Prevalence of Nonalcoholic Fatty Liver Disease in the United States: The Third National Health and Nutrition Examination Survey, 1988–1994

Lazo, Mariana; Hernáez, Rubén; Eberhardt, Mark S.; Bonekamp, Susanne; Kamel, Ihab R.; Güallar, Eliseo; Koteish, Ayman; Brancati, Frederick L.; Clark, Jeanne M.

doi:10.1093/aje/kws448

Cited by 733 publications

(583 citation statements)

References 37 publications

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“…The prevalence rates of hepatic steatosis and NAFLD are 21.4% and 19.0%, respectively in the US [2]. Fat accumulation in the liver due to defects in lipoprotein assembly or transport can lead to hepatic steatosis or NAFLD [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Mea6 controls VLDL transport through the coordinated regulation of COPII assembly

et al. 2016

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Lipid accumulation, which may be caused by the disturbance in very low density lipoprotein (VLDL) secretion in the liver, can lead to fatty liver disease. VLDL is synthesized in endoplasmic reticulum (ER) and transported to Golgi apparatus for secretion into plasma. However, the underlying molecular mechanism for VLDL transport is still poorly understood. Here we show that hepatocyte-specific deletion of meningioma-expressed antigen 6 (Mea6)/cutaneous T cell lymphoma-associated antigen 5C (cTAGE5C) leads to severe fatty liver and hypolipemia in mice. Quantitative lipidomic and proteomic analyses indicate that Mea6/cTAGE5 deletion impairs the secretion of different types of lipids and proteins, including VLDL, from the liver. Moreover, we demonstrate that Mea6/cTAGE5 interacts with components of the ER coat protein complex II (COPII) which, when depleted, also cause lipid accumulation in hepatocytes. Our findings not only reveal several novel factors that regulate lipid transport, but also provide evidence that Mea6 plays a critical role in lipid transportation through the coordinated regulation of the COPII machinery.

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Section: Introductionmentioning

confidence: 99%

Mea6 controls VLDL transport through the coordinated regulation of COPII assembly

et al. 2016

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“…Some studies report higher prevalence in men. (6,7) Genetic factors, such as patatin-like phospholipase domain containing 3 (PNPLA3) gene polymorphism, are associated with increased hepatic fat concentration. (10) Posttransplant NAFLD affects 18%-40% of liver transplantation (LT) recipients (11)(12)(13) and even 39%-70% (14,15) of those transplanted for NAFLD-related cirrhosis.…”

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confidence: 99%

Prevalence and risk factors of steatosis after liver transplantation and patient outcomes

et al. 2016

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Steatosis occurs frequently after liver transplantation (LT). We aimed to determine the prevalence of steatosis in adult LT recipients, to determine the effects of significant (>33%; grades 2-3) steatosis on patient survival, and to identify risk factors for the development of significant steatosis and its effect on fibrosis progression. We retrospectively examined 2360 posttransplant biopsies of 548 LT recipients. Survival was compared between patients with significant steatosis and those with grades 0-1 steatosis. Patients with significant steatosis were compared to controls without steatosis (grade 0) for clinical and laboratory factors and fibrosis progression. Steatosis was found in 309 (56.4%) patients, including 93 (17.0%) patients with significant steatosis. Steatohepatitis (nonalcoholic fatty liver disease activity score 5) was diagnosed in 57 (10.4%) patients. The prevalence of steatosis increased from 30.3% at 1 year to 47.6% at 10 years after LT (P < 0.001). Survival times did not differ between groups (P 5 0.29). On multivariate analysis of pretransplant factors and initial immunosuppression (IS), alcohol-induced cirrhosis (P < 0.001) and high body mass index (BMI; P 5 0.002) were associated with the development of significant steatosis, whereas increased levels of alkaline phosphatase (P 5 0.01) and mycophenolate mofetil given initially (P 5 0.009) appeared to protect against significant steatosis. On multivariate analysis of posttransplant factors, high BMI (P < 0.001), serum triglycerides (P < 0.001), alcohol consumption (P 5 0.005), and type 2 diabetes mellitus (P 5 0.048) were associated with significant steatosis, whereas high creatinine (P 5 0.02) appeared to protect against significant steatosis. Significant steatosis was not associated with a higher fibrosis stage (P 5 0.62). Posttransplant steatosis affects 56.4% of LT recipients, and the prevalence increases with time after LT. Recipient factors and types of IS affect the risk for significant steatosis, which is not associated with a higher fibrosis stage or worse patient survival.Liver Transplantation 22 644-655 2016 AASLD.

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“…The increasing worldwide prevalence of obesity is considered one of the most serious public health problems of the 21st century (1,2). Obesity is a predisposing factor for various metabolic disorders, including type 2 diabetes, cardiovascular disease, and non-alcoholic fatty liver disease (NAFLD) 3 (3,4).…”

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confidence: 99%

XBP1s Is an Anti-lipogenic Protein

Herrema

Zhou

Zhang

et al. 2016

Journal of Biological Chemistry

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Endoplasmic reticulum (ER) stress has been shown to contribute to various metabolic diseases, including non-alcoholic fatty liver disease and type 2 diabetes. Reduction of ER stress by treatment with chemical chaperones or overexpression of ER chaperone proteins alleviates hepatic steatosis. Nonetheless, X-box binding protein 1s (XBP1s), a key transcription factor that reduces ER stress, has been proposed as a lipogenic transcription factor. In this report, we document that XBP1s leads to suppression of lipogenic gene expression and reduction of hepatic triglyceride and diacylglycerol content in livers of dietinduced obese and genetically obese and insulin-resistant ob/ob mice. Furthermore, we also show that PKC⑀ activity, which correlates with fatty liver and which causes insulin resistance, was significantly reduced in diet-induced obese mice. Finally, we have shown that XBP1s reduces the hepatic fatty acid synthesis rate and enhances macrolipophagy, an initiating step in lipolysis. Our results reveal that XBP1s reduces hepatic lipogenic gene expression and improves hepatosteatosis in mouse models of obesity and insulin resistance, which leads us to conclude that XBP1s has anti-lipogenic properties in the liver.

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Prevalence of Nonalcoholic Fatty Liver Disease in the United States: The Third National Health and Nutrition Examination Survey, 1988–1994

Cited by 733 publications

References 37 publications

Mea6 controls VLDL transport through the coordinated regulation of COPII assembly

Mea6 controls VLDL transport through the coordinated regulation of COPII assembly

Prevalence and risk factors of steatosis after liver transplantation and patient outcomes

XBP1s Is an Anti-lipogenic Protein

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