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Related Concept Videos

Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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Pathophysiology of Diabetes01:20

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Carbohydrate metabolism is a fundamental biochemical process that ensures a constant supply of energy to living cells. The most important carbohydrate is glucose, which can be broken down via glycolysis to enter into the Krebs cycle and eventually lead to the production of ATP through oxidative phosphorylation.
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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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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: 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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Updated: Oct 8, 2025

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish
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Hyperglycemia induces corneal endothelial dysfunction through attenuating mitophagy.

Chen Chen1, Qingjun Zhou2, Zongyi Li2

  • 1Department of Ophthalmology, Clinical Medical College of Shandong University, Jinan, 250012, China; State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, 266071, China.

Experimental Eye Research
|December 24, 2021
PubMed
Summary
This summary is machine-generated.

Hyperglycemia damages corneal endothelial cells by reducing key proteins and impairing mitophagy. Activating mitophagy with CCCP offers a potential treatment for diabetic corneal endothelial dysfunction.

Keywords:
CCCPCorneal endotheliumDiabetes mellitusHyperglycemiaMitophagy

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Area of Science:

  • Ophthalmology
  • Endocrinology
  • Cell Biology

Background:

  • Hyperglycemia is linked to corneal endothelial dysfunction, affecting structure and function.
  • The precise mechanisms underlying hyperglycemia-induced corneal damage are not fully understood.

Purpose of the Study:

  • To investigate the impact of hyperglycemia on corneal endothelial cells.
  • To elucidate the role of mitophagy in diabetic corneal endothelial dysfunction.
  • To explore mitophagy activation as a therapeutic strategy.

Main Methods:

  • Assessed expression of Na+/K+ ATPase and ZO-1 in hyperglycemic conditions.
  • Examined mitochondrial morphology and dynamics in vitro.
  • Quantified mitophagy levels using Western blotting and LC3B-Mitotracker Immunofluorescence.
  • Administered mitophagy agonist CCCP to cells and diabetic mice.

Main Results:

  • Hyperglycemia reduced Na+/K+ ATPase and ZO-1 expression.
  • Observed abnormal mitochondrial morphology and dynamics in vitro.
  • Demonstrated decreased mitophagy levels in hyperglycemic conditions.
  • CCCP treatment upregulated mitophagy, restoring Na+/K+ ATPase and ZO-1 levels.
  • CCCP reversed corneal opacity and thickness in diabetic mice.

Conclusions:

  • Mitophagy plays a critical role in the pathogenesis of diabetic corneal endothelial dysfunction.
  • Activating mitophagy presents a potential therapeutic approach for diabetic corneal complications.