ArticlePloS one2011
Consistency of the disposition index in the face of diet induced insulin resistance: potential role of FFA.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 33 citations in OpenAlex.
- Pancreatic β cell function versus insulin resistance: application of the hyperbolic law of glucose tolerance.The Journal of clinical investigation · 2024Article
- Central Nervous System Control of Glucose Homeostasis: A Therapeutic Target for Type 2 Diabetes?Annual review of pharmacology and toxicology · 2022Review
- Hyperinsulinemic Compensation for Insulin Resistance Occurs Independent of Elevated Glycemia in Male Dogs.Endocrinology · 2021Article
- Article
- Sudden 'cure' of type two diabetes due to pancreatic insulinoma: A case report.Molecular and clinical oncology · 2020Article
- Origins and History of the Minimal Model of Glucose Regulation.Frontiers in endocrinology · 2020Article
- Glucoregulatory responses to hypothalamic preoptic area cooling.Brain research · 2019Article
- Vascular endothelial growth factor-B: Impact on physiology and pathology.Cell adhesion & migration · 2018Article
- Exenatide Treatment Alone Improves β-Cell Function in a Canine Model of Pre-Diabetes.PloS one · 2016Article
- Rapid development of cardiac dysfunction in a canine model of insulin resistance and moderate obesity.Diabetologia · 2016Article
- Influence of endogenous NEFA on beta cell function in humans.Diabetologia · 2015Article
- Increase in visceral fat per se does not induce insulin resistance in the canine model.Obesity (Silver Spring, Md.) · 2015Article
- Beta cell dysfunction and insulin resistance.Frontiers in endocrinology · 2013Article
- Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveInsulin resistance induces hyperinsulinemic compensation, which in turn maintains almost a constant disposition index. However, the signal that gives rise to the hyperinsulinemic compensation for insulin resistance remains unknown.
methodsIn a dog model of obesity we examined the possibility that potential early-week changes in plasma FFA, glucose, or both could be part of a cascade of signals that lead to compensatory hyperinsulinemia induced by insulin resistance.
resultsHypercaloric high fat feeding in dogs resulted in modest weight gain, and an increase in adipose tissue with no change in the non-adipose tissue size. To compensate for the drop in insulin sensitivity, there was a significant rise in plasma insulin, which can be attributed in part to a decrease in the metabolic clearance rate of insulin and increased insulin secretion. In this study we observed complete compensation for high fat diet induced insulin resistance as measured by the disposition index. The compensatory hyperinsulinemia was coupled with significant changes in plasma FFAs and no change in plasma glucose.
conclusionsWe postulate that early in the development of diet induced insulin resistance, a change in plasma FFAs may directly, through signaling at the level of β-cell, or indirectly, by decreasing hepatic insulin clearance, result in the observed hyperinsulinemic compensation.
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