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Related Concept Videos

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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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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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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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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The pancreas, a vital organ within the abdominal cavity, plays dual roles in the digestive and endocrine systems, collaborating with exocrine and endocrine cells to maintain optimal digestion and blood sugar levels.
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Isolated Pancreatic Islet Treatment and Apoptosis Measurement
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Cytokines and Pancreatic β-Cell Apoptosis.

L A Berchtold1, M Prause1, J Størling2

  • 1University of Copenhagen, Copenhagen, Denmark.

Advances in Clinical Chemistry
|June 28, 2016
PubMed
Summary

Inflammatory cytokines impact pancreatic beta-cell function bimodal responses. Research identifies the caspase-dependent intrinsic apoptosis pathway as key in cytokine-induced beta-cell death, guiding new diabetes treatments.

Keywords:
ApoptosisCytokinesDiabetesER stressInflammationMitochondrial stressOxidative stressProgrammed cell deathSignaling

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Area of Science:

  • Endocrinology and Immunology
  • Cellular Biology
  • Diabetes Research

Background:

  • Inflammatory cytokines induce concentration and time-dependent bimodal responses in pancreatic beta-cell function and viability.
  • This discovery shifted research from toxic chemical models to in vitro cytokine exposure, mimicking in vivo inflammatory effects.
  • Understanding these responses is crucial for comprehending beta-cell failure in diabetes.

Purpose of the Study:

  • To review cellular, preclinical, and clinical evidence on death pathways activated by inflammatory cytokines in pancreatic beta-cells.
  • To identify potential antidiabetic targets based on inflammatory cytokine-induced beta-cell apoptosis mechanisms.
  • To guide the development of precise, specific, and safe anti-inflammatory treatments for diabetes.

Main Methods:

  • Analysis of cellular and preclinical studies on cytokine-induced beta-cell apoptosis.
  • Review of emerging clinical trial data on anticytokine therapies for diabetes.
  • Examination of signaling pathways, including nuclear factor kappa B and mitogen-activated protein kinases.

Main Results:

  • Cytokine exposure elicits bimodal responses, with low concentrations stimulating and high concentrations inhibiting beta-cell function.
  • Proapoptotic responses involve nuclear factor kappa B and mitogen-activated protein kinase activation, leading to endoplasmic reticulum stress and mitochondrial dysfunction.
  • Cellular and preclinical data strongly implicate the caspase-dependent intrinsic apoptosis pathway in inflammatory beta-cell death.

Conclusions:

  • The caspase-dependent intrinsic apoptosis pathway is the primary mechanism of inflammatory beta-cell apoptosis.
  • Anticytokine therapies show promise in preclinical models and early clinical trials.
  • Further research is needed to optimize dosing, timing, and combinations for effective clinical application in diabetes treatment.