Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Type II Diabetes I: Introduction

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 II Diabetes II: Pathophysiology

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 I Diabetes II: Pathophysiology

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 Pathways

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...

Type I Diabetes I: Introduction

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Non-insulin treatments for Type 1 diabetes: critical appraisal of the available evidence and insight into future directions.

Diabetic medicine : a journal of the British Diabetic Association·2019

Same author

Exploring residual risk for diabetes and microvascular disease in the Diabetes Prevention Program Outcomes Study (DPPOS).

Diabetic medicine : a journal of the British Diabetic Association·2017

Same author

Efficient continuous synthesis of high purity deep eutectic solvents by twin screw extrusion.

Chemical communications (Cambridge, England)·2016

Same author

Steroid Sex Hormones, Sex Hormone-Binding Globulin, and Diabetes Incidence in the Diabetes Prevention Program.

The Journal of clinical endocrinology and metabolism·2015

Same author

The duodenal glucose load impacts the oral disposition index in healthy subjects.

Diabetic medicine : a journal of the British Diabetic Association·2015

Same author

Visceral abdominal fat accumulation predicts the conversion of metabolically healthy obese subjects to an unhealthy phenotype.

International journal of obesity (2005)·2015

Same journal

Relationship Between hsCRP, Glycaemic Control and Response to Sotagliflozin in Type 1 Diabetes: A Post Hoc Analysis of the inTandem3 Trial.

Diabetes, obesity & metabolism·2026

Same journal

Early Weight Regain After GLP-1 Receptor Agonist Discontinuation: Mechanisms and Implications for Treatment De-Escalation Strategies.

Diabetes, obesity & metabolism·2026

Same journal

First-Line Dapagliflozin, Metformin, or Combination Therapy in Type 2 Diabetes: Vascular and Molecular Outcomes of a Randomised Controlled Trial.

Diabetes, obesity & metabolism·2026

Same journal

Trends in Prevalence of Diabetes, Pre-Diabetes, and Cardiometabolic Risk Factor Control Among U.S. Adults, 2013-2023.

Diabetes, obesity & metabolism·2026

Same journal

Metabolic Risk-Attributable Dementia Burden: A Life-Course and Cautious Attribution Perspective.

Diabetes, obesity & metabolism·2026

Same journal

A Highly Powered Large Outcomes Randomised Controlled Trial Will Usually, but Not Always, Have Balanced Groups at Baseline.

Diabetes, obesity & metabolism·2026

See all related articles

Search research articles

Related Experiment Video

Updated: May 19, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Interactions between genetic background, insulin resistance and β-cell function.

S E Kahn¹, S Suvag, L A Wright

¹Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108, USA. skahn@u.washington.edu

Diabetes, Obesity & Metabolism

|August 30, 2012

Summary

This summary is machine-generated.

Genetic and environmental factors interact to cause type 2 diabetes. Advanced genetic analysis identified 40 genes linked to type 2 diabetes, primarily affecting beta-cell function and insulin sensitivity.

More Related Videos

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Published on: January 7, 2018

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

Related Experiment Videos

Last Updated: May 19, 2026

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance

Published on: February 17, 2023

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Published on: January 7, 2018

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

Area of Science:

Genetics
Endocrinology
Metabolic Diseases

Background:

Type 2 diabetes pathogenesis involves gene-environment interactions.
Recent advances in genetic techniques have identified numerous genes associated with type 2 diabetes.
Most identified genes impact beta-cell function, with some linked to insulin resistance and obesity.

Purpose of the Study:

To explore the genetic underpinnings of type 2 diabetes.
To understand the role of specific gene variants in glucose regulation and disease development.
To uncover novel molecular players in beta-cell physiology and pathophysiology.

Main Methods:

Utilizing sophisticated techniques for gene variant analysis.
Analyzing genetic data to identify associations with type 2 diabetes.
Employing quantitative traits (continuous measures) instead of dichotomous diagnostic criteria.

Main Results:

Approximately 40 genes have been associated with type 2 diabetes.
Gene variants influencing fasting or post-prandial glucose are not always linked to a type 2 diabetes diagnosis.
Novel insights into beta-cell physiology and pathophysiology have been gained.

Conclusions:

Gene-environment interactions are central to type 2 diabetes development.
Genetic discoveries offer new perspectives on beta-cell function and dysfunction.
Further research into identified gene variants can reveal previously unknown molecular mechanisms in diabetes.