Chronic Hepatitis C virus has the potential of inducing insulin resistance and type 2 Diabetes Mellitus in vitro as well as in vivo . Structural and non-structural proteins of HCV modulate cellular gene expression in such a way that insulin signaling is hampered, concomitantly leads toward diabetes mellitus. A number of mechanisms have been proposed in regard to the HCV induced insulin resistance involving the upregulation of Inflammatory cytokine TNF-α, hypophosphorylation of IRS-1 and IRS-2, phosphorylation of Akt, up-regulation of gluconeogenic genes, accumulation of lipids and targeting lipid storage organelles. This review provides an insight of molecular mechanisms by which HCV structural and non-structural proteins can induce insulin resistance.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3206488PMC
http://dx.doi.org/10.1186/1743-422X-8-474DOI Listing

Publication Analysis

Top Keywords

insulin resistance
16
hepatitis virus
8
diabetes mellitus
8
structural non-structural
8
non-structural proteins
8
insulin
5
virus infection
4
infection molecular
4
molecular pathways
4
pathways insulin
4

Similar Publications

Modulation of placental angiogenesis by metformin in a rat model of gestational diabetes.

Histochem Cell Biol

January 2025

Medical Histology and Cell Biology Department, Faculty of Medicine, Mansoura University, Mansoura, 35516, Egypt.

Gestational diabetes mellitus (GDM) significantly disrupts placental structure and function, leading to complications such as intrauterine growth restriction (IUGR) and preeclampsia. This study aimed to investigate the effects of GDM on placental histology, angiogenesis, and oxidative stress, as well as evaluate metformin's protective role in mitigating these changes. A total of 60 pregnant Sprague-Dawley rats were divided into four groups: control, metformin-treated, GDM, and GDM with metformin.

View Article and Find Full Text PDF

Noninvasive evaluations of hormones can contribute to the assessment of health and welfare of animals. Variations in insulin levels and sensitivity, for example, have been linked to health concerns in non-human and human primates including insulin resistance, diabetes, and heart disease, the leading cause of death in zoo-housed gorillas. Few published studies have assessed insulin concentrations in western lowland gorillas (Gorilla gorilla gorilla), and all did so using serum.

View Article and Find Full Text PDF

Obesity is a rapidly growing health problem worldwide, affecting both adults and children and increasing the risk of chronic diseases such as type 2 diabetes, hypertension and cardiovascular disease (CVD). In addition, obesity is closely linked to chronic kidney disease (CKD) by either exacerbating diabetic complications or directly causing kidney damage. Obesity-related CKD is characterized by proteinuria, lipid accumulation, fibrosis and glomerulosclerosis, which can gradually impair kidney function.

View Article and Find Full Text PDF

Background: The triglyceride-glucose (TyG) index has emerged as a validated and cost-effective indicator of insulin resistance (IR). Given the significant association between visceral obesity and IR, this study aimed to investigate the utility of the TyG index in estimating visceral obesity in patients with gastric cancer (GC).

Methods: The visceral fat area (VFA), subcutaneous fat area (SFA), and VFA-to-SFA ratio (VSR) were determined through the analysis of CT images at the lumbar 3 level.

View Article and Find Full Text PDF

Sulforaphane acutely activates multiple starvation response pathways.

Front Nutr

January 2025

Aging and Metabolism Research Program, Oklahoma City, OK, United States.

Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables that has demonstrated anti-cancer, anti-microbial and anti-oxidant properties. SFN ameliorates various disease models in rodents (e.g.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!