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Cited by 106Diabetes, Cardiovascular Risks, and LipoproteinsCardiovascular and exercise physiologyPhysical Activity and Health

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Modulation of Insulin Sensitivity by Exercise Training: Implications for Cardiovascular Prevention

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Iaccarino, Guido, Franco, Danilo, Sorriento, Daniela, Strisciuglio, Teresa, Barbato, Emanuele, Morisco, Carmine·2021·Journal of Cardiovascular Translational Research
DOI 10.1007/s12265-020-10057-wPMC PMC8043859
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Abstract

The beneficial effects of physical activity on the cardiovascular system nowadays have achieved the relevance of clinical evidence. In fact, several studies have documented the benefits of exercise training in the prevention of the cardiovascular risk. Abnormalities of insulin signaling transduction account for the impairment of insulin sensitivity and development of insulin resistance, which, in turn, is responsible for the enhancement of cardiovascular risk. Insulin sensitivity is related to the degree of physical activity, and physical training has been shown to ameliorate insulin action in insulin-resistant subjects. This effect is mediated by the improvement of the molecular abnormalities that are responsible of the insulin resistance, contributing in this way to restore the physiological insulin sensitivity. However, it should be underlined that mechanisms that account for this phenomenon are extremely complex and still unclear. Further studies are required to better clarify the molecular basis of the exercise-evoked improvement of insulin signal. Graphical abstract.

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Graphical abstractCC BY · PubMed Central
Fig. 1 The effects of exercise training on the conventional determinant of CV risk. HbA1c: glycosylated hemoglobin, HDL: high-density lipoprotein, WC: waist circumference, DBP: diastolic blood pressure, SBP: systolic blood pressure, BW: body weight
Fig. 1 The effects of exercise training on the conventional determinant of CV risk. HbA1c: glycosylated hemoglobin, HDL: high-density lipoprotein, WC: waist circumference, DBP: diastolic blood pressure, SBP: systolic blood pressure, BW: body weightCC BY · PubMed Central
Fig. 2 Schematic representation of early steps of insulin signaling, and the principal mechanisms that account for insulin resistance. Binding of insulin to the α-subunit of its own receptor induces the autophosphorylation of tyrosine residues of β-subunit which, in turn, induces the tyrosine phosphorylation of IR substrates (IRS), IRS-1, and IRS-2. The binding of phosphorylated IRS1/2 to the regulatory subunit p85 of phosphoinositide-3 kinase (PI3K) activates the catalytic subunit p110, which, in turn, phosphorylates/activates the serine/threonine kinase Akt (called also PKB), which stimulates the glucose uptake through the translocation of the major glucose transporter GLUT-4 to the plasma membrane. In addition, AKT promotes cell survival and cell growth, and is involved in the regulation of vascular tone and metabolic homeostasis. Insulin resistance evoked by oxidative stress, neuro-hormonal stimulation, hyperinsulinemia, and etc. may be due to defect(s) of downstream signaling components, such as receptor structure, number, binding affinity, and/or signaling capacity. P: phosphorylation, Tyr: tyrosine, IR. insulin receptor, IL-6: interleukine-6, Pro Exp: protein expression, TNF: tumor necrosis factor
Fig. 2 Schematic representation of early steps of insulin signaling, and the principal mechanisms that account for insulin resistance. Binding of insulin to the α-subunit of its own receptor induces the autophosphorylation of tyrosine residues of β-subunit which, in turn, induces the tyrosine phosphorylation of IR substrates (IRS), IRS-1, and IRS-2. The binding of phosphorylated IRS1/2 to the regulatory subunit p85 of phosphoinositide-3 kinase (PI3K) activates the catalytic subunit p110, which, in turn, phosphorylates/activates the serine/threonine kinase Akt (called also PKB), which stimulates the glucose uptake through the translocation of the major glucose transporter GLUT-4 to the plasma membrane. In addition, AKT promotes cell survival and cell growth, and is involved in the regulation of vascular tone and metabolic homeostasis. Insulin resistance evoked by oxidative stress, neuro-hormonal stimulation, hyperinsulinemia, and etc. may be due to defect(s) of downstream signaling components, such as receptor structure, number, binding affinity, and/or signaling capacity. P: phosphorylation, Tyr: tyrosine, IR. insulin receptor, IL-6: interleukine-6, Pro Exp: protein expression, TNF: tumor necrosis factorCC BY · PubMed Central
Fig. 3 Effects of acute exercise on glucose uptake and insulin signaling. Acute exercise evokes an increase of glucose uptake which is time-dependently regulated by insulin-independent and insulin-dependent mechanisms. The exercise-induced enhanced insulin sensitivity is mediated by different pathways that work in parallel with the canonical insulin signaling cascade. AMPK: AMP-activated protein kinase; AS 160: AS 160 protein; GLUT4: insulin-responsive glucose transporter; IRS: insulin receptor substrates; PI3K: phosphoinositide 3-kinase
Fig. 3 Effects of acute exercise on glucose uptake and insulin signaling. Acute exercise evokes an increase of glucose uptake which is time-dependently regulated by insulin-independent and insulin-dependent mechanisms. The exercise-induced enhanced insulin sensitivity is mediated by different pathways that work in parallel with the canonical insulin signaling cascade. AMPK: AMP-activated protein kinase; AS 160: AS 160 protein; GLUT4: insulin-responsive glucose transporter; IRS: insulin receptor substrates; PI3K: phosphoinositide 3-kinaseCC BY · PubMed Central

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  1. (2010). In Global recommendations on physical activity for health (WHO Guidelines Approved by the Guidelines Review Committee). Geneva.

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Metadata

Authors
Iaccarino, G., Franco, D., Sorriento, D., Strisciuglio, T., Barbato, E., & Morisco, C.
Affiliations
University of Naples Federico II (IT)
Corresponding author
Morisco, Carmine
ORCID
Venue
Journal of Cardiovascular Translational Research
Publisher
Springer Science and Business Media LLC
Published
2020-07-31
Volume
14
Issue
2
Pages
256-270
ISSN
  • 1937-5387 (ISSN-L)
  • 1937-5395
DOI
10.1007/s12265-020-10057-w
PMC
PMC8043859
OpenAlex
W3046313480
Cited by
106
References
129
Citations by year
2026: 17 · 2025: 16 · 2024: 14 · 2023: 22 · 2022: 21 · 2021: 14 · 2020: 2
FWCI
2.26
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Cardiovascular Translational Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by)
Funders
Cardiopath PhD program
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Physical Activity and Health
Keywords
insulin sensitivity, exercise training, insulin resistance, insulin signaling, cardiovascular risk prevention, physical activity
MeSH terms
Healthy Lifestyle, Heart Disease Risk Factors, Animals, Cardiovascular Diseases, Health Status, Humans, Insulin Resistance, Prognosis, Biomarkers, Exercise, Risk Assessment, Risk Reduction Behavior, Protective Factors

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