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Insulin Resistance in Chronic Heart Failure: Relation to Severity and Etiology of Heart Failure
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Citations
Cites
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“In normal subjects infusion of insulin increases sympathetic activity (11), but infusions of either epinephrine or norepinephrine reduce insulin levels (12,13), suggesting a possible negative feedback mechanism.”
BackgroundEpinephrine-induced insulin resistance in man
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“However, some studies (14,15) have implicated increased catecholamine levels as a cause of insulin resistance (and hyperinsulinemia) in patients without heart disease, indicating that a disturbance of the normal feedback mechanism may occur in insulin-resistant states.”
BackgroundAdrenergic Mechanisms for the Effects of Epinephrine on Glucose Production and Clearance in Man
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“However, some studies (14,15) have implicated increased catecholamine levels as a cause of insulin resistance (and hyperinsulinemia) in patients without heart disease, indicating that a disturbance of the normal feedback mechanism may occur in insulin-resistant states.”
Background
Cited by
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Pathogenesis of insulin resistance in skeletal muscle
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Noncardiac comorbidities in heart failure with reduced versus preserved ejection fraction
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Diabetes, left ventricular systolic dysfunction, and chronic heart failure
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Functional class in patients with heart failure is associated with the development of diabetes
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Metadata
- Authors
- Swan, J. W., Anker, S. D., Walton, C., Godsland, I. F., Clark, A. L., Leyva, F., Stevenson, J. C., & Coats, A. J. S.
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 1997-08
- Volume
- 30
- Issue
- 2
- Pages
- 527-532
- ISSN
- 0735-1097 (ISSN-L)
- OpenAlex
- W1982509198
- Cited by
- 533
- References
- 4
- FWCI
- 7.52
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
