Mild suppression of hyperinsulinemia to treat obesity and insulin resistance
Open accessAbstract
Insulin plays roles in lipid uptake, lipolysis, and lipogenesis, in addition to controlling blood glucose levels. Excessive circulating insulin is associated with adipose tissue expansion and obesity, yet a causal role for hyperinsulinemia in the development of mammalian obesity has proven controversial, with many researchers suggesting it as a consequence of insulin resistance. Recently, evidence that specifically reducing hyperinsulinemia can prevent and reverse obesity in animal models has been presented. Our experiments, and others in this field, question the current dogma that hyperinsulinemia is a response to obesity and/or insulin resistance. In this review, we discuss preclinical evidence in the context of the broader literature and speculate on the possibility of clinical translation of alternative approaches for treating obesity.
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Hyperinsulinemia has been proposed to be an early crucial driver in the progression of adiposity.
“In this regard, hyperinsulinemia has been proposed to be an early crucial driver in the progression of adiposity [265,266,267,268].”
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“It has been reported that although there is a causal role of hyperinsulinemia in the progression of obesity with a well-established connection, its contribution varies [9].”
BackgroundNutritional guidelines for the management of insulin resistance
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Self-citation
- Authors
- Page, M. M., & Johnson, J. D.
- Affiliations
- University of British Columbia (CA)
- Corresponding author
- Johnson, James D.
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 29
- Issue
- 6
- Pages
- 389-399
- ISSN
- 1043-2760 (ISSN-L)
- OpenAlex
- W2796621520
- Cited by
- 99
- References
- 108
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 11 · 2023: 16 · 2022: 15 · 2021: 17 · 2020: 21 · 2019: 7 · 2018: 3
- FWCI
- 1.71
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- hyperinsulinemia, obesity, insulin resistance, insulin signaling, adipose tissue expansion, lipolysis, lipogenesis, lipid uptake, obesity treatment, animal models of obesity
- MeSH terms
- Animals, Glucose, Homeostasis, Humans, Hyperinsulinism, Insulin, Insulin Resistance, Obesity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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