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A comparison of associations of alanine aminotransferase and gamma-glutamyltransferase with fasting glucose, fasting insulin, and glycated hemoglobin in women with and without diabetes

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TLDR
E elevation of liver enzymes and hepatic insulin resistance as reflected by fasting insulin occur in the early stages of insulin resistance and highlight the central role of the liver in insulin resistance in the general population.
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This article is published in Hepatology.The article was published on 2007-07-01 and is currently open access. It has received 63 citations till now. The article focuses on the topics: Insulin resistance & Insulin.

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ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries

TL;DR: The evaluation of hepatocellular injury includes testing for viral hepatitis A, B, and C, assessment for nonalcoholic fatty liver disease and alcoholic liver disease, screening for hereditary hemochromatosis, autoimmune hepatitis, Wilson’s disease, and alpha-1 antitrypsin deficiency.
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Elevated Serum Alanine Aminotransferase and γ-Glutamyltransferase and Mortality in the United States Population

TL;DR: In the US population, elevated GGT was associated with mortality from all causes, liver disease, cancer, and diabetes, while ALT was associated only with liver disease mortality.
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Prevalence of elevated alanine aminotransferase among US adolescents and associated factors: NHANES 1999-2004.

TL;DR: AlT level is associated with waist circumference and insulin resistance even in a young population and could be utilized to identify adolescents who may benefit from screening for NAFLD, offering an opportunity to prevent disease progression at an early age.
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Low Hemoglobin A1c and Risk of All-Cause Mortality Among US Adults Without Diabetes

TL;DR: Low HbA1c was associated with increased all-cause mortality among US adults without diabetes and remained statistically significant after further multivariable adjustment for lifestyle, cardiovascular factors, metabolic factors, red blood cell indices, iron storage indices, and liver function indices.
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The metabolic syndrome and nonalcoholic fatty liver disease in children.

TL;DR: The close association between NAFLD and the MetS supports screening for other comorbidities associated with themetS, and its close association with MetS argues for a focus on strategies designed to improve insulin resistance and components of the metS.
References
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Journal ArticleDOI

Homeostasis model assessment : insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man

TL;DR: The correlation of the model's estimates with patient data accords with the hypothesis that basal glucose and insulin interactions are largely determined by a simple feed back loop.
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Nonalcoholic fatty liver disease a feature of the metabolic syndrome

TL;DR: 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.
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The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes.

TL;DR: Greater understanding of the relative roles of insulin resistance and beta-cell dysfunction in Type 2 diabetes can anticipate advances in the identification of genes contributing to the development of the disease as well as approaches to the treatment and prevention of Type 1 diabetes.
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Updated Definitions of Healthy Ranges for Serum Alanine Aminotransferase Levels

TL;DR: This study redefined ALT limits in blood donors at low risk for NAFLD and without hepatitis B or C and tested the sensitivity and specificity of the ranges obtained from these participants in the clinical evaluation of anti-HCVpositive persons with and without chronic liver damage.
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Mechanism of Hepatic Insulin Resistance in Non-alcoholic Fatty Liver Disease

TL;DR: The hypothesis hepatic steatosis leads to hepatic insulin resistance by stimulating gluconeogenesis and activating PKC-ϵ and JNK1, which may interfere with tyrosine phosphorylation of IRS-1 and IRS-2 and impair the ability of insulin to activate glycogen synthase is supported.
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