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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...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
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...
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 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...
Cell Specific Gene Expression01:58

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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...

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Efficient Differentiation of Pluripotent Stem Cells to NKX6-1+ Pancreatic Progenitors
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AGEs decrease insulin synthesis in pancreatic β-cell by repressing Pdx-1 protein expression at the post-translational

Tingting Shu1, Yunxia Zhu, Hongdong Wang

  • 1Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, Jiangsu, China.

Plos One
|May 3, 2011
PubMed
Summary
This summary is machine-generated.

Advanced glycation end products (AGEs) impair pancreatic beta-cell function by increasing nuclear Foxo1, which reduces Pdx-1 stability and insulin synthesis. This mechanism contributes to diabetic complications.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Diabetology

Background:

  • Advanced glycation end products (AGEs) are linked to diabetic complications.
  • The role of AGEs in pancreatic beta-cell dysfunction is not fully understood.
  • Previous studies show AGEs impair insulin secretion and transcription.

Purpose of the Study:

  • To investigate the molecular mechanisms by which AGEs suppress insulin synthesis in pancreatic beta-cells.
  • To elucidate the role of Foxo1 and Pdx-1 in AGE-induced beta-cell dysfunction.

Main Methods:

  • Using the rat pancreatic beta-cell line INS-1.
  • Treating cells with AGEs and analyzing Foxo1 and Pdx-1 expression and localization.
  • Investigating Pdx-1 regulation at transcriptional and post-transcriptional levels.
  • Utilizing RAGE inhibition and Foxo1 manipulation.

Main Results:

  • AGEs induced Foxo1 dephosphorylation and nuclear accumulation.
  • Nuclear Foxo1 inhibited Pdx-1 levels without affecting mRNA.
  • Pdx-1 protein levels decreased due to reduced stability.
  • RAGE antibody and DN-Foxo1 partially reversed AGE-induced effects.

Conclusions:

  • AGEs promote pancreatic beta-cell dysfunction by inducing Foxo1 nuclear translocation.
  • This leads to decreased Pdx-1 protein stability and expression.
  • Reduced Pdx-1 ultimately impairs insulin synthesis, contributing to diabetic pathology.