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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 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 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.
Tissue Renewal without Stem Cells01:23

Tissue Renewal without Stem Cells

After cellular or tissue damage, the resident stem cells present in the human body can locally repair and regenerate the damaged tissue or organ. However, even though some tissues do not have stem cells, they can repair and regenerate with the help of pre-existing cells. For example, beta cells of the pancreas and hepatocytes of the liver can divide to renew and regenerate the tissue. Here, both cell division and cell death are well regulated by homeostasis.
However, failure of such a system...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
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...

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Related Experiment Video

Updated: Jun 6, 2026

Differentiation of Human Pluripotent Stem Cells into Insulin-Producing Islet Clusters
08:41

Differentiation of Human Pluripotent Stem Cells into Insulin-Producing Islet Clusters

Published on: June 23, 2023

Distinct senescent β-cell senotypes differentially drive islet aging and dysfunction.

Kanako Iwasaki1, Hui Pan1, Jonathan Dreyfuss1

  • 1Joslin Diabetes Center/Harvard Medical School, Boston, MA.

Biorxiv : the Preprint Server for Biology
|June 5, 2026
PubMed
Summary
This summary is machine-generated.

Biological aging impairs glucose handling and increases type 2 diabetes risk. This study reveals two distinct pancreatic senescent cell types, one maladaptive and one adaptive, offering new therapeutic targets for diabetes.

Related Experiment Videos

Last Updated: Jun 6, 2026

Differentiation of Human Pluripotent Stem Cells into Insulin-Producing Islet Clusters
08:41

Differentiation of Human Pluripotent Stem Cells into Insulin-Producing Islet Clusters

Published on: June 23, 2023

Area of Science:

  • Endocrinology
  • Gerontology
  • Cell Biology

Background:

  • Biological aging affects glucose metabolism and is a key risk factor for type 2 diabetes (T2D).
  • Cellular senescence in the human endocrine pancreas and its role in aging are not well understood at the single-cell level.
  • Senolytic therapies show promise, but heterogeneity of senescent cells requires further investigation.

Purpose of the Study:

  • To investigate the heterogeneity and functional roles of senescent cells in the aging human pancreas at a single-cell resolution.
  • To identify distinct subpopulations of senescent cells (SnCs) and their specific characteristics.
  • To provide a framework for developing targeted senescence therapies for T2D.

Main Methods:

  • Single-cell-resolved spatial proteomics and transcriptomics on intact human pancreas (26 donors, ages 20-80).
  • Multiplexed single-cell RNA sequencing and functional assays on dispersed human islets (14 donors, ages 34-69).
  • Identification and characterization of senescent cell subpopulations based on gene expression (CDKN1A, CDKN2A).

Main Results:

  • Two distinct senescent cell subpopulations (SnCs) were identified: CDKN1A⁺ and CDKN2A⁺.
  • CDKN1A⁺ SnCs showed loss of beta-cell identity, reduced insulin secretion, and a pro-inflammatory senescence-associated secretory phenotype (SASP), correlating with increased islet immune infiltration.
  • CDKN2A⁺ SnCs maintained transcriptional identity and function with lower inflammatory signaling.

Conclusions:

  • Human pancreatic senescence is heterogeneous, with distinct senotypes.
  • An adaptive (CDKN2A⁺) and a maladaptive (CDKN1A⁺) senescence program exists in the pancreas.
  • These findings offer a mechanism-guided approach for developing senescence-targeted therapies for T2D.