On the causal relationships between hyperinsulinaemia, insulin resistance, obesity and dysglycaemia in type 2 diabetes

Hundreds of millions of people are affected by hyperinsulinaemia, insulin resistance, obesity and the dysglycaemia that mark a common progression from metabolic health to type 2 diabetes. Although the relative contribution of these features and the order in which they appear may differ between indiv...

Full description

Saved in:
Bibliographic Details
Published in:Diabetologia 2021-10, Vol.64 (10), p.2138-2146
Main Author: Johnson, James D.
Format: Article
Language:English
Subjects:
Animals
Beta cells
Clinical trials
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2
For Debate
Human Physiology
Humans
Hyperinsulinism
Insulin
Insulin Resistance
Insulin secretion
Internal Medicine
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolism
Obesity
Obesity - complications
Pathophysiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Hundreds of millions of people are affected by hyperinsulinaemia, insulin resistance, obesity and the dysglycaemia that mark a common progression from metabolic health to type 2 diabetes. Although the relative contribution of these features and the order in which they appear may differ between individuals, the common clustering and seemingly progressive nature of type 2 diabetes aetiology has guided research and clinical practice in this area for decades. At the same time, lively debate around the causal relationships between these features has continued, as new data from human trials and highly controlled animal studies are presented. This ‘For debate’ article was prompted by the review in Diabetologia by Esser, Utzschneider and Kahn ( https://doi.org/10.1007/s00125-020-05245-x ), with the purpose of reviewing established and emerging data that provide insight into the relative contributions of hyperinsulinaemia and impaired glucose-stimulated insulin secretion in progressive stages between health, obesity and diabetes. It is concluded that these beta cell defects are not mutually exclusive and that they are both important, but at different stages. Graphical abstract
ISSN:0012-186X
1432-0428
DOI:10.1007/s00125-021-05505-4