Nonalcoholic fatty liver disease a feature of the metabolic syndrome
Giulio Marchesini,Mara Brizi,Giampaolo Bianchi,Sara Tomassetti,Elisabetta Bugianesi,Marco Lenzi,Arthur J. McCullough,S. Natale,Gabriele Forlani,Nazario Melchionda +9 more
TLDR
It is concluded that NAFLD, in the presence of normoglycemia and normal or moderately increased body weight, is characterized by clinical and laboratory data similar to those found in diabetes and obesity.Abstract:
Insulin sensitivity (euglycemic clamp, insulin infusion rate: 40 mU m(-2) min(-1)) was studied in 30 subjects with biopsy-proven nonalcoholic fatty liver disease (NAFLD), normal glucose tolerance, and a BMI <30 kg/m(2) Of those 30 subjects, 9 had pure fatty liver and 21 had evidence of steatohepatitis In addition, 10 patients with type 2 diabetes under good metabolic control and 10 healthy subjects were studied Most NAFLD patients had central fat accumulation, increased triglycerides and uric acid, and low HDL cholesterol, irrespective of BMI Glucose disposal during the clamp was reduced by nearly 50% in NAFLD patients, as well as in patients with normal body weight, to an extent similar to that of the type 2 diabetic patients Basal free fatty acids were increased, whereas insulin-mediated suppression of lipolysis was less effective (-69% in NAFLD vs -84% in control subjects; P = 0003) Postabsorptive hepatic glucose production (HGP), measured by [6,6-(2)H(2)]glucose, was normal In response to insulin infusion, HGP decreased by only 63% of basal in NAFLD vs 84% in control subjects (P = 0002) Compared with type 2 diabetic patients, NAFLD patients were characterized by lower basal HGP, but with similarly reduced insulin-mediated suppression of HGP There was laboratory evidence of iron overload in many NAFLD patients, but clinical, histological, and biochemical data (including insulin sensitivity) were not correlated with iron status Four subjects were heterozygous for mutation His63Asp of the HFE gene of familiar hemochromatosis We concluded that NAFLD, in the presence of normoglycemia and normal or moderately increased body weight, is characterized by clinical and laboratory data similar to those found in diabetes and obesity NAFLD may be considered an additional feature of the metabolic syndrome, with specific hepatic insulin resistanceread more
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Should nonalcoholic fatty liver disease be renamed
TL;DR: The introduction of a positive criterion also mentioned in its definition would benefit the diagnosis of NAFLD and of steatohepatitis observed in the setting of other liver diseases, help to estimate the risk of its progression and aid the treatment of metabolic (fatty) liver disorders.
Journal ArticleDOI
Reduced expression of peroxisome proliferator‐activated receptor‐α may have an important role in the development of non‐alcoholic fatty liver disease
Jong Eun Yeon,Kyung Mook Choi,Sei Hyun Baik,Kyoung Oh Kim,Hyoung Joon Lim,Kiho Park,Jin Yong Kim,Jong-Jae Park,Jae Seon Kim,Young-Tae Bak,Kwan Soo Byun,Chang Hong Lee +11 more
TL;DR: The role of PPAR‐α and AOX in the development of NAFLD is defined using the Otsuka Long‐Evans Tokushima fatty (OLETF) rat model.
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Renin-Angiotensin System Inhibitors, Type 2 Diabetes and Fibrosis Progression: An Observational Study in Patients with Nonalcoholic Fatty Liver Disease.
Serena Pelusi,Salvatore Petta,Chiara Rosso,V. Borroni,Anna Ludovica Fracanzani,Paola Dongiovanni,Antonio Craxì,Elisabetta Bugianesi,Silvia Fargion,Luca Valenti +9 more
TL;DR: NASH is not required for fibrosis progression in NAFLD, whereas T2D seems to drive fibrogenesis independently of hepatic inflammation, especially in high-risk patients affected by T1D.
Journal ArticleDOI
Synthesis and biological activity of novel barbituric and thiobarbituric acid derivatives against non-alcoholic fatty liver disease
Liang Ma,Shilin Li,Hao Zheng,Jinying Chen,Lin Lin,Xia Ye,Zhizhi Chen,Qinyuan Xu,Tao Chen,Jincheng Yang,Neng Qiu,Guangcheng Wang,Aihua Peng,Yi Ding,Yuquan Wei,Lijuan Chen +15 more
TL;DR: Histopathological evaluation of liver sections by Oil Red O and H&E staining confirmed 3s as a potent, orally active molecule for reducing fat deposition against non-alcoholic fatty liver disease.
Journal Article
An overview of nonalcoholic steatohepatitis: past, present and future directions.
TL;DR: Nonalcoholic steatohepatitis emerged from an anecdotal disease first described in 1981 to the most common cause of incident chronic liver disease at the end of the current decade and some of the landmark changes in perception and understanding of this disease are described.
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