Dataset Information

C-Reactive Protein Causes Adult-Onset Obesity Through Chronic Inflammatory Mechanism.

ABSTRACT: Obesity is characterized by low-grade chronic inflammation. As an acute-phase reactant to inflammation and infection, C-reactive protein (CRP) has been found to be the strongest factor associated with obesity. Here we show that chronic elevation of human CRP at baseline level causes the obesity. The obesity phenotype is confirmed by whole-body magnetic resonance imaging (MRI), in which the total fat mass is 6- to 9- fold higher in the CRP rats than the control rats. Univariate linear regression analysis showed different growth rates between the CRP rats and the control rats, and that the difference appears around 11 weeks old, indicating that they developed adult-onset obesity. We also found that chronic elevation of CRP can prime molecular changes broadly in the innate immune system, energy expenditure systems, thyroid hormones, apolipoproteins, and gut flora. Our data established a causal role of CRP elevation in the development of adult-onset obesity.

SUBMITTER: Li Q

PROVIDER: S-EPMC7044181 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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C-Reactive Protein Causes Adult-Onset Obesity Through Chronic Inflammatory Mechanism.

Li Qiling Q Wang Qi Q Xu Wei W Ma Yamin Y Wang Qing Q Eatman Danita D You Shaojin S Zou Jin J Champion James J Zhao Lanbo L Cui Ye Y Li Wenzhi W Deng Yangyang Y Ma Li L Wu Biao B Wang Guangdi G Zhang Xiaodong X Wang Qingwei Q Bayorh Mohamed A MA Song Qing Q

Frontiers in cell and developmental biology 20200220

Obesity is characterized by low-grade chronic inflammation. As an acute-phase reactant to inflammation and infection, C-reactive protein (CRP) has been found to be the strongest factor associated with obesity. Here we show that chronic elevation of human CRP at baseline level causes the obesity. The obesity phenotype is confirmed by whole-body magnetic resonance imaging (MRI), in which the total fat mass is 6- to 9- fold higher in the CRP rats than the control rats. Univariate linear regression ...[more]

PMID: 32154244

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Project description:BackgroundObesity and the metabolic syndrome occur in approximately one-third of patients with alcoholic liver disease (ALD). The increased consumption of fructose parallels the increased prevalence of obesity and the metabolic syndrome in the United States and worldwide. In this study, we investigated whether dietary high fructose potentiates chronic alcohol-induced liver injury, and explored potential mechanism(s).MethodsSix-week-old male C57BL/6J mice were assigned to 4 groups: control, high fructose, chronic ethanol (EtOH), and high fructose plus chronic alcohol. The mice were fed either control diet or high-fructose diet (60%, w/w) for 18 weeks. Chronic alcohol-fed mice were given 20% (v/v) ethanol (Meadows-Cook model) ad libitum as the only available liquid from the 9th week through the 18th week. Liver injury, steatosis, hepatic inflammatory gene expression, and copper status were assessed.ResultsHigh-fructose diet and chronic alcohol consumption alone each induce hepatic fat accumulation and impair copper status. However, the combination of dietary high fructose plus chronic alcohol synergistically induced liver injury as evidenced by robustly increased plasma alanine aminotransferase and aspartate aminotransferase, but the combination did not exacerbate hepatic fat accumulation nor worsen copper status. Moreover, FE-fed mice were characterized by prominent microvesicular steatosis. High-fructose diet and chronic alcohol ingestion together led to a significant up-regulation of Kupffer cell (KC) M1 phenotype gene expression (e.g., tumor necrosis factor-α and monocyte chemoattractant protein-1), as well as Toll-like receptor 4 (TLR4) signaling gene expression, which is also associated with the up-regulation of KCs and activation marker gene expression, including Emr1, CD68, and CD163.ConclusionsOur data suggest that dietary high fructose may potentiate chronic alcohol consumption-induced liver injury. The underlying mechanism might be due to the synergistic effect of dietary high fructose and alcohol on the activation of the TLR4 signaling pathway, which in turn leads to KC activation and phenotype switch toward M1 polarization. This study suggests that alcohol-fructose combination contributes to ALD progression.

Dataset Information

C-Reactive Protein Causes Adult-Onset Obesity Through Chronic Inflammatory Mechanism.

Publications

C-Reactive Protein Causes Adult-Onset Obesity Through Chronic Inflammatory Mechanism.

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