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Related Concept Videos

Pathophysiology of Diabetes01:20

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...
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 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...
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...
Diabetes Mellitus: Introduction01:26

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...
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis01:25

Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis

Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...

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Related Experiment Video

Updated: Jun 22, 2026

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy

Published on: December 7, 2017

Pathophysiology of prediabetes.

Muhammad A Abdul-Ghani1, Ralph A DeFronzo

  • 1Diabetes Division, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. abdulghani@uthscsa.edu

Current Diabetes Reports
|June 4, 2009
PubMed
Summary

Prediabetes, characterized by impaired glucose levels, increases the risk of type 2 diabetes and cardiovascular disease. Understanding the distinct metabolic issues in impaired fasting glucose and impaired glucose tolerance is crucial for risk assessment.

Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Cardiovascular Health

Background:

  • Prediabetes encompasses impaired fasting glucose (IFG) and impaired glucose tolerance (IGT).
  • Both IFG and IGT elevate the risk of type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD).
  • Distinct metabolic derangements characterize IFG and IGT, contributing to differential risks.

Purpose of the Study:

  • To delineate the specific metabolic abnormalities associated with impaired fasting glucose.
  • To outline the metabolic abnormalities characteristic of impaired glucose tolerance.
  • To explain how these distinct metabolic abnormalities contribute to the heightened risk of T2DM and CVD.

Main Methods:

  • Review of existing literature on prediabetes phenotypes.

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

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Last Updated: Jun 22, 2026

Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
08:47

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Published on: December 7, 2017

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

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

  • Analysis of metabolic profiles in subjects with IFG and IGT.
  • Correlation of metabolic abnormalities with T2DM and CVD risk factors.

    • Main Results:

    • Impaired fasting glucose is primarily associated with hepatic insulin resistance.
    • Impaired glucose tolerance is predominantly linked to pancreatic beta-cell dysfunction.
    • Both conditions share some metabolic derangements but differ in their primary drivers.

    Conclusions:

    • Differentiating between IFG and IGT is essential for understanding individual risk.
    • Targeted interventions may be more effective when tailored to the specific metabolic profile.
    • Further research into the distinct pathways of IFG and IGT can inform T2DM and CVD prevention strategies.