Related Experiment Video

Updated: Aug 16, 2026

Improving Strength, Power, Muscle Aerobic Capacity, and Glucose Tolerance through Short-term Progressive Strength Training Among Elderly People
12:59

Improving Strength, Power, Muscle Aerobic Capacity, and Glucose Tolerance through Short-term Progressive Strength Training Among Elderly People

Published on: July 5, 2017

Reduction of postchallenge hyperglycaemia prevents acute endothelial dysfunction in subjects with impaired glucose

T C Wascher1, I Schmoelzer, A Wiegratz

  • 1Department of Internal Medicine, Medical University of Graz, Austria. thomas.wascher@meduni-graz.at

European Journal of Clinical Investigation
|September 1, 2005
PubMed
Abstract

Insights

Reducing high blood sugar after meals improves early vascular function in people with impaired glucose tolerance. This effect is linked to glucose levels, not ADMA, highlighting the importance of glycemic control.

Area of Science:

  • Cardiovascular Research
  • Metabolic Disorders
  • Vascular Biology

Background:

  • Endothelial dysfunction is an early sign of vascular disease.
  • Impaired glucose tolerance is a risk factor for cardiovascular events.
  • Postchallenge hyperglycemia may acutely impair endothelial function.

Purpose of the Study:

  • To determine if reducing postchallenge hyperglycemia affects acute endothelial dysfunction.
  • To investigate the role of acarbose in managing endothelial function in impaired glucose tolerance.
  • To explore the relationship between glycemic control and vascular function.

Main Methods:

  • Randomized, double-blind, placebo-controlled, cross-over study.
  • 28 subjects with impaired glucose tolerance received acarbose or placebo.
  • Flow-mediated dilation (FMD) and asymmetrical dimethylarginine (ADMA) were measured.

Main Results:

  • A negative correlation was found between glucose changes and FMD.
  • Acarbose significantly reduced blood glucose and improved FMD.
  • The beneficial effect of acarbose was observed in subjects with higher glucose increases.
  • No changes in ADMA levels were detected.

Conclusions:

  • Acute elevation of blood glucose postchallenge impairs vascular function in impaired glucose tolerance.
  • Selective reduction of hyperglycemia improves endothelial function.
  • This vascular effect is not mediated by ADMA.

Related Concept Videos

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
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.
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...
Oral Hypoglycemic Agents: Glinides01:06

Oral Hypoglycemic Agents: Glinides

Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively manages...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

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...