Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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.
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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 uptake of...
Complications of Diabetes Mellitus01:22

Complications of Diabetes Mellitus

Diabetes mellitus is a chronic metabolic disorder characterized by persistent hyperglycemia due to insulin deficiency, resistance, or both. Prolonged hyperglycemia disrupts metabolic homeostasis and leads to acute and chronic complications.Acute ComplicationsAcute complications result from sudden metabolic imbalance.Diabetic ketoacidosis (DKA) mainly appears in type 1 diabetes but may also develop in type 2 diabetes, particularly under extreme stress. It arises from severe insulin deficiency,...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

An Almond Meal-Rich Diet Improves Red Blood Cell Count and Reduces Odds of Anemia in a Mouse Model of Aging.

Antioxidants (Basel, Switzerland)·2026
Same author

Metabolic dysfunction-associated steatotic liver disease in spinal cord injury and obesity: A narrative review of divergent mechanisms, convergent outcomes.

Nutrition research (New York, N.Y.)·2026
Same author

Dietary Supplementation with the Probiotic <i>Bacillus velezensis</i> BV379 Decreases Abdominal Bloating Without Perturbing the Commensal Gut Microbiota: A Randomized, Double-Blind, Placebo-Controlled Trial in Healthy Adults.

Journal of the American Nutrition Association·2025
Same author

SALSA: a novel flow cytometry assay to detect ascorbate at the single-cell level.

Redox biology·2025
Same author

Bridging nutritional mechanisms and global challenges: The 2024 David Kritchevsky award winners.

Nutrition research (New York, N.Y.)·2025
Same author

Perspective: Framework for Developing Prediction Equations for Estimating the Absorption and Bioavailability of Nutrients from Foods.

Advances in nutrition (Bethesda, Md.)·2025

Related Experiment Video

Updated: May 16, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
08:22

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Published on: March 20, 2017

Postprandial hyperglycemia on vascular endothelial function: mechanisms and consequences.

Eunice Mah1, Richard S Bruno

  • 1Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.

Nutrition Research (New York, N.Y.)
|November 14, 2012
PubMed
Summary

Postprandial hyperglycemia (PPH) impairs vascular function, even in healthy individuals, and predicts cardiovascular disease (CVD) mortality. Oxidative stress and nitric oxide disruption are key mechanisms contributing to PPH-related vascular endothelial dysfunction.

More Related Videos

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
06:35

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Related Experiment Videos

Last Updated: May 16, 2026

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
08:22

Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion

Published on: March 20, 2017

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
06:35

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test

Published on: April 27, 2016

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Vascular Biology

Background:

  • Vascular endothelial dysfunction is a precursor to atherosclerosis and a major contributor to cardiovascular disease (CVD).
  • Chronic hyperglycemia, common in diabetes, impairs vascular function, but acute postprandial hyperglycemia (PPH) also transiently affects vascular health.
  • PPH is a stronger predictor of CVD mortality than fasting glucose in both diabetic and non-diabetic individuals.

Purpose of the Study:

  • To review clinical evidence demonstrating that PPH impairs vascular function.
  • To discuss the role of oxidative stress in nitric oxide (NO) dysregulation and PPH-mediated vascular dysfunction.
  • To identify knowledge gaps and suggest future research directions for PPH as a CVD risk factor.

Main Methods:

  • Review of clinical studies utilizing functional indices of vascular function.
  • Analysis of evidence linking PPH to oxidative stress and NO homeostasis.
  • Synthesis of current understanding and identification of research limitations.

Main Results:

  • Clinical studies confirm that PPH impairs vascular function.
  • Oxidative stress and subsequent disruption of NO homeostasis are implicated in PPH-induced vascular endothelial dysfunction.
  • PPH poses a significant risk for CVD, particularly when vascular recovery mechanisms are compromised.

Conclusions:

  • Postprandial hyperglycemia is an independent risk factor for cardiovascular disease.
  • Understanding the mechanisms of PPH-induced vascular dysfunction, particularly the role of oxidative stress, is crucial.
  • Further research is needed to fully elucidate PPH's contribution to CVD and inform preventative strategies.