Hyperinsulinaemia as a cause of obesity and cardiometabolic diseases
(2026) In Nature Reviews Endocrinology- Abstract
This narrative Review explores the role of hyperinsulinaemia as a potential independent contributor to obesity and cardiometabolic diseases. We argue that scientific discussions about the role of hyperinsulinaemia as a causal factor in these conditions have not sufficiently distinguished between postprandial insulin excursions and chronically elevated basal levels of insulin. We summarize findings from observational and experimental human trials, as well as preclinical models, and outline how reasonable evidence suggests that chronic (basal) exposure to elevated levels of insulin, rather than normal postprandial insulin excursions in isolation, might have a role in promoting or exacerbating the development of adiposity. We discuss the... (More)
This narrative Review explores the role of hyperinsulinaemia as a potential independent contributor to obesity and cardiometabolic diseases. We argue that scientific discussions about the role of hyperinsulinaemia as a causal factor in these conditions have not sufficiently distinguished between postprandial insulin excursions and chronically elevated basal levels of insulin. We summarize findings from observational and experimental human trials, as well as preclinical models, and outline how reasonable evidence suggests that chronic (basal) exposure to elevated levels of insulin, rather than normal postprandial insulin excursions in isolation, might have a role in promoting or exacerbating the development of adiposity. We discuss the putative contributors to hyperinsulinaemia, including genetic predisposition, early-life influences, diet, environmental pollutants and physical inactivity, highlighting causality knowledge gaps relevant to the prevention of obesity and cardiometabolic diseases.
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- author
- Guess, Nicola ; Johnson, James D ; Vaag, Allan LU ; Tahrani, Abd A ; Corkey, Barbara ; Bruin, Jennifer E and Little, Jon P
- organization
- publishing date
- 2026-03-09
- type
- Contribution to journal
- publication status
- epub
- subject
- in
- Nature Reviews Endocrinology
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:105033294713
- pmid:41803509
- ISSN
- 1759-5037
- DOI
- 10.1038/s41574-026-01240-1
- language
- English
- LU publication?
- yes
- additional info
- © 2026. Springer Nature Limited.
- id
- 52700e26-7d85-461c-850e-e6db507327d1
- date added to LUP
- 2026-03-11 13:48:07
- date last changed
- 2026-05-15 09:38:16
@article{52700e26-7d85-461c-850e-e6db507327d1,
abstract = {{<p>This narrative Review explores the role of hyperinsulinaemia as a potential independent contributor to obesity and cardiometabolic diseases. We argue that scientific discussions about the role of hyperinsulinaemia as a causal factor in these conditions have not sufficiently distinguished between postprandial insulin excursions and chronically elevated basal levels of insulin. We summarize findings from observational and experimental human trials, as well as preclinical models, and outline how reasonable evidence suggests that chronic (basal) exposure to elevated levels of insulin, rather than normal postprandial insulin excursions in isolation, might have a role in promoting or exacerbating the development of adiposity. We discuss the putative contributors to hyperinsulinaemia, including genetic predisposition, early-life influences, diet, environmental pollutants and physical inactivity, highlighting causality knowledge gaps relevant to the prevention of obesity and cardiometabolic diseases.</p>}},
author = {{Guess, Nicola and Johnson, James D and Vaag, Allan and Tahrani, Abd A and Corkey, Barbara and Bruin, Jennifer E and Little, Jon P}},
issn = {{1759-5037}},
language = {{eng}},
month = {{03}},
publisher = {{Nature Publishing Group}},
series = {{Nature Reviews Endocrinology}},
title = {{Hyperinsulinaemia as a cause of obesity and cardiometabolic diseases}},
url = {{http://dx.doi.org/10.1038/s41574-026-01240-1}},
doi = {{10.1038/s41574-026-01240-1}},
year = {{2026}},
}