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Obesity as a cardiovascular risk factor
Abstract
The prevalence of overweight and obesity continues to increase rapidly in the United States, with more than half of all adults currently overweight or obese. In general, people become obese because of a combination of inherited genes and a lifestyle consisting of low levels of physical activity and consumption of excess calories. Obesity, especially the central or visceral type, is a predisposing factor for the development of type 2 diabetes mellitus, hypertension, and cardiovascular disease (CVD). Obesity and type 2 diabetes are associated with insulin resistance. The relation among obesity, insulin resistance, and CVD appears to develop at a relatively young age. Central obesity is linked with hyperinsulinemia, insulin resistance, dyslipidemia, and proinflammatory and prothrombotic clinical states. Adipose tissue synthesizes and secretes biologically active molecules that may affect CVD risk factors. These chemical messengers include adiponectin, resistin, leptin, plasminogen activator inhibitor-1, tumor necrosis factor-alpha, and interleukin-6. In overweight and obese individuals, weight loss may improve insulin sensitivity, leading to reduction in risk factors for CVD and, consequently, the potential for cardiovascular events. Agents that improve insulin sensitivity, such as the thiazolidinediones, have been shown to reduce visceral obesity. Decreases in visceral adipose tissue contribute to improvements in insulin sensitivity and blood pressure, and weight loss reduces serum levels of triglycerides and low-density lipoprotein cholesterol while increasing serum levels of high-density lipoprotein cholesterol. Reduction of risk factors suggests that the development of cardiovascular disease will be reduced by the improvement of insulin sensitivity and weight loss.
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“Indeed, central obesity is undeniably a risk marker, and probably a risk factor for the development and progression of coronary artery disease (43, 105, 185–188, 229, 241, 328).”
From Cardiac remodeling in obesity (2008) · cites this paper as [328]
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Metadata
- Authors
- Sowers, J. R.
- Affiliations
- Harry S. Truman Memorial Veterans' Hospital (US)
- Corresponding author
- Sowers, James R
- ORCID
- Sowers, James R
- Venue
- The American Journal of Medicine
- Publisher
- Elsevier BV
- Published
- 2003-12
- Volume
- 115
- Issue
- 8
- Pages
- 37-41
- ISSN
- 0002-9343 (ISSN-L)
- OpenAlex
- W2053454761
- Cited by
- 584
- References
- 53
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 14 · 2023: 20 · 2022: 17 · 2021: 23 · 2020: 24 · 2019: 15 · 2018: 27 · 2017: 20 · 2016: 23 · 2015: 28 · 2014: 29 · 2013: 21 · 2012: 21
- FWCI
- 5.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The American Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01-HL63904-01)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- obesity, cardiovascular disease, abdominal obesity, visceral adipose tissue, insulin resistance, type 2 diabetes, hyperinsulinemia, dyslipidemia, adipokines, leptin, adiponectin, resistin, weight loss, thiazolidinediones, hypertension, cardiovascular risk factors
- MeSH terms
- Adipose Tissue, Blood Pressure, Cardiovascular Diseases, Humans, Insulin Resistance, Motor Activity, Obesity, Risk Factors, United States, Prevalence
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