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Related Concept Videos

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 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.
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 I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
Diabetes Mellitus: Overview and Type I Subtype01:22

Diabetes Mellitus: Overview and Type I Subtype

Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...
Type I Diabetes I: Introduction01:12

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...

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Related Experiment Video

Updated: Jun 17, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
08:22

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Published on: March 20, 2017

HIF-1alpha dysfunction in diabetes.

Hariharan Thangarajah1, Ivan N Vial, Raymon H Grogan

  • 1Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA.

Cell Cycle (Georgetown, Tex.)
|December 18, 2009
PubMed
Summary
This summary is machine-generated.

Deferoxamine (DFO) improves diabetic wound healing by restoring hypoxia-inducible factor-1alpha (HIF-1alpha) activity, crucial for blood vessel formation. This iron chelator shows promise for treating diabetic foot ulcers and other ischemic conditions.

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A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
05:18

A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes

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Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
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Published on: March 20, 2017

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A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
05:18

A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes

Published on: February 17, 2023

Area of Science:

  • Biomedical Science
  • Wound Healing Research
  • Diabetic Complications

Background:

  • Diabetic wounds, particularly foot ulcers, lead to significant amputations due to poor healing.
  • Impaired wound healing in diabetes stems from compromised blood vessel formation (neovascularization) caused by high glucose levels.
  • High glucose impairs hypoxia-inducible factor-1alpha (HIF-1alpha) activity, essential for vascular endothelial growth factor (VEGF) expression and neovascularization.

Purpose of the Study:

  • To investigate the precise mechanism of high glucose-induced HIF-1alpha dysfunction in diabetic wound healing.
  • To further evaluate the therapeutic potential of deferoxamine (DFO) in improving diabetic wound healing and tissue viability.

Main Methods:

  • Assessed HIF-1alpha activity versus stability in high glucose conditions.
  • Examined the impact of high glucose-induced HIF-1alpha hydroxylation on its activity.
  • Investigated DFO's effects on VEGF expression, vascular proliferation, and tissue viability in a mouse model of diabetic wounds.

Main Results:

  • High glucose impairs HIF-1alpha *activity*, not protein stability, hindering transactivation.
  • Constitutive HIF-1alpha overexpression did not overcome high glucose-induced impairment.
  • High glucose-induced hydroxylation of HIF-1alpha's transactivation domain did not affect its activity.
  • DFO treatment normalized healing, increased VEGF expression, and promoted vascular proliferation, improving tissue viability in diabetic mice.

Conclusions:

  • High glucose disrupts diabetic wound healing by impairing HIF-1alpha transactivation activity.
  • DFO effectively reverses these impairments, promoting neovascularization and healing.
  • DFO is a promising therapeutic candidate for diabetic wound healing and other ischemic conditions due to its established clinical use.