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Abstract：
Obesity is the result of energy intake (EI) chronically exceeding energy expenditure. However, the potential metabolic factors, including insulin resistance, remain unclear. This study longitudinally investigated factors associated with changes in body weight.
A cohort of 707 adults without diabetes were investigated at the 4-year follow-up visit. The habitual intake of energy and macronutrients during the past 12 months was assessed using a validated Food Frequency Questionnaire for the local population. Homeostatic model assessment of β-cell function and insulin resistance (HOMA-IR) was used as a surrogate measure of insulin resistance. Additionally, PNPLA3 was genotyped.
Eighty-seven participants were weight gainers (G; cutoff value = 5 kg), and 620 were non-gainers (NG). Initial anthropometric (G vs. NG: age, 44 ± 13 vs 51 ± 13 years, P < 0.001; body mass index, 27.8 ± 6.5 vs 28.1 ± 5.1 kg/m2, P = ns; body weight, 76.7 ± 22.1 vs 74.2 ± 14.7 kg, P = ns; final body weight, 86.3 ± 23.7 vs 72.9 ± 14.2 kg, P < 0.001) and diet characteristics, as well as insulin concentrations and HOMA-IR values, were similar in both groups. Four years later, G showed significantly increased EI, insulin concentrations, and HOMA-IR values. G had a higher prevalence of the PNPLA3 CG and GG alleles than NG (P < 0.05). The presence of G was independently associated with age (OR = 1.031), EI change (OR = 2.257), and unfavorable alleles of PNPLA3 gene (OR = 1.700). Final body mass index, waist circumference, and EI were independently associated with final HOMA-IR (P < 0.001).
EI is associated with body weight gain, and genetic factors may influence the energy balance. Insulin resistance is a consequence of weight gain, suggesting a possible intracellular protective mechanism against substrate overflow.
ISRCTN15840340.
A cohort of 707 adults without diabetes were investigated at the 4-year follow-up visit. The habitual intake of energy and macronutrients during the past 12 months was assessed using a validated Food Frequency Questionnaire for the local population. Homeostatic model assessment of β-cell function and insulin resistance (HOMA-IR) was used as a surrogate measure of insulin resistance. Additionally, PNPLA3 was genotyped.
Eighty-seven participants were weight gainers (G; cutoff value = 5 kg), and 620 were non-gainers (NG). Initial anthropometric (G vs. NG: age, 44 ± 13 vs 51 ± 13 years, P < 0.001; body mass index, 27.8 ± 6.5 vs 28.1 ± 5.1 kg/m2, P = ns; body weight, 76.7 ± 22.1 vs 74.2 ± 14.7 kg, P = ns; final body weight, 86.3 ± 23.7 vs 72.9 ± 14.2 kg, P < 0.001) and diet characteristics, as well as insulin concentrations and HOMA-IR values, were similar in both groups. Four years later, G showed significantly increased EI, insulin concentrations, and HOMA-IR values. G had a higher prevalence of the PNPLA3 CG and GG alleles than NG (P < 0.05). The presence of G was independently associated with age (OR = 1.031), EI change (OR = 2.257), and unfavorable alleles of PNPLA3 gene (OR = 1.700). Final body mass index, waist circumference, and EI were independently associated with final HOMA-IR (P < 0.001).
EI is associated with body weight gain, and genetic factors may influence the energy balance. Insulin resistance is a consequence of weight gain, suggesting a possible intracellular protective mechanism against substrate overflow.
ISRCTN15840340.
摘要：
背景：肥胖是能量摄入（EI）长期超过能量消耗的结果。然而,潜在的代谢因素，包括胰岛素抵抗，仍然不清楚。这项研究纵向调查了与体重变化相关的因素。
方法：在4年的随访中对707名没有糖尿病的成年人进行了调查。使用经过验证的食物频率问卷对过去12个月的能量和大量营养素的习惯性摄入量进行评估。β细胞功能和胰岛素抵抗的稳态模型评估(HOMA-IR)用作胰岛素抵抗的替代测量。此外,对PNPLA3进行基因分型。
结果：87名参与者是体重增加者（G；截止值=5公斤），620为非涨幅者（NG）。初始人体测量(Gvs.NG：年龄，44±13vs51±13年，P<0.001；体重指数，27.8±6.5vs28.1±5.1kg/m2,P=ns;体重,76.7±22.1vs74.2±14.7kg，P=ns；最终体重，86.3±23.7vs72.9±14.2kg，P<0.001）和饮食特征，以及胰岛素浓度和HOMA-IR值，两组相似。四年后,G显示EI显著增加，胰岛素浓度，和HOMA-IR值。G的PNPLA3CG和GG等位基因的患病率高于NG（P<0.05）。G的存在与年龄独立相关（OR=1.031），EI变化（OR=2.257），和PNPLA3基因的不良等位基因（OR=1.700）。最终体重指数,腰围,EI与最终HOMA-IR独立相关(P<0.001)。
结论：EI与体重增加有关，遗传因素可能会影响能量平衡。胰岛素抵抗是体重增加的结果，提示可能的细胞内保护机制对抗底物溢出。
背景：ISRCTN15840340。
方法：在4年的随访中对707名没有糖尿病的成年人进行了调查。使用经过验证的食物频率问卷对过去12个月的能量和大量营养素的习惯性摄入量进行评估。β细胞功能和胰岛素抵抗的稳态模型评估(HOMA-IR)用作胰岛素抵抗的替代测量。此外,对PNPLA3进行基因分型。
结果：87名参与者是体重增加者（G；截止值=5公斤），620为非涨幅者（NG）。初始人体测量(Gvs.NG：年龄，44±13vs51±13年，P<0.001；体重指数，27.8±6.5vs28.1±5.1kg/m2,P=ns;体重,76.7±22.1vs74.2±14.7kg，P=ns；最终体重，86.3±23.7vs72.9±14.2kg，P<0.001）和饮食特征，以及胰岛素浓度和HOMA-IR值，两组相似。四年后,G显示EI显著增加，胰岛素浓度，和HOMA-IR值。G的PNPLA3CG和GG等位基因的患病率高于NG（P<0.05）。G的存在与年龄独立相关（OR=1.031），EI变化（OR=2.257），和PNPLA3基因的不良等位基因（OR=1.700）。最终体重指数,腰围,EI与最终HOMA-IR独立相关(P<0.001)。
结论：EI与体重增加有关，遗传因素可能会影响能量平衡。胰岛素抵抗是体重增加的结果，提示可能的细胞内保护机制对抗底物溢出。
背景：ISRCTN15840340。
