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Betaine is a food component with well-reported hepatoprotection effects. However, the effects and mechanisms of betaine on liver fibrosis development are still insufficient. Because metabolic functions of chicken and human liver is similar, we established a chicken model with carbon Tetrachloride- (CCl4-) induced fibrosis for studying antifibrotic effect of betaine in vivo and in vitro. Two-week-old male chicks were supplemented with betaine (1%, w/v) in drinking water for 2 weeks prior to the initiation of CCl4 treatment (i.p.) until sacrifice. Primary chicken hepatocytes were treated with CCl4 and betaine to mimic the in vivo supplementation. The supplementation of betaine significantly alleviated liver fibrosis development along with the inhibition of lipid peroxidation, hepatic inflammation cytokine, and transforming growth factor-β1 expression levels. These inhibitive effects were also accompanied with the attenuation of hepatic stellate cell activation. Furthermore, our in vitro studies confirmed that betaine provides antioxidant capacity for attenuating the hepatocyte necrosis by CCl4. Altogether, our results highlight the antioxidant ability of betaine, which alleviates CCl4-induced fibrogenesis process along with the suppression of hepatic stellate cells activation. Since betaine is a natural compound without toxicity, we suggest betaine can be used as a potent nutritional or therapeutic factor for reducing liver fibrosis.

The AdipoR1 transgene enabled mice to resist diet-induced obesity while decreasing lipid accumulation, oxidative stress and autophagic damage. These effects might contribute to the improvement of heart functions in diet-induced obese mice.

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AdipoR1 enhances fatty acid metabolism and cell viability in palmitate-treated HepG2 cells partially by activating AKT signaling. Therefore, AdipoR1 has therapeutic potential in the treatment of nonalcoholic fatty liver disease.

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Circulating leukocyte subtypes and monocyte subsets are independent predictors of cardiovascular events. We hypothesized that an increased leukocyte subtype would predict severe coronary stenosis and extensive plaque involvement. We retrospectively analyzed clinical, laboratory, and coronary CT data in a total of 588 asymptomatic adults (69% men; mean age, 57 ± 9 years) undergoing a general health check-up. Intermediate CD14CD16 monocyte count had the strongest association with mixed and calcified plaque scores, whereas the numbers of neutrophils and classical CD14CD16 monocytes were significantly associated with non-calcified plaque score. Only high CD14CD16 monocyte count (>12 cells/μL) significantly predicted extensive plaque involvement [odds ratio 3.16 (95% confidence interval 1.84-5.43), P < 0.001; quartile 4 vs. 1-3] and severe coronary stenosis [3.67 (1.84-7.33), P < 0.001; quartile 4 vs. 1-3] after adjustments for Framingham Risk Score (FRS), metabolic syndrome, and C-reactive protein. The CD14CD16 monocyte count, when added to FRS, significantly reclassified 30.4 and 26.7% of the overall and 50.2 and 36.2% of the intermediate-risk population (FRS 6-20%) for predicting extensive plaque involvement and severe coronary stenosis, respectively. Thus, in asymptomatic individuals, intermediate CD14CD16 monocyte could independently predict severe CAD and improve risk stratification.