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Related Concept Videos

Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
Viral Hepatitis I: Introduction01:28

Viral Hepatitis I: Introduction

Viral hepatitis is an inflammatory condition of the liver caused by infection with hepatotropic viruses, most commonly hepatitis A, B, C, D, and E. Despite variations in structure and transmission, all viruses mentioned infect hepatocytes and provoke immune responses that can hinder liver function. Additionally, some non-hepatotropic viruses can also lead to hepatic inflammation.Hepatitis A VirusHepatitis A virus (HAV) is transmitted through the fecal–oral route, typically by ingestion of food...

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An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes
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An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes

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Insulin resistance and hepatitis C.

Manuel Romero-Gómez1

  • 1Unit for The Clinical Management of Digestive Diseases. Hospital Universitario de Valme. Ctra de Cadiz s/n. Sevilla 41014, Spain. mromerog@supercable.es

World Journal of Gastroenterology
|November 30, 2006
PubMed
Summary

Hepatitis C virus infection promotes insulin resistance, leading to liver steatosis and fibrosis. This insulin resistance also contributes to interferon resistance, hindering treatment effectiveness in chronic hepatitis C patients.

Area of Science:

  • Hepatology
  • Virology
  • Endocrinology

Background:

  • Insulin resistance is a key feature of metabolic syndrome, impacting insulin secretion and sensitivity.
  • Chronic hepatitis C (HCV) patients exhibit higher rates of insulin resistance and type 2 diabetes mellitus compared to controls.
  • HCV infection exacerbates insulin resistance through increased TNF and SOC-3, inhibiting PI3K/Akt pathways.

Purpose of the Study:

  • To investigate the mechanisms by which HCV infection induces insulin resistance.
  • To explore the consequences of insulin resistance in chronic hepatitis C, including its impact on liver disease progression and treatment response.
  • To elucidate the interplay between insulin, HCV, and interferon efficacy.

Main Methods:

  • Analysis of insulin resistance markers in chronic hepatitis C patients.

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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
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  • Investigation of molecular pathways (TNF, SOC-3, PI3K, Akt) involved in HCV-induced insulin resistance.
  • In vitro experiments using Huh-7 cells to assess the effect of insulin on interferon-alpha's ability to block HCV replication and PKR synthesis.

    • Main Results:

    • HCV infection promotes insulin resistance via TNF and SOC-3, blocking PI3K and Akt phosphorylation.
    • Insulin resistance in HCV contributes to steatosis, fibrosis progression, hyperleptinemia, and impaired PPARgamma expression.
    • Insulin resistance is associated with poorer treatment outcomes (lower sustained response rates) to peginterferon plus ribavirin, particularly in genotype 1 patients.
    • High insulin levels (hyperinsulinemia) interfere with interferon-alpha's antiviral activity by abolishing PKR synthesis.

    Conclusions:

    • Hepatitis C virus infection directly promotes insulin resistance.
    • Insulin resistance exacerbates liver disease (steatosis, fibrosis) and impairs treatment response in chronic hepatitis C.
    • The interaction between insulin and interferon highlights a mechanism for treatment resistance in HCV patients with hyperinsulinemia.