calorie restricted meal replacement (CRMR), and calorie restricted meal replacement with fish oil supplementation (CRMRF)] for 12 weeks. Abdominal obesity was defined as a waist circumference (WC) ≥ 80 cm in women. Hp phenotyping was performed by plasma gel electrophoresis. RESULTS: The prevalence of the Hp 1-1, 2-1, and 2-2 phenotypes were 12.58%, 41.06% and 46.35%, respectively. The mean age was 50.59 ± 12.22 years, and mean reduction in the percent body weight was 4.7% ± 3.8%. The Hp 1-1 phenotype exhibited significant decreases in the WC, body fat mass, plasma insulin levels, free hemoglobin and homeostatic model assessment of insulin resistance (HOMA-IR) compared to the Hp 2-1 or Hp 2-2 phenotypes after adjusting for the baseline age, WC, metabolic syndrome (MetS), and dietary programs (all adjusted p < 0.05). A greater improvement in the prevalence of central obesity and, to a lesser extent, MetS was also found in women with the Hp 1-1 phenotype. CONCLUSIONS: Obese women with the Hp 1-1 phenotype might obtain greater benefits in terms of reducing abdominal fat and improving insulin sensitivity in response to hypocaloric diet-induced weight reduction. The findings from this study support potential gene-diet interactions affecting weight loss. This trial was registered at ClinicalTrials.gov as NCT01768169. CLINICAL TRIAL REGISTRY: This trial was registered at ClinicalTrials.gov as NCT01768169.
