Diabetes, obesity & metabolism · 2025
Acute inflammation amplifies the diabetogenic effect of excess adiposity: Evidence from a real-life, prospective cohort.
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Lan Yulong, Wu Dan, Feng Baoyu, Ding Xiong, Xu Lingyu, Zheng Huancong, Wu Kuangyi, Li Xingang, Balmer Lois, Wang Wei, Wu Shouling, Chen Youren
Аннотация
AIMS: Mounting evidence has suggested the probable involvement of infections in obesity-associated type 2 diabetes. This study aims to evaluate the association between acute inflammation and type 2 diabetes risk and to examine whether this association is modified by adiposity status.
MATERIALS AND METHODS: This study analysed 82 314 participants without pre-existing diabetes from a real-life, prospective cohort in China. Acute immune response was defined as high-sensitivity C-reactive protein (hsCRP) ≥10 mg/L, and overweight/obesity as body mass index (BMI) ≥24 kg/m2. Multivariable Cox regression models estimated diabetes risk, and both multiplicative and additive interactions were evaluated.
RESULTS: During a median follow-up of 11 years, 14 189 participants developed diabetes. Both elevated hsCRP and overweight/obesity independently increased diabetes risk. Acute inflammation was associated with a higher diabetes risk [hazard ratio (HR): 1.14; 95% confidence interval (CI): 1.04-1.22], particularly among those with excess adiposity [HR: 1.24 (1.13-1.36)] compared to those with normal weight [HR: 1.00 (0.83-1.21); P-interaction = 0.0112]. A supra-additive interaction was observed (relative excess risk due to interaction: 0.27; 95% CI: 0.02-0.52), with stronger synergistic effects seen in individuals under 60 and differences noted by sex.
CONCLUSIONS: Acute inflammation significantly elevates diabetes risk in overweight/obese individuals but not in those with normal weight, highlighting the synergistic role of adiposity and immune activation in diabetes pathogenesis and the importance of weight control in prevention strategies.
MATERIALS AND METHODS: This study analysed 82 314 participants without pre-existing diabetes from a real-life, prospective cohort in China. Acute immune response was defined as high-sensitivity C-reactive protein (hsCRP) ≥10 mg/L, and overweight/obesity as body mass index (BMI) ≥24 kg/m2. Multivariable Cox regression models estimated diabetes risk, and both multiplicative and additive interactions were evaluated.
RESULTS: During a median follow-up of 11 years, 14 189 participants developed diabetes. Both elevated hsCRP and overweight/obesity independently increased diabetes risk. Acute inflammation was associated with a higher diabetes risk [hazard ratio (HR): 1.14; 95% confidence interval (CI): 1.04-1.22], particularly among those with excess adiposity [HR: 1.24 (1.13-1.36)] compared to those with normal weight [HR: 1.00 (0.83-1.21); P-interaction = 0.0112]. A supra-additive interaction was observed (relative excess risk due to interaction: 0.27; 95% CI: 0.02-0.52), with stronger synergistic effects seen in individuals under 60 and differences noted by sex.
CONCLUSIONS: Acute inflammation significantly elevates diabetes risk in overweight/obese individuals but not in those with normal weight, highlighting the synergistic role of adiposity and immune activation in diabetes pathogenesis and the importance of weight control in prevention strategies.