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Related Concept Videos

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...
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...

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Related Experiment Video

Updated: Jun 7, 2026

A Model of Chronic Nutrient Infusion in the Rat
08:18

A Model of Chronic Nutrient Infusion in the Rat

Published on: August 14, 2013

[3T3L1 adipocytes induce rat beta-cell dysfunction].

Yu-fan Wang1, Xiao-hua Li, Yong-de Peng

  • 1Department of Endocrinology, Shanghai Jiao Tong University Affiliated First People's Hospital, China.

Zhonghua Yi Xue Za Zhi
|October 29, 2010
PubMed
Summary

Adipocytes impair rat beta-cell function by reducing glucose-stimulated insulin secretion and downregulating key genes and proteins involved in insulin signaling, potentially contributing to type 2 diabetes development.

More Related Videos

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

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

Published on: February 17, 2023

Related Experiment Videos

Last Updated: Jun 7, 2026

A Model of Chronic Nutrient Infusion in the Rat
08:18

A Model of Chronic Nutrient Infusion in the Rat

Published on: August 14, 2013

Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
09:48

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

Published on: February 17, 2023

Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Research

Context:

  • Adipocyte dysfunction is linked to insulin resistance.
  • Beta-cell function is crucial for glucose homeostasis.
  • Understanding inter-organ communication is vital for metabolic disease research.

Purpose:

  • To investigate the impact of adipocytes on rat beta-cell function.
  • To establish a co-culture system of 3T3L1 adipocytes and rat islet cells.
  • To analyze insulin secretion, gene expression, and protein signaling pathways.

Summary:

  • Co-culture of rat islet cells with 3T3L1 adipocytes reduced glucose-stimulated insulin secretion (GSIS) and the stimulation index.
  • mRNA levels of GCK, GLUT2, and Kir6.2 were downregulated in the co-culture group.
  • Protein expression and tyrosine phosphorylation of insulin receptor beta (IR-beta) and insulin receptor substrate-1 (IRS-1) were decreased.

Impact:

  • 3T3L1 adipocytes contribute to beta-cell dysfunction.
  • This dysfunction may be mediated by reduced GSIS-related gene expression.
  • Suppression of islet cell insulin signaling pathways is implicated in type 2 diabetes pathogenesis.