Background

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.

Subjects

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.

Results

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).

Conclusions

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.

Clinical trial registration

ISRCTN15840340.

中文翻译：

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与体重增加和胰岛素抵抗相关的因素：一项纵向研究

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，仍不清楚。这项研究纵向调查了与体重变化相关的因素。

科目

在 4 年随访中对 707 名没有糖尿病的成年人进行了调查。使用经过验证的当地居民食物频率调查问卷评估了过去 12 个月内能量和常量营养素的习惯摄入量。 β细胞功能和胰岛素抵抗的稳态模型评估（HOMA-IR）被用作胰岛素抵抗的替代指标。此外，还对PNPLA3进行了基因分型。

结果

87 名参与者体重增加者（G；截止值 = 5 公斤），620 名参与者体重未增加（NG）。初始人体测量（G vs. NG：年龄，44 ± 13 vs 51 ± 13 岁，P  < 0.001；体重指数，27.8 ± 6.5 vs 28.1 ± 5.1 kg/m ²，P  = ns；体重，76.7 ± 22.1 vs两组的 最终体重（74.2 ± 14.7 kg，P = ns；86.3 ± 23.7 vs 72.9 ± 14.2 kg， P  < 0.001）和饮食特征以及胰岛素浓度和 HOMA-IR 值相似。四年后，G 的 EI、胰岛素浓度和 HOMA-IR 值显着增加。 G 的 PNPLA3 CG 和 GG 等位基因患病率高于 NG（P  < 0.05）。 G 的存在与年龄 (OR = 1.031)、EI 变化 (OR = 2.257) 和 PNPLA3 基因的不利等位基因 (OR = 1.700) 独立相关。最终体重指数、腰围和EI与最终HOMA-IR独立相关（P  <0.001）。

结论

EI与体重增加有关，遗传因素可能影响能量平衡。胰岛素抵抗是体重增加的结果，这表明可能存在针对底物溢出的细胞内保护机制。

临床试验注册

ISRCTN15840340。