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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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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.
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Hormones Regulating Blood Glucose01:16

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
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Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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Cell Specific Gene Expression01:58

Cell Specific Gene Expression

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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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Glucagon-like Receptor Agonists01:24

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
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Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
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Assessing Replication and Beta Cell Function in Adenovirally-transduced Isolated Rodent Islets
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Glucose potentiates β-cell function by inducing Tph1 expression in rat islets.

Yuqing Zhang1, Ruyuan Deng1, Xue Yang1

  • 1Department of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|August 11, 2017
PubMed
Summary
This summary is machine-generated.

High glucose levels increase tryptophan hydroxylase 1 (Tph1) expression in pancreatic beta cells, enhancing insulin secretion. Promoting Tph1 offers a new strategy for type 2 diabetes treatment.

Keywords:
diabetesislet functionserotonintryptophan hydroxylase 1

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Type 2 diabetes is characterized by impaired pancreatic beta-cell function.
  • Mechanisms of beta-cell adaptation to chronic hyperglycemia are not fully understood.

Purpose of the Study:

  • To investigate the role of glucose-induced gene expression in beta-cell adaptation.
  • To identify novel therapeutic targets for type 2 diabetes.

Main Methods:

  • Global gene expression profiling in rat islets.
  • Analysis of Tph1 promoter activity and transcription factor binding.
  • In vitro and in vivo studies of Tph1 function in beta cells.
  • Manipulation of Tph1 expression (knockdown and overexpression).

Main Results:

  • Tryptophan hydroxylase 1 (Tph1) was significantly upregulated in rat islets under high glucose conditions.
  • Glucose-stimulated Tph1 transcription was mediated by calcium and cAMP signaling pathways.
  • In vivo high glucose infusion induced Tph1 expression and enhanced islet function.
  • Tph1 inhibition reduced glucose-potentiated insulin secretion, while overexpression augmented it.
  • Exendin-4 stimulated Tph1 expression in a glucose-dependent manner, impacting insulin secretion.

Conclusions:

  • Tph1 plays a crucial role in mediating glucose-induced compensation of pancreatic beta-cell function.
  • Targeting Tph1 expression in beta cells presents a potential therapeutic strategy for type 2 diabetes mellitus.