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Body weight gain rather than body weight variability associated with increased risk of nonalcoholic fatty liver disease.

ABSTRACT: Weight loss, the most established therapy for nonalcoholic fatty liver disease (NAFLD), is frequently followed by weight regain and fluctuation. The aim of this study was to investigate whether body weight change and variability were independent risk factors for incident NAFLD. We conducted a longitudinal cohort study. Among the 1907 participants, incident NAFLD occurred in 420 (22.0%) cases during median follow-up of 5.6 years. In the multivariate analysis, there was no significant association between weight variability and the risk of incident NAFLD. The risk of incident NAFLD was significantly higher in subjects with weight gain ≥ 10% and 7% < gain ≤ 10% [hazard ratios (HR), 2.43; 95% confidence intervals (CI), 1.65-3.58 and HR, 1.73; 95% CI, 1.26-2.39, respectively], while the risk of incident NAFLD was significantly lower in those with -7% < weight loss ≤ --3% (HR, 0.33; 95% CI, 0.22-0.51). Overall body weight gain rather than bodyweight variability was independently associated with the risk of incident NAFLD. Understanding the association between body weight variability and incident NAFLD may have future clinical implications for the quantification of weight loss as a treatment for patients with NAFLD.

SUBMITTER: Cho EJ

PROVIDER: S-EPMC8277820 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature

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Body weight gain rather than body weight variability associated with increased risk of nonalcoholic fatty liver disease.

Cho Eun Ju EJ Yu Su Jong SJ Jung Gu Cheol GC Kwak Min-Sun MS Yang Jong In JI Yim Jeong Yoon JY Chung Goh Eun GE

Scientific reports 20210713 1

Weight loss, the most established therapy for nonalcoholic fatty liver disease (NAFLD), is frequently followed by weight regain and fluctuation. The aim of this study was to investigate whether body weight change and variability were independent risk factors for incident NAFLD. We conducted a longitudinal cohort study. Among the 1907 participants, incident NAFLD occurred in 420 (22.0%) cases during median follow-up of 5.6 years. In the multivariate analysis, there was no significant association ...[more]

PMID: 34257374

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Project description:Our objective was to examine risk factors associated with development of nonalcoholic fatty liver disease (NAFLD) among women with endometrial cancer who underwent surgical staging with or without oophorectomy.This is a retrospective study that evaluated endometrial cancer cases that underwent surgical staging (n = 666) and endometrial hyperplasia cases that underwent hysterectomy-based treatment (n = 209). This study included 712 oophorectomy cases and 163 nonoophorectomy cases. Archived records were reviewed for participant demographics, medical comorbidities, operative notes, histology results, and radiology reports for NAFLD. Cumulative risks of NAFLD after surgical operation were correlated to demographics and medical comorbidities.The cumulative prevalence of NAFLD in 875 women with endometrial tumor was 14.1%, 20.5%, and 38.4% at 1, 2, and 5 years after surgical operation, respectively. On multivariate analysis, after controlling for age, ethnicity, body mass index, medical comorbidities, tumor type, hormonal treatment pattern, and oophorectomy status, age younger than 40 years (2-y cumulative prevalence, 26.6% vs 16.8%; hazard ratio [HR], 1.85; 95% CI, 1.27-2.71; P = 0.001) and age 40 to 49 years (2-y cumulative prevalence, 23.1% vs 16.8%; HR, 1.49; 95% CI, 1.08-2.04; P = 0.015) remained significant predictors for developing NAFLD after surgical operation compared with age 50 years or older. Oophorectomy was an independent predictor for increased risk of NAFLD (20.9% vs 15.9%; HR, 1.70; 95% CI, 1.01-2.86; P = 0.047). In addition, NAFLD was significantly associated with postoperative development of diabetes mellitus (39.2% vs 15.3%; HR, 2.26; 95% CI, 1.52-3.35; P < 0.0001) and hypercholesterolemia (34.3% vs 17.5%; HR, 1.71; 95% CI, 1.12-2.63; P = 0.014).Oophorectomy in young women with endometrial cancer significantly increases the risk of NAFLD. This is associated with development of diabetes mellitus and hypercholesterolemia after oophorectomy.

Project description:Background & Aims: Overnutrition is one of the major causes of non-alcoholic fatty liver disease (NAFLD) and its advanced form non-alcoholic steatohepatitis (NASH). Besides the quantity of consumed calories, distinct dietary components are increasingly recognized as important contributor to the pathogenesis of NASH. We aimed to develop and characterize a hitherto missing murine model which resembles both the pathology and nutritional situation of NASH-patients in Western societies. Methods: We developed a NASH-inducing diet (ND) enriched with sucrose, cholesterol and a high concentration of fats rich in saturated fatty acids in a composition which mimics Western food. C57Bl6/N mice were fed with the ND or control chow for 12 weeks. Biochemical, real-time polymerase chain reaction, Western Blot and immunohistochemical analyses were performed to characterize systemic and hepatic changes induced by ND-feeding. Immunohistochemistry was used to assess c-Jun levels and activation in 110 human NAFLD and control liver specimens applying tissue micro array technology. Results: ND-fed mice showed significant body weight gain, impaired glucose tolerance, elevated fasting blood glucose levels as well as decreased adiponectin and increased leptin serum levels compared to control mice. In the liver, ND-feeding led to marked steatosis, enhanced cholesterol levels, distinct signs of oxidative stress, hepatocellular damage, inflammation, activation of hepatic stellate cells, and beginning fibrosis. Transcriptome-wide hepatic gene expression analysis comparing ND-fed mice and control mice indicated main alterations in lipid metabolism and inflammatory processes. Search for over-represented transcription factor target sites among the differentially expressed genes identified AP-1 as the most likely factor to cause the transcriptional changes in ND-livers. Combining differentially expressed gene and protein-protein interaction network analysis identified c-Jun (a component of the AP-1 complex) as hub in the largest connected deregulated sub-network in ND-livers. In accordance, ND-livers revealed c-Jun-phosphorylation and nuclear translocation. Moreover, hepatic c-Jun RNA and protein expression was enhanced in ND-fed compared to control mice. Also NAFLD-patients showed enhanced hepatic c-Jun levels, which correlated with inflammation, and notably, with the degree of hepatic steatosis. Conclusions: The new dietary mouse-model shows important pathological changes also found in human NASH and indicates c-jun/AP-1 activation as critical regulator of hepatic alterations. Abundance of c-jun in NAFLD likely facilitates development and progression of NASH, and thus, c-jun appears as attractive prognostic and therapeutic target of NAFLD progression. 14-weeks old male C57BL/6N mice were fed with either regular diet or a newly designed NASH-inducing diet for 12 weeks. Hepatic gene expression levels were measured thereafter.

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Body weight gain rather than body weight variability associated with increased risk of nonalcoholic fatty liver disease.

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Body weight gain rather than body weight variability associated with increased risk of nonalcoholic fatty liver disease.

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