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 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 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...

Pathophysiology of Diabetes

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational 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...

Diabetes Mellitus: Introduction

Diabetes Mellitus: Introduction

Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term...

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...

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...

You might also read

Related Articles

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

Sort by

Same author

Endogenous Opioids and Exercise-Related Hypoalgesia: Modern Models, Measurement, and Mechanisms of Action.

Advances in neurobiology·2024

Same author

The effects of peripheral hormone responses to exercise on adult hippocampal neurogenesis.

Frontiers in endocrinology·2023

Same author

The effects of separate and simultaneous upper and lower body cycling on cardiorespiratory responses in young men.

The Journal of sports medicine and physical fitness·2023

Same author

Hemodynamics and Arterial Stiffness in Response to Oral Glucose Loading in Individuals with Type II Diabetes and Controlled Hypertension.

High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension·2023

Same author

Maximal Respiratory Pressure Reference Values for Hopi Children Ages 4-13.

Cardiopulmonary physical therapy journal·2022

Same author

Impaired postprandial adipose tissue microvascular blood flow responses to a mixed-nutrient meal in first-degree relatives of adults with type 2 diabetes.

American journal of physiology. Endocrinology and metabolism·2022

Search research articles

Related Experiment Video

Updated: May 20, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Metabolic dysfunction in diabetic offspring: deviations in metabolic flexibility.

Ryan D Russell¹, Robert R Kraemer, Arnold G Nelson

¹Department of Kinesiology, Louisiana State University, Baton Rouge, LA, USA. rrussell@medicine.umaryland.edu

Medicine and Science in Sports and Exercise

|July 20, 2012

Summary

Family history of type 2 diabetes (T2D) is linked to metabolic inflexibility, even without impaired blood glucose control. Passive stretching (PS) reveals early mitochondrial dysfunction in those with a family history of T2D.

More Related Videos

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection

Published on: May 17, 2024

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

Published on: February 28, 2013

Related Experiment Videos

Last Updated: May 20, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection

Monitoring Blood Glucose in Mouse Offspring After Intracytoplasmic Sperm Injection

Published on: May 17, 2024

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

Published on: February 28, 2013

Area of Science:

Metabolic physiology
Endocrinology
Mitochondrial function

Background:

Type 2 diabetes (T2D) is characterized by insulin resistance, lipotoxicity, poor glucoregulation, and reduced metabolic flexibility.
A key debate in T2D research is whether metabolic inflexibility precedes or follows insulin resistance.

Purpose of the Study:

To investigate if a family history of T2D (FH+) predisposes individuals to metabolic inflexibility.
To identify early markers of metabolic dysfunction in individuals with a family history of T2D.

Main Methods:

Compared metabolic characteristics of individuals with T2D, FH+, and controls (FH-) using a metabolic cart.
Assessed metabolic responses at rest, during passive stretching (PS) with recovery, and after an oral glucose load.
Measured expired gas and blood glucose (BG) levels under fasting conditions.

Main Results:

Passive stretching (PS) reduced blood glucose (BG) in FH- and FH+ groups more than in the T2D group.
Carbohydrate (CHO) use increased with PS across all groups, notably in the T2D group.
Metabolic flexibility during an oral glucose load showed no difference between FH- and T2D groups, but differed between FH- and FH+ groups.

Conclusions:

Passive stretching (PS) enhances glycolytic activity in T2D without altering BG, suggesting its utility in assessing metabolic flexibility.
Reductions in metabolic flexibility are present in both T2D and FH+ individuals.
The FH+ group exhibits early-stage mitochondrial dysfunction without glucoregulatory impairment, indicating metabolic inflexibility precedes overt T2D symptoms.