Related Experiment Video
Updated: Jul 27, 2026

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
Published on: February 28, 2013
[Genetic susceptibility to diabetes and hypertension]
Hiroshi Ikegami1, Toshio Ogihara
1Department of Geriatric Medicine, Osaka University Graduate School of Medicine.
Abstract:
Both type 2 diabetes and hypertension are multifactorial diseases. Several lines of evidence suggested that common genetic factors contribute to both conditions. Genes responsible for obesity and insulin resistance are candidates for common genetic factors. Among candidate genes are genes encoding glycogen synthase, beta 3-adrenergic receptor, glycogen-associated regulatory subunit of protein phosphatase-1, peroxisome proliferator--activated receptor-gamma (PPAR gamma), leptin and adiponectin. In addition, recent genome scans mapped loci linked to type 2 diabetes, hypertension and/or metabolic syndrome. Identification of genes responsible for both type 2 diabetes and hypertension will increase our understanding of molecular mechanisms of these conditions and facilitate the development of effective methods for prevention and intervention of diabetes and hypertension as well as metabolic syndrome.
More Related Videos
09:52Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)
Published on: April 19, 2013
10:31Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Related Concept Videos
Diabetes Mellitus: Type 2 and Gestational
Pathophysiology of Diabetes
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...
Hypertension II: Pathophysiology
Type I Diabetes I: Introduction
Type II Diabetes I: Introduction
Type II Diabetes II: Pathophysiology