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Related Concept Videos

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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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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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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Hypoglycemia and Glucagon01:15

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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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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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Updated: Sep 10, 2025

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
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Endothelial function can be modulated by acute hyperglycemia.

Hassanain Qambari1,2, Paula K Yu1, Chandrakumar Balaratnasingam1,2

  • 1Centre for Ophthalmology and Visual Science, The University of Western Australia, Perth, Australia.

Scientific Reports
|August 20, 2025
PubMed
Summary
This summary is machine-generated.

Acute hyperglycemia temporarily enhances ocular endothelial function, but prolonged exposure in diabetic rats leads to incomplete recovery, suggesting irreversible dysfunction. This impacts microvascular disease development.

Keywords:
Acute hyperglycemiaEndothelial dysfunctionGlycemic controlStreptozotocin-induced diabetesVascular disease

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Area of Science:

  • Ophthalmology
  • Endocrinology
  • Vascular Biology

Background:

  • Endothelial dysfunction from chronic hyperglycemia contributes to microvascular diseases like diabetic retinopathy.
  • The impact and recovery of vascular endothelium from acute hyperglycemia are not well understood.

Purpose of the Study:

  • To investigate the effects of acute and prolonged hyperglycemia on ocular microvascular endothelium function and recovery in streptozotocin (STZ)-induced diabetic rats.
  • To assess histological changes including capillary density, diameter, pericyte distribution, eNOS, and advanced glycated end products (AGEs).

Main Methods:

  • Isolated perfused eye preparation from normoglycemic and 1- to 4-week STZ-diabetic rats.
  • Sequential perfusion with varying glucose concentrations (6 mM, 12 mM, 24 mM, then 6 mM).
  • Measurement of acetylcholine (Ach)-induced vasodilatory response and histological examination.

Main Results:

  • Acute high glucose enhanced Ach-induced vasodilation in all groups.
  • Recovery of Ach response was observed in 1- to 3-week diabetic eyes upon return to normoglycemia.
  • 4-week diabetic eyes showed persistent enhanced vasodilation despite normoglycemia.
  • Increased pericyte distribution in 3- and 4-week diabetic eyes; increased eNOS in 1-week diabetic eyes; AGEs detected in 1-week diabetic eyes.

Conclusions:

  • Short-term hyperglycemia allows for endothelial function recovery.
  • Prolonged hyperglycemia (≥4 weeks) in diabetic rats leads to incomplete functional recovery, indicating a potential shift towards irreversible endothelial dysfunction.
  • Findings highlight the progressive nature of hyperglycemia-induced vascular damage in the eye.