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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Disordered Lipid Metabolism and the Pathogenesis of Insulin Resistance
TL;DR: Recent human studies exploring the mechanistic links between disorders of fatty acid/lipid metabolism and insulin resistance are reviewed, mainly involving the use of isotopes and/or magnetic resonance spectroscopy.
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A position statement on NAFLD/NASH based on the EASL 2009 special conference ☆
TL;DR: This poster presents a meta-modelling procedure called “spot-spot analysis” that allows for the direct comparison of the response of the immune system to various types of carbohydrates and its role in disease.
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Beyond Insulin Resistance in NASH: TNF-alpha or Adiponectin?
Jason M. Hui,Alex Hodge,Geoffrey C. Farrell,James G. Kench,Adamandia D. Kriketos,Jacob George +5 more
TL;DR: Reduced adiponectin level is associated with more extensive necroinflammation and may contribute to the development of necroinflammatory forms of NAFLD.
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Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity
Elisa Fabbrini,Faidon Magkos,B. Selma Mohammed,Terri A. Pietka,Nada A. Abumrad,Bruce W. Patterson,Adewole L. Okunade,Samuel Klein +7 more
TL;DR: Data demonstrate that IHTG, not VAT, is a better marker of the metabolic derangements associated with obesity, and alterations in tissue fatty acid transport could be involved in the pathogenesis of ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue toward other tissues.
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Insulin resistance: A metabolic pathway to chronic liver disease†
TL;DR: The ability of insulin‐sensitizing, pharmacological agents to treat NAFLD by reducing IR in the liver (metformin) and in the periphery (thiazolidinediones) are discussed.
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