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Related Concept Videos

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...
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 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...
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.

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Related Experiment Video

Updated: Jul 11, 2026

Echocardiographic Measurement of Right Ventricular Diastolic Parameters in Mouse
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Right ventricular dysfunctions in type 1 diabetic mice: A longitudinal study.

Jian-Jian Yu1,2, Jian-Ge Han2,3, Yi Tan1,4

  • 1Pediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, KY 40202, United States.

World Journal of Diabetes
|October 20, 2025
PubMed
Summary

In type 1 diabetes (T1D) mice, left ventricular dysfunction occurs before right ventricular dysfunction. Pulmonary arterial hypertension develops later, potentially impacting right ventricular function.

Keywords:
Cardiac dysfunctionCardiac remodelingDiabetic cardiomyopathyLeft ventricleRight ventricleType 1 diabetes

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Area of Science:

  • Cardiology
  • Endocrinology
  • Diabetology

Background:

  • Diabetes mellitus is a global metabolic disease with cardiovascular complications as a leading cause of mortality.
  • Diabetic cardiomyopathy, a diabetes-specific condition, affects cardiac function, particularly in type 1 diabetes (T1D).
  • While left ventricular (LV) dysfunction in T1D is well-studied, right ventricular (RV) dysfunction is gaining research attention, especially in pediatric T1D.

Purpose of the Study:

  • To longitudinally assess RV and LV functional and structural changes in female transgenic OVE26 T1D mice over 30 weeks.
  • To compare cardiac function between T1D mice and wild-type controls.

Main Methods:

  • Transthoracic echocardiography was used to evaluate RV and LV structure and function.
  • RV systolic pressure was measured using a pressure catheter.
  • Histological analyses (Sirius-red, wheat germ agglutinin) and molecular techniques (qPCR, Western blotting) assessed fibrosis, cardiomyocyte size, miRNA expression, and protein levels.

Main Results:

  • LV systolic function declined in T1D mice by 30 weeks, while RV systolic function remained similar to controls.
  • RV diastolic dysfunction significantly increased from 18 weeks onwards, accompanied by RV fibrosis and hypertrophy.
  • Pulmonary arterial hypertension developed in T1D mice by 30 weeks, indicated by elevated RV systolic pressure and altered pulmonary blood flow dynamics.

Conclusions:

  • In OVE26 T1D mice, RV diastolic dysfunction emerges later than LV dysfunction.
  • Late-stage T1D is associated with mild pulmonary arterial hypertension, which may contribute to RV systolic impairment and remodeling.