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 Experiment Videos

Islet dysfunction in non-insulin-dependent diabetes mellitus.

S E Kahn1, D Porte

  • 1Department of Medicine, University of Washington School of Medicine, Seattle.

The American Journal of Medicine
|November 28, 1988
PubMed
Summary

Non-insulin-dependent diabetes mellitus involves elevated fasting glucose due to pancreatic islet, liver, and tissue defects. Impaired insulin secretion and action by beta cells are central to this condition.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Exploring residual risk for diabetes and microvascular disease in the Diabetes Prevention Program Outcomes Study (DPPOS).

Diabetic medicine : a journal of the British Diabetic Association·2017
Same author

Regulation of food intake and body weight by insulin.

Diabetologia·2016
Same author

Peptides and the control of meal size.

Diabetologia·2016
Same author

Steroid Sex Hormones, Sex Hormone-Binding Globulin, and Diabetes Incidence in the Diabetes Prevention Program.

The Journal of clinical endocrinology and metabolism·2015
Same author

The duodenal glucose load impacts the oral disposition index in healthy subjects.

Diabetic medicine : a journal of the British Diabetic Association·2015
Same author

Visceral abdominal fat accumulation predicts the conversion of metabolically healthy obese subjects to an unhealthy phenotype.

International journal of obesity (2005)·2015

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Diabetes Research

Background:

  • Non-insulin-dependent diabetes mellitus (NIDDM) presents with fasting hyperglycemia.
  • Defects in pancreatic islets, liver, and peripheral tissues disrupt glucose homeostasis.
  • A feedback loop involving these organs regulates glucose levels.

Purpose of the Study:

  • To review the role of pancreatic A and B cells in coordinating hepatic glucose production and peripheral glucose utilization.
  • To elucidate the mechanisms underlying hyperglycemia in NIDDM.
  • To examine the relationship between islet dysfunction and fasting hyperglycemia.

Main Methods:

  • Review of existing literature on NIDDM pathophysiology.
  • Analysis of the interplay between hepatic glucose production, insulin secretion, and tissue glucose uptake.

Related Experiment Videos

  • Correlation of islet function testing with fasting hyperglycemia levels.

    • Main Results:

    • Elevated basal hepatic glucose production correlates with fasting hyperglycemia in NIDDM.
    • Impaired hepatic insulin sensitivity and reduced insulin secretion contribute to increased glucose release.
    • Beta-cell dysfunction, characterized by reduced secretory capacity, impairs both basal and stimulated insulin release.
    • Peripheral tissue glucose uptake is compromised by decreased insulin secretion and defective insulin action.
    • The degree of beta-cell responsiveness to glucose is curvilinearly related to fasting hyperglycemia.

    Conclusions:

    • NIDDM is characterized by a regulated elevation of plasma glucose concentration.
    • Islet dysfunction, specifically impaired beta-cell function, is a necessary component of NIDDM pathophysiology.
    • Therapeutic interventions targeting islet function, hepatic glucose production, or tissue glucose uptake effectively lower fasting glucose levels.