On the causal relationships between hyperinsulinaemia, insulin resistance, obesity and dysglycaemia in type 2 diabetes.
Dysglycaemia
Human studies
Hyperinsulinaemia
Insulin resistance
Insulin secretion
Mouse models
Obesity
Pancreatic islet beta cells
Review
Type 2 diabetes
Journal
Diabetologia
ISSN: 1432-0428
Titre abrégé: Diabetologia
Pays: Germany
ID NLM: 0006777
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
11
02
2021
accepted:
23
04
2021
pubmed:
24
7
2021
medline:
12
2
2022
entrez:
23
7
2021
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 34296322
doi: 10.1007/s00125-021-05505-4
pii: 10.1007/s00125-021-05505-4
doi:
Substances chimiques
Insulin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Comment
Langues
eng
Sous-ensembles de citation
IM
Pagination
2138-2146Subventions
Organisme : CIHR
ID : P-168857
Pays : Canada
Organisme : CIHR
ID : P-168854
Pays : Canada
Commentaires et corrections
Type : CommentOn
Type : CommentIn
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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