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Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease that affects over 30% of the world's population. For decades, the heterogeneity of non-alcoholic fatty liver disease (NAFLD) has impeded our understanding of the disease mechanism and the development of effective medications. However, a recent change in the nomenclature from NAFLD to MASLD emphasizes the critical role of systemic metabolic dysfunction in the pathophysiology of this disease and therefore promotes the progress in the pharmaceutical treatment of MASLD. In this review, we focus on the mechanism underlying the abnormality of hepatic lipid metabolism in patients with MASLD, and summarize the latest progress in the therapeutic medications of MASLD that target metabolic disorders. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the association of serum betatrophin with the status and progression of nonalcoholic fatty liver disease (NAFLD). Methods: A total of 249 subjects who received ultrasonic examination of liver fat content (LFC) were recruited. Anthropometric and biochemical examinations were performed. Serum betatrophin was measured by ELISA. Results: Compared with control group, serum betatrophin significantly increased in NAFLD group (P < 0.05). There was significant difference in serum betatrophin among control, low liver fat content (LLFC), and high liver fat content (HLFC) groups (P < 0.01). After adjustment for gender, age, BMI, FPG and HbA1c, the betatrophin positively correlated with LFC (r = 0.185, P < 0.01) and TG (r = 0.195, P < 0.01). Stepwise multiple regression analysis indicated serum betatrophin was independently related to LFC (P < 0.05). Multivariate logistic regression analysis revealed subjects in the highest tertile of serum betatrophin had higher odds of having NAFLD after adjustment for traditional NAFLD risk factors (OR = 2.88, 95%CI: 1.15–7.19) (P<0.05). Conclusion: Serum betatrophin is an independent risk factor for NAFLD and potential non-invasive marker for its progression. Serum betatrophin may be helpful for the early diagnosis of NAFLD and improvement of its prognosis. [ABSTRACT FROM AUTHOR]

Background/Objectives: Vitamin D exerts metabolic activities. We investigated whether the 25-hydroxy vitamin D [25(OH)D] is associated with liver fat content (LFC) and non-alcoholic fatty liver disease (NAFLD) in a middle-aged, elderly Chinese population. Subject/Methods: A total of 2,960 participants (954 men and 2,006 women) aged over 45 years old were enrolled. Each participant underwent a standard interview, anthropometric measurements and laboratory examinations. Vitamin D deficiency and insufficiency was diagnosed when serum 25(OH) D level was < 50 and 50–75nmol/L. An ultrasound quantitative method was used to assess the LFC. Results: Among the 2,960 participants, 1,982 (67.0%) subjects had vitamin D deficiency, 769 (26.0%) had vitamin D insufficiency, and 209 (7%) had normal vitamin D. Male subjects with vitamin D deficiency and insufficiency had significantly higher LFC than those with normal 25(OH)D (P = 0.034), while the LFC values showed no significant difference among the female subjects with vitamin D sufficiency, insufficiency and deficiency (P = 0.396). Univariate correlation analysis showed that 25(OH)D had a significantly negative association with LFC in men (r = -0.085, P = 0.009), but not in women. After adjusting for age, cigarette smoking, examination season, serum calcium, PTH and all possible confounders that displayed significant associations with LFC in univariate correlation analysis, serum 25(OH)D remained associated with LFC in middle-aged and elderly Chinese men. Conclusion: Serum 25(OH)D level was inversely associated with LFC in middle-aged and elderly Chinese men. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is closely associated with type 2 diabetes mellitus. We investigated whether the deposition of fat in the liver is associated with glycemic abnormalities and evaluated the contribution of the liver fat content (LFC) to the impaired glucose regulation. We conducted a community-based study among 2836 residents (1018 males and 1818 females) without prior known diabetes mellitus from the Changfeng Study who were at least 45 years old. A standard interview, anthropometrics and laboratory parameters were performed for each participant. The standardised ultrasound hepatic-renal echo-intensity and hepatic echo-intensity attenuation rate were used to assess the LFC. The cohort was stratified according to the quintiles for LFC. Two-hour glucose and fasting blood glucose increased across the LFC quintiles after adjustment for age and gender. LFC increased continuously among glucose categories after adjustment for age and gender (NGT: 7.7±0.3%, IFG: 10.0±0.8%, IGT: 11.8±0.5%, IFG+IGT: 11.7±0.9%, new- DM: 12.4±0.6%, P<0.001). By logistic regression analysis, 1% LFC increment independently predicted prediabetes and diabetes (OR 1.032, 1.019–1.045, P<0.001; 1.021, 1.005–1.037, P = 0.012, respectively) after adjustment for all potential confounders. Furthermore, participants with LFC higher than 10% had higher odds ratios of impaired glucose regulation as compared with those with LFC below 10% in fully adjusted logistic models. These results suggest that the LFC is strongly associated with impaired glucose regulation in the Chinese population, and that an even slightly elevated LFC is associated with increased glucose dysregulation. [ABSTRACT FROM AUTHOR]