Anna Mae Diehl

ORCID: 0000-0003-1859-089X
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Liver Disease Diagnosis and Treatment
  • Liver physiology and pathology
  • Hedgehog Signaling Pathway Studies
  • Diet, Metabolism, and Disease
  • Liver Disease and Transplantation
  • Alcohol Consumption and Health Effects
  • Epigenetics and DNA Methylation
  • Hepatitis B Virus Studies
  • Endoplasmic Reticulum Stress and Disease
  • Liver Diseases and Immunity
  • Genetic and Kidney Cyst Diseases
  • Cancer-related Molecular Pathways
  • Pediatric Hepatobiliary Diseases and Treatments
  • Organ Transplantation Techniques and Outcomes
  • Diet and metabolism studies
  • Pancreatic function and diabetes
  • Pancreatitis Pathology and Treatment
  • Adipose Tissue and Metabolism
  • Drug-Induced Hepatotoxicity and Protection
  • Lipid metabolism and disorders
  • Phagocytosis and Immune Regulation
  • Adipokines, Inflammation, and Metabolic Diseases
  • Regulation of Appetite and Obesity
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Gut microbiota and health

Duke University
2016-2025

Duke Medical Center
2015-2024

University of Miami
2024

Duke University Health System
2018-2023

American Nephrology Nurses Association
2023

Duke University Hospital
2008-2021

Clinical Research Institute
2017-2019

Genetic Analysis (Norway)
2016

Block Center
2015

Durham Technical Community College
2015

These recommendations are based on the following: (1) a formal review and analysis of recently published world literature topic [Medline search up to June 2011]; (2) American College Physicians' Manual for Assessing Health Practices Designing Practice Guidelines;1 (3) guideline policies three societies approving this document; (4) experience authors independent reviewers with regards NAFLD. Intended use by physicians allied health professionals, these suggest preferred approaches diagnostic,...

10.1002/hep.25762 article EN Hepatology 2012-04-06

Chronic liver disease is a major cause of morbidity and mortality in the United States. Although often used to detect disease, prevalence etiology elevated aminotransferases are unknown. We analyzed data on adults ages 17 yr older (N = 15,676) from Third National Health Nutrition Examination Survey (1988-1994). Participants were classified as having aminotransferase levels if either aspartate or alanine was above normal. Aminotransferase elevation "explained" there laboratory evidence...

10.1111/j.1572-0241.2003.07486.x article EN The American Journal of Gastroenterology 2003-05-01

Several animal studies have emphasized the role of gut microbiota in nonalcoholic fatty liver disease (NAFLD). However, data about dysbiosis human NAFLD remain scarce literature, especially including whole spectrum lesions. We aimed to evaluate association between and severe lesions, that is, steatohepatitis (NASH) fibrosis, a well-characterized population adult NAFLD. Fifty-seven patients with biopsy-proven were enrolled. Taxonomic composition was determined using 16S ribosomal RNA gene...

10.1002/hep.28356 article EN Hepatology 2015-11-24

Obesity is associated with an increased incidence of infection, diabetes, and cardiovascular disease, which together account for most obesity-related morbidity mortality. Decreased expression leptin or functional receptors results in hyperphagia, decreased energy expenditure, obesity. It unclear, however, whether defective leptin-dependent signal transduction directly promotes any the conditions that frequently complicate Abnormalities tumor necrosis factor alpha have been noted each above...

10.1096/fasebj.12.1.57 article EN The FASEB Journal 1998-01-01

In the early stages of nonalcoholic fatty liver disease (NAFLD), triglycerides accumulate in hepatocytes. Diacylglycerol acyltransferase 2 (DGAT2) catalyzes final step hepatocyte triglyceride biosynthesis. DGAT2 antisense oligonucleotide (ASO) treatment improved hepatic steatosis dramatically a previous study obese mice. According to 2-hit hypothesis for progression NAFLD, is risk factor steatohepatitis (NASH) and fibrosis. To evaluate this hypothesis, we inhibited mouse model NASH induced...

10.1002/hep.21655 article EN Hepatology 2007-05-03

Ob/ob mice, a model for nonalcoholic fatty liver disease (NAFLD), develop intestinal bacterial overgrowth and overexpress tumor necrosis factor α (TNF-α). In animal models alcoholic (AFLD), decontaminating the intestine or inhibiting TNF-α improves AFLD. Because AFLD NAFLD may have similar pathogenesis, treatment with probiotic (to modify flora) anti-TNF antibodies inhibit activity) improve in ob/ob mice. To evaluate this hypothesis, 48 mice were given either high-fat diet alone (ob/ob...

10.1053/jhep.2003.50048 article EN Hepatology 2003-02-01

Genetically obese fatty/fatty rats and obese/obese mice exhibit increased sensitivity to endotoxin hepatotoxicity, quickly developing steatohepatitis after exposure low doses of lipopolysaccharide (LPS). Among animals, females are more sensitive liver injury than males. LPS induction tumor necrosis factor alpha (TNF alpha), the proven affecter injury, is no greater in livers, white adipose tissues, or sera animals those lean controls. Indeed, lowest serum concentrations TNF occur female...

10.1073/pnas.94.6.2557 article EN Proceedings of the National Academy of Sciences 1997-03-18

The rising incidence of obesity and diabetes coincides with a marked increase in fructose consumption. Fructose consumption is higher individuals nonalcoholic fatty liver disease (NAFLD) than age-matched body mass index (BMI)-matched controls. Because elicits metabolic perturbations that may be hepatotoxic, we investigated the relationship between severity NAFLD. We studied 427 adults enrolled NASH Clinical Research Network for whom Block food questionnaire data were collected within 3...

10.1002/hep.23535 article EN Hepatology 2010-01-28

Preamble These recommendations are based on the following: (i) a formal review and analysis of recently published world literature topic (Medline search up to June 2011); (ii) American College Physicians' Manual for Assessing Health Practices Designing Practice Guidelines; (1) (iii) guideline policies three societies approving this document; (iv) experience authors independent reviewers with regards non-alcoholic fatty liver disease (NAFLD). Intended use by physicians allied health...

10.1038/ajg.2012.128 article EN The American Journal of Gastroenterology 2012-05-29

Inhibition of apoptosis signal-regulating kinase 1, a serine/threonine kinase, leads to improvement in inflammation and fibrosis animal models nonalcoholic steatohepatitis. We evaluated the safety efficacy selonsertib, selective inhibitor alone or combination with simtuzumab, patients steatohepatitis stage 2 3 liver fibrosis. In this multicenter phase trial, 72 were randomized receive 24 weeks open-label treatment either 6 18 mg selonsertib orally once daily without once-weekly injections...

10.1002/hep.29514 article EN cc-by-nc-nd Hepatology 2017-09-11

To determine the efficacy of a corticosteroid in reducing short-term mortality patients with severe alcoholic hepatitis.Randomized, double-blind, placebo-controlled multicenter trial.Four university teaching hospitals.We enrolled 66 hepatitis and either spontaneous hepatic encephalopathy or discriminant function value greater than 32, calculated using formula: 4.6 (prothrombin time - control time) + serum bilirubin [in mumol/L]/17.1. Fifty-nine (89%) completed study. Two withdrew from trial....

10.7326/0003-4819-110-9-685 article EN Annals of Internal Medicine 1989-05-01

Obesity is associated with an increased incidence of infection, diabetes, and cardiovascular disease, which together account for most obesity-related morbidity mortality. Decreased expression leptin or functional receptors results in hyperphagia, decreased energy expenditure, obesity. It unclear, however, whether defective leptin-dependent signal transduction directly promotes any the conditions that frequently complicate Abnormalities tumor necrosis factor α have been noted each above...

10.1096/fsb2fasebj.12.1.57 article EN The FASEB Journal 1998-01-01

ContextThe mechanisms that drive progression from fatty liver to steatohepatitis and cirrhosis are unknown. In animal models, obese mice with livers vulnerable adenosine triphosphate (ATP) depletion necrosis, suggesting altered hepatic energy homeostasis may be involved.ObjectiveTo determine if patients disease exhibit impaired recovery ATP depletion.DesignLaboratory analysis of stores monitored by nuclear magnetic resonance spectroscopy before after transient was induced fructose injection....

10.1001/jama.282.17.1659 article EN JAMA 1999-11-03
Coming Soon ...