alexa Visceral Fat and Association with Metabolic Risk Factors | OMICS International
ISSN: 2161-1165
Epidemiology: Open Access

Like us on:

Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

Visceral Fat and Association with Metabolic Risk Factors

Leonardo S. Roever-Borges1*, Resende ES1

1Department of Clinical Research, Federal University of Uberlândia,San Paulo, Brazil.

*Corresponding Author:
Leonardo S. Roever-Borges
MHS Av. Pará, 1720 - Bairro Umuarama
Uberlândia - MG - CEP 38400-902
Tel: +553488039878
E-mail: [email protected]

Received date: February 13, 2015; Accepted date: February 16, 2015; Published date: February 20, 2015

Citation: Roever-Borges LS, Resende ES (2015) Visceral Fat and Association with Metabolic Risk Factors. Epidemiology(sunnyvale) 5:e118. doi:10.4172/2161-1165.1000E118

Copyright: © 2015 Roever. L et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Epidemiology: Open Access

Abstract

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the world. Globally, more than one billion adults are overweight (BMI≥25 kg/m2). At least 300 million are obese (BMI≥30 kg/m2). Visceral fat (VF) is a risk factor for multiple CVD risk factors, including endothelial dysfunction, hypertension, dyslipidemia, diabetes, impaired glucose metabolism, insulin resistance, metabolic syndrome (MetS), liver insulin resistance, non-alcoholic fatty liver disease, sleep apnea, increased predisposition to cancers of the colon, breast and prostate, and it is associated with prolonged hospital stays,increased incidence of infections and non-infectious complications, and increased mortality in hospital. Age, gender, genetics, and ethnicity are factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage may involve sex hormones, local cortisol production in abdominal adipose tissues, dietary fructose endocannabinoids and growth hormone.

Editorial

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the world. Globally, more than one billion adults are overweight (BMI≥25 kg/m2). At least 300 million are obese (BMI≥30 kg/m2) [1]. The visceral fat (VF) is a risk factor for multiple CVD risk factors, including endothelial dysfunction, hypertension, dyslipidemia, diabetes, impaired glucose metabolism, insulin resistance, metabolic syndrome (MetS), liver insulin resistance, non-alcoholic fatty liver disease, sleep apnea, increased predisposition to cancers of the colon, breast and prostate, and it is associated with prolonged hospital stays, increased incidence of infections and non-infectious complications, and increased mortality in hospital [2-5]. Age, gender, genetics, and ethnicity are factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage may involve sex hormones, local cortisol production in abdominal adipose tissues, dietary fructose endocannabinoids and growth hormone. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storagecapacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral fat [6].

Abdominal obesity itself is an independent component of MetS and VF accumulation also determines a comprehensive cardiovascular risk profile and increases the susceptibility to ischaemic heart disease and arterial hypertension [7-8].

The VF releases different bioactive molecules and hormones, such as adiponectin, leptin, tumour necrosis factor( TNF-α), resistin and interleutin (IL-6, IL-1β)), resistin, adipocyte fatty acid binding protein (A-FABP), omentin-1, and chemerin. Adipokines contribute to the modulation of adipogenesis, immune cell migration into adipose tissue, adipocyte metabolism and function. Adiponectin is inversely correlated with the amount of VF, while decreased concentrations of adiponectin are associated with hypertension, type 2 diabetes, elevated glucose levels, cardiovascular disease and certain malignancies. Hypertriglyceridemia is a central correlate of visceral obesity. It is caused by a combination of increased liver VLDL triglyceride production and impaired clearance from the circulation [9-13].

An important contribution to evaluation of the influence of obesity on cardiovascular risk is the InterHeart Study, which shows evidence that abdominal obesity makes a higher contribution than BMI to the probability of these events[14]. Yusuf et al. defining the results more accurately, showing that the association between abdominal adiposity and coronary heart disease risk is highly significant in all geographical areas in which InterHeart Study data were collected [15].

In a population of 1,498 Caucasian, already showed that there was a strong independent association with VF and both cardiovascular (odd ratio (95% CI):2.45 (1.52–3.95)) and cerebrovascular events (odd ratio (95% CI):1.63 (1.06–2.50)); in the same study, a (ROC) analysis proved greater sensitivity and specificity of VF, compared to its individual components (WC, BMI, HDL, and TG) with regard to cardiovascular and cerebrovascular events [16]. In a large case-control study, a high VF is associated with elevated risk of CHD in Chinese men and women [17]. As visceral obesity is associated with poor prognosis, metabolic disturbances and degree of pathology also occur in several chronic diseases. The VF is metabolically active and associated with insulin resistance, atherosclerosis, metabolic syndrome and CVD. To develop novel aetiology based strategies for the prevention and treatment of these diseases, a better understanding of the molecular mechanisms underlying obesity and its relationship to metabolic and cardiovascular diseases is essential.

Therefore, the identification of VF that regulates the atherosclerotic process might provide new opportunities for developing more effective approaches for preventing and treatment of cardiovascular disease.

References

  1. Go A, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, et al. (2015) Heart Disease and Stroke Statistics—2015 Update A Report From the American Heart Association. Circulation 131: e29-e322.
  2. Ritchie SA, Connell JM (2007) The link between abdominal obesity, metabolic syndrome and cardiovascular disease. NutrMetabCardiovasc Dis 17: 319-326.
  3. Fox CS, Massaro JM, Hoffmann U, Pou KM, Maurovich-Horvat P, et al. (2007) Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study. Circulation 116: 39-48.
  4. Oh TH, Byeon JS, Myung SJ, Yang SK, Choi KS, et al. (2008) Visceral obesity as a risk factor for colorectal neoplasm. J GastroenterolHepatol 23: 411-417
  5. Von H P, Pina F, Pérez A, Tavares M, Barros H (2004) Visceral fat accumulation as a risk factor for prostate cancer. Obes Res 12: 1930-1935
  6. Tchernof A, Després JP (2013) Pathophysiology of human visceral obesity: an update. Physiol Rev 93(1): 359-404.
  7. Mathieu P, Pibarot P, Larose E, Poirier P, Marette A, et al. (2008) Visceral obesity and the heart. Int J Biochem Cell Biol 40: 821-836.
  8. Lamarche B, Lemieux S, Dagenais GR, Després JP (1998) Visceral obesity and the risk of ischaemic heart disease: insights from the Québec Cardiovascular Study. Growth Horm IGF Res 8 Suppl B: 1-8.
  9. Shuster A, Patlas, M, Pinthus, JH, Mourtzakis M (2012) The clinical importance of visceral adiposity: a critical review of methods for visceral adipose tissue analysis. Br J Radiol 85(1009): 1-10.
  10. Kanaya AM, Harris T, Goodpaster BH, Tylavsky F, Cummings SR (2004) Adipocytokines attenuate the association between visceral adiposity and diabetes in older adults. Diabetes Care 27: 1375-1380.
  11. Yatagai T, Nagasaka S, Taniguchi A, Fukushima M, Nakamura T, et al. (2003) Hypoadiponectinemia is associated with visceral fat accumulation and insulin resistance in Japanese men with type 2 diabetes mellitus. Metabolism 52: 1274-1278.
  12. Ebrahimi-Mamaeghani M, Mohammadi S, Arefhosseini SR, Fallah P, Bazi Z (2015) Adiponectin as a potential biomarker of vascular disease. Vasc Health Risk Manag 11: 55-70.
  13. Taskinen MR, Adiels M, Westerbacka J, Soderlund S, Kahri J, et al. (2011) Dual metabolic defects are required to produce hypertriglyceridemia in obese subjects. ArteriosclerThrombVascBiol 31: 2144-2150.
  14. Yusuf S, Hawken S, Ounpuu S (2004) Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. The Lancet 364(9438)(937): 952.
  15. Yusuf S, Hawken S, Ôunpuu S, Bautista L, Franzosi MG, et al. (2005) Obesity and the risk of myocardial infarction in 27 000 participants from 52 countries: a case-control study. The Lancet 366(9497): 1640-1649.
  16. Amato MC, Giordano C, Galia M (2010) Visceral adiposity index: a reliable indicator of visceral fat function associated with cardiometabolic risk. Diabetes Care 33(4): 920-922.
  17. Zhang X, Shu XO, Li H (2013) Visceral adiposity and risk of coronary heart disease in relatively lean Chinese adults. International Journal of Cardiology 168(3): 2141-2145.
Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Relevant Topics

Article Usage

  • Total views: 12008
  • [From(publication date):
    March-2015 - Jul 16, 2018]
  • Breakdown by view type
  • HTML page views : 8200
  • PDF downloads : 3808
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2018-19
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri & Aquaculture Journals

Dr. Krish

[email protected]

+1-702-714-7001Extn: 9040

Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001Extn: 9040

Clinical Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

Food & Nutrition Journals

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

General Science

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics & Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Materials Science Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Nursing & Health Care Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

Ann Jose

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001Extn: 9042

 
© 2008- 2018 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
Leave Your Message 24x7