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Related Concept Videos

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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Insulin: The Receptor and Signaling Pathways01:28

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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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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.
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Type II Diabetes II: Pathophysiology01:24

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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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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Related Experiment Video

Updated: May 2, 2026

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
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Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

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SIK2 regulates insulin secretion.

Bengt-Frederik Belgardt1, Markus Stoffel1

  • 1Institute of Molecular Health Sciences and the Competence Centre for Systems Physiology and Metabolic Diseases, ETH Zurich, Otto-Stern-Weg 7, 8093 Zurich, Switzerland.

Nature Cell Biology
|March 1, 2014
PubMed
Summary

The salt-inducible kinase 2 (SIK2) is stabilized in pancreatic beta cells after glucose intake. This regulation improves glucose homeostasis by controlling calcium flux and insulin secretion.

Area of Science:

  • Endocrinology
  • Metabolic regulation
  • Pancreatic beta-cell function

Background:

  • Insulin secretion is vital for maintaining blood glucose levels.
  • Dysregulation of insulin secretion contributes to metabolic disorders.
  • Pancreatic beta-cells are key endocrine cells responsible for insulin production and release.

Purpose of the Study:

  • To investigate the role of salt-inducible kinase 2 (SIK2) in pancreatic beta-cell function.
  • To determine how SIK2 influences insulin secretion and glucose homeostasis.
  • To elucidate the regulatory mechanisms of SIK2 in response to glucose stimulation.

Main Methods:

  • Utilized pancreatic beta-cell models and in vivo studies.
  • Investigated the stabilization of SIK2 upon glucose stimulation.

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  • Analyzed the impact of SIK2 on cellular calcium flux and insulin secretion.
  • Assessed effects on systemic glucose homeostasis.

    • Main Results:

    • SIK2 protein is stabilized in pancreatic beta-cells following glucose stimulation.
    • SIK2 stabilization enhances insulin secretion.
    • SIK2 modulates cellular calcium flux, contributing to improved insulin release.
    • Increased SIK2 activity leads to better systemic glucose homeostasis.

    Conclusions:

    • SIK2 plays a critical role in the glucose-stimulated regulation of insulin secretion.
    • Stabilization of SIK2 in pancreatic beta-cells is a key mechanism for maintaining glucose homeostasis.
    • Targeting SIK2 may offer therapeutic potential for metabolic disorders related to impaired insulin secretion.