Insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift
Open accessAbstract
While few dispute the existence of the metabolic syndrome as a clustering of factors indicative of poor metabolic health, its utility above that of its individual components in the clinical care of individual patients is questioned. This is likely a consequence of the failure of clinicians and scientists to agree on a unifying mechanism to explain the metabolic syndrome. Insulin resistance has most commonly been proposed for this role and is generally considered to be a root causative factor for not only metabolic syndrome but also for its associated conditions of non-alcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS), obesity-related type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD). An alternative view, for which evidence is mounting, is that hyper-responsiveness of islet β-cells to a hostile environment, such as westernised lifestyle, is primary and that the resulting hyperinsulinaemia drives the other components of the metabolic syndrome. Importantly, within this new conceptual framework, insulin resistance, while always a biomarker and state of poor metabolic health, is not considered to be harmful, but a protective adaptive response of critical tissues including the myocardium against insulin-induced metabolic stress. This major shift in how metabolic syndrome can be considered puts insulin hypersecretion into position as the unifying mechanism. If shown to be correct, this new conceptual framework has major implications for the future prevention and management of the metabolic syndrome, including its associated conditions of NAFLD, PCOS, obesity-related T2D and ASCVD.
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Being able to vary the sensitivity and physiological action of insulin is thought to have conferred a significant adaptive survival role in many animals throughout evolutionary history.
“Nevertheless, being able to vary the sensitivity and physiological action of insulin is thought to have conferred a significant adaptive survival role in many animals throughout evolutionary history [146,159].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [146]
The section “Insulin sensitivity: adaptable to physiological demands” describes changes in insulin sensitivity that help partition nutrients during feast and famine, pregnancy, and other physiological demands. It does not establish that this flexibility conferred a significant survival advantage across many animals throughout evolutionary history. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPhysiological regulation of insulin function can be viewed as an adaptive mechanism to regulate the metabolic pathway of insulin signaling (PI-3K) in response to changing environmental conditions or during normal alterations of internal states.
“Physiological regulation of insulin function can be viewed as an adaptive mechanism to regulate the metabolic pathway of insulin signaling (PI-3K), in response to changing environmental conditions [starvation, fear, stress] [164,165] or during normal alterations of internal states (pregnancy, lactation, adolescence) [65,146,152].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [146]
The section “Insulin sensitivity: adaptable to physiological demands” describes adaptive changes in insulin sensitivity with dietary intake, physical activity, puberty and pregnancy. It does not identify PI-3K as the pathway being regulated or mention lactation, so those specifics are not supported by our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThere is no consensus on the definition of insulin resistance.
“There is no consensus on the definition of IR [145,146]”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [146]
The Abstract discusses controversy over the definition of metabolic syndrome and differing views of insulin resistance’s role, but it does not say whether there is consensus on the definition of insulin resistance. Searches for a definition of insulin resistance found no passage addressing that point. (LLM, conf=0.73)
Experimental — accuracy not yet measuredInsulin resistance results from alterations to cellular membrane insulin-receptor function or intracellular signaling, enzyme, metabolic or gene function.
“IR results from alterations to cellular membrane insulin-receptor function or intracellular signaling, enzyme, metabolic or gene function [146,160,161].”
From Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment (2022) · cites this paper as [146]
The section ‘Insulin resistance: a protective mechanism against nutrient-induced intracellular metabolic stress’ describes insulin resistance as an adaptive response to chronic overnutrition, but does not identify alterations in insulin-receptor function, intracellular signaling, enzymes, metabolism, or genes as its causes. Searches for the quoted list and for receptor-signaling mechanisms found no passage in our copy that addresses that specific claim; the available passages have no page numbers. (LLM, conf=0.72)
Experimental — accuracy not yet measuredTo sustain a stable levels of blood glucose, islet β cells secret excessive insulin to compensate, leading to hyperinsulinemia.
“In order to sustain a stable levels of blood glucose, islet β cells secret excessive insulin to compensate, leading to hyperinsulinemia (86).”
From Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments (2020) · cites this paper as [86]
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- Authors
- Nolan, C. J., & Prentki, M.
- Affiliations
- Australian National University (AU)
- Université de Montréal (CA)
- Corresponding author
- Prentki, Marc
- Venue
- Diabetes and Vascular Disease Research
- Publisher
- SAGE Publications
- Published
- 2019-02-15
- Volume
- 16
- Issue
- 2
- Pages
- 118-127
- ISSN
- 1479-1641 (ISSN-L)
- 1752-8984
- OpenAlex
- W2913033190
- Semantic Scholar
- d0dde31c6f8816e74167f424d5ccb49470d3254a
- Cited by
- 292
- References
- 54
- Citations by year
- 2026: 18 · 2025: 43 · 2024: 43 · 2023: 53 · 2022: 56 · 2021: 42 · 2020: 27 · 2019: 10
- FWCI
- 5.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes and Vascular Disease Research (publishedVersion)
- PubMed (publishedVersion)
- ANU Open Research (Australian National University) (submittedVersion)
- Funders
- Canadian Institutes of Health Research
- Medical Research Council
- National Health and Medical Research Council (1128442)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- metabolic syndrome, insulin resistance, insulin hypersecretion, hyperinsulinemia, type 2 diabetes, non-alcoholic fatty liver disease, polycystic ovary syndrome, atherosclerotic cardiovascular disease, obesity
- MeSH terms
- Animals, Blood Glucose, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Female, Health Status, Humans, Insulin, Insulin Resistance, Male, Obesity, Polycystic Ovary Syndrome, Prognosis, Risk Factors, Biomarkers, Metabolic Syndrome, Insulin-Secreting Cells, Secretory Pathway, Non-alcoholic Fatty Liver Disease
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