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Pathogenesis and Pathophysiology of the Cardiometabolic Syndrome
Open accessAbstract
The cardiometabolic syndrome represents a cluster of metabolic abnormalities that are risk factors for cardiovascular disease. The mechanism(s) responsible for developing the cardiometabolic syndrome is not known, but it is likely that multi‐organ insulin resistance, which is a common feature of the cardiometabolic syndrome, is involved. Insulin resistance is an important risk factor for type 2 diabetes and can cause vasoconstriction and renal sodium reabsorption, leading to increased blood pressure. Alterations in adipose tissue fatty acid and adipokine metabolism are involved in the pathogenesis of insulin resistance. Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Noninfectious systemic inflammation associated with adipocyte and adipose tissue macrophage cytokine production can also cause insulin resistance. In addition, increased free fatty acid delivery to the liver can stimulate hepatic very low‐density lipoprotein triglyceride production, leading to dyslipidemia.
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“Weight loss is the cornerstone of therapy for people with obesity because it can ameliorate or completely resolve the metabolic risk factors for diabetes, coronary artery disease, and obesity-associated cancers.”
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Additional file 1 of The conceptualisation of cardiometabolic disease policy model in the UK
Putri, S., Ciminata, G., Lewsey, J., Jani, B., McMeekin, N., & Geue, C. (2024) · Figshare · doi:10.6084/m9.figshare.27019301
Additional file 2 of The conceptualisation of cardiometabolic disease policy model in the UK
Putri, S., Ciminata, G., Lewsey, J., Jani, B., McMeekin, N., & Geue, C. (2024) · Figshare · doi:10.6084/m9.figshare.27019304
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820853
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820871
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820868
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820859
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820838
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820844
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820862
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820847
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820856
Artegoitia, V. M., Krishnan, S., Bonnel, E. L., Stephensen, C. B., Keim, N. L., & Newman, J. W. (2021) · Figshare · doi:10.6084/m9.figshare.14820841
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Metadata
- Authors
- Kirk, E. P., & Klein, S.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Klein, Samuel
- ORCID
- Klein, Samuel
- Venue
- The Journal of Clinical Hypertension
- Publisher
- Wiley
- Published
- 2009-12
- Volume
- 11
- Issue
- 12
- Pages
- 761-765
- ISSN
- 1524-6175 (ISSN-L)
- 1751-7176
- PMC
- PMC2859214
- OpenAlex
- W1972602644
- Cited by
- 195
- References
- 46
- Citations by year
- 2026: 24 · 2025: 29 · 2024: 19 · 2023: 12 · 2022: 14 · 2021: 25 · 2020: 10 · 2019: 5 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 6 · 2013: 8 · 2012: 5
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Hypertension (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK078738)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- cardiometabolic syndrome, insulin resistance, type 2 diabetes, hypertension, adipose tissue, adipokines, fatty acid metabolism, systemic inflammation, adipose tissue macrophages, hepatic glucose production, muscle glucose uptake, free fatty acids, dyslipidemia, VLDL, cardiovascular risk
- MeSH terms
- Cardiovascular Diseases, Diabetes Mellitus, Type 2, Fatty Acids, Humans, Hypertension, Insulin Resistance, Obesity, Risk Factors, Vasoconstriction, Prevalence, Muscle, Skeletal, Metabolic Syndrome
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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