Mediators of inflammation · 2026
C1q/TNF-Related Protein 4 (C1QTNF4) Acts as an Adipokine That Ameliorates Diet-Induced Obesity by Improving Energy Metabolism and Alleviating Adipose Inflammation.
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Na Daxiang, He Yanwei, Liu Xinrui, Huang Mingjun, Xie Shuo, Li Hexin, Liu Jingying, Zhang Hong, Wang Lu
Аннотация
BACKGROUND: The C1q/TNF-related protein (C1QTNF) plays a crucial role in the intricate connection between obesity and inflammation, acting as a significant adipokine. This study aims to investigate the potential of C1QTNF4 as an antiobesity and anti-inflammatory adipokine.
METHODS: Forty-eight subjects, with or without obesity and diabetes mellitus (DM), were categorized into two groups based on their health condition. Measurements of C1QTNF4, glucose, and adipokine concentrations were conducted. Seven-week-old C57BL/6J mice were segregated into four groups, with eight mice in each group of both sexes. C1QTNF4 transgenic (Tg) mice and their corresponding littermate controls were subjected to either a high-fat (HF) diet (HFD) or a standard chow diet for 14 weeks.
RESULTS: C1QTNF4 and leptin levels increased, while adiponectin levels decreased in subjects with obesity and DM compared to normal individuals. C1QTNF4 Tg mice on a HFD exhibited resistance to weight gain, accompanied by an amelioration of insulin resistance (IR). Fatty liver and chronic adipose inflammation were also mitigated. In the liver and skeletal muscle of C1QTNF4 Tg mice, C1QTNF4 activated the AMP-activated protein kinase (AMPK) pathway associated with insulin sensitivity and energy expenditure. Plasma IL-6 decreased in Tg mice on a HFD, indicating that C1QTNF4 alleviates inflammation via the IL-6-JAK1/2-STAT3 pathway.
CONCLUSIONS: C1QTNF4 emerges as an adipokine with a regulatory role in adipogenesis, addressing energy imbalances and reducing inflammation. This study suggests that C1QTNF4 represents a potential drug target for treating obesity, IR, and inflammation.
METHODS: Forty-eight subjects, with or without obesity and diabetes mellitus (DM), were categorized into two groups based on their health condition. Measurements of C1QTNF4, glucose, and adipokine concentrations were conducted. Seven-week-old C57BL/6J mice were segregated into four groups, with eight mice in each group of both sexes. C1QTNF4 transgenic (Tg) mice and their corresponding littermate controls were subjected to either a high-fat (HF) diet (HFD) or a standard chow diet for 14 weeks.
RESULTS: C1QTNF4 and leptin levels increased, while adiponectin levels decreased in subjects with obesity and DM compared to normal individuals. C1QTNF4 Tg mice on a HFD exhibited resistance to weight gain, accompanied by an amelioration of insulin resistance (IR). Fatty liver and chronic adipose inflammation were also mitigated. In the liver and skeletal muscle of C1QTNF4 Tg mice, C1QTNF4 activated the AMP-activated protein kinase (AMPK) pathway associated with insulin sensitivity and energy expenditure. Plasma IL-6 decreased in Tg mice on a HFD, indicating that C1QTNF4 alleviates inflammation via the IL-6-JAK1/2-STAT3 pathway.
CONCLUSIONS: C1QTNF4 emerges as an adipokine with a regulatory role in adipogenesis, addressing energy imbalances and reducing inflammation. This study suggests that C1QTNF4 represents a potential drug target for treating obesity, IR, and inflammation.