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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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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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Glucose Homeostasis: Regulation of Blood Glucose01:02

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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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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Type I Diabetes II: Pathophysiology01:26

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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...
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Cells and Secretions of the Pancreas01:16

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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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Updated: Apr 28, 2026

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Evidence That Oscillations in Glucose Metabolism Promote Optimal Islet Function.

Brian P List1, Nicholas B Whitticar1,2, Kathryn L Corbin1

  • 1Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH 45701, USA.

Metabolites
|April 27, 2026
PubMed
Summary

Pulsatile delivery of D-mannoheptulose (MH) improved islet function under high glucose conditions more effectively than continuous delivery, restoring glucose sensing and beta-cell function in type 2 diabetes research.

Keywords:
D-mannoheptuloseintracellular calciumoscillationsoscillatorypulsatilepulsatility

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Cell Biology

Background:

  • Impaired pulsatile insulin release is an early marker of type 2 diabetes and insulin resistance.
  • Pulsatile insulin delivery to the liver enhances glucose-lowering effects compared to continuous delivery.
  • The impact of pulsatility on islet function itself remains largely unexplored.

Purpose of the Study:

  • To investigate whether pulsatile versus continuous delivery of D-mannoheptulose (MH) affects its efficacy in improving islet function.
  • To determine if MH's benefits are enhanced by oscillatory delivery in islets adapted to hyperglycemia.

Main Methods:

  • Mouse islets were exposed to high glucose (20 mM) for 24-48 hours.
  • A perifusion system imposed pulsatile MH delivery (3 min MH, 3 min high glucose) for 18 hours.
  • Compared pulsatile MH with continuous MH (2.5 mM or 1.25 mM).

Main Results:

  • Pulsatile MH delivery more effectively reversed hyperglycemia-induced effects and restored glucose sensing compared to continuous delivery.
  • Intracellular calcium imaging revealed pulsatile MH reduced elevated basal calcium and improved the glucose stimulation index.
  • Pulsatile MH enhanced phase 0 response, indicating improved glucose-stimulated calcium uptake by the endoplasmic reticulum.

Conclusions:

  • Loss of oscillatory glucose metabolism in islets directly contributes to beta-cell dysfunction.
  • Pulsatile administration of MH demonstrates superior efficacy in restoring islet function under hyperglycemic stress.
  • These findings highlight the importance of oscillatory dynamics in maintaining beta-cell health.