Skip to main content
Log in

Impact of Obesity and Bariatric Surgery on Metabolism and Coronary Circulatory Function

  • Nuclear Cardiology (V Dilsizian, Section Editor)
  • Published:
Current Cardiology Reports Aims and scope Submit manuscript

Abstract

Increases in intra-abdominal visceral adipose tissue have been widely appreciated as a risk factor for metabolic disorders such as dyslipidemia, hypertension, insulin resistance, and type 2 diabetes, whereas this is not the case for peripheral or subcutaneous obesity. While the underlying mechanisms that contribute to these differences in adipose tissue activity remain uncertain, increases in visceral fat commonly induce metabolic dysregulation, in part because of increased venous effluent of fatty acids and/or adipokines/cytokines to the liver. Increased body weight, paralleled by an increase in plasma markers of the insulin-resistance syndrome and chronic inflammation, is independently associated with coronary circulatory dysfunction. Recent data suggest that plasma proteins originating from the adipose tissue, such as endocannabinoids (EC), leptin, and adiponectin (termed adipocytes) play a central role in the regulation and control of coronary circulatory function in obesity. Positron emission tomography (PET) in concert with tracer kinetic modeling is a well established technique for quantifying regional myocardial blood flow at rest and in response to various forms of vasomotor stress. Myocardial flow reserve assessed by PET provides a noninvasive surrogate of coronary circulatory function. PET also enables the monitoring and characterization of coronary circulatory function in response to gastric bypass-induced weight loss in initially morbidly obese individuals, to medication and/or behavioral interventions related to weight, diet, and physical activity. Whether the observed improvement in coronary circulatory dysfunction via weight loss may translate to diminution in cardiovascular events awaits clinical confirmation.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2
Fig. 3

Similar content being viewed by others

References

Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

  1. • Apovian CM, Gokce N. Obesity and cardiovascular disease. Circulation. 2012;125:1178–82. This review article provides an excellent update on the relationship between obesity and cardiovascular disease.

    Article  PubMed Central  PubMed  Google Scholar 

  2. Cornier MA, Despres JP, Davis NE, et al. Assessing adiposity: a scientific statement from the American Heart Association. Circulation. 2011;124:1996–2019.

    Article  PubMed  Google Scholar 

  3. Rexrode KM, Carey VJ, Hennekens CH, Walters EE, Colditz GA, Stampfer MJ, et al. Abdominal adiposity and coronary heart disease in women. JAMA. 1998;280:1843–8.

    Article  CAS  PubMed  Google Scholar 

  4. Lissner L, Björkelund C, Heitmann BL, Seidell JC, Bengtsson C. Larger hip circumference independently predicts health and longevity in a Swedish female cohort. Obes Res. 2001;9:644–6.

    Article  CAS  PubMed  Google Scholar 

  5. Brook RD, Bard RL, Rubenfire M, Ridker PM, Rajagopalan S. Usefulness of visceral obesity (waist/hip ratio) in predicting vascular endothelial function in healthy overweight adults. Am J Cardiol. 2001;88:1264–9.

    Article  CAS  PubMed  Google Scholar 

  6. •• Schindler TH, Cardenas J, Prior JO, Facta AD, Kreissl MC, Zhang X-L, et al. Relationship between increasing body weight, insulin resistance, inflammation, adipocytokine leptin, and coronary circulatory function. J Am Coll Cardiol. 2006;47:1188–95. These observations are the first to describe independent adverses effects of increased body weight on coronary circulatory function.

    Article  CAS  PubMed  Google Scholar 

  7. Pascot A, Després JP, Lemieux I, Bergeron J, Nadeau A, Prud’homme D, et al. Contribution of visceral obesity to the deterioration of the metabolic risk profile in men with impaired glucose tolerance. Diabetologia. 2000;43:1126–35.

    Article  CAS  PubMed  Google Scholar 

  8. Reaven G. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988;37:1595–607.

    Article  CAS  PubMed  Google Scholar 

  9. Widén E, Lehto M, Kanninen T, Walston J, Shuldiner AR, Groop LC. Association of a polymorphism in the beta 3-adrenergic-receptor gene with features of the insulin resistance syndrome in Finns. N Engl J Med. 1995;333:348–51.

    Article  PubMed  Google Scholar 

  10. Yokota T, Oritani K, Takahashi I, Ishikawa J, Matsuyama A, Ouchi N, et al. Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages. Blood. 2000;96:1723–32.

    CAS  PubMed  Google Scholar 

  11. •• Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444:860–7. This review provides very valuable information on mediators and the inflammatory state in obesity.

    Article  CAS  PubMed  Google Scholar 

  12. Conway JM, Yanovski SZ, Avila NA, Hubbard VS. Visceral adipose tissue differences in black and white women. Am J Clin Nutr. 1995;61:765–71.

    CAS  PubMed  Google Scholar 

  13. •• Hamdy O, Porramatikul S, Al-Ozairi E. Metabolic obesity: the paradox between visceral and subcutaneous fat. Curr Diabetes Rev. 2006;2:367–73. This review article provides a very thorough update on metabolic differences between intraabdominal visceral and subcutaneous fat.

    Article  PubMed  Google Scholar 

  14. Pouliot MC, Després JP, Nadeau A, Moorjani S, Prud’Homme D, Lupien PJ, et al. Visceral obesity in men. Associations with glucose tolerance, plasma insulin, and lipoprotein levels. Diabetes. 1992;41:826–34.

    Article  CAS  PubMed  Google Scholar 

  15. Tankó LB, Bagger YZ, Alexandersen P, Larsen PJ, Christiansen C. Peripheral adiposity exhibits an independent dominant antiatherogenic effect in elderly women. Circulation. 2003;107:1626–31.

    Article  PubMed  Google Scholar 

  16. Seidell JC, Pérusse L, Després JP, Bouchard C. Waist and hip circumferences have independent and opposite effects on cardiovascular disease risk factors: the Quebec Family Study. Am J Clin Nutr. 2001;74:315–21.

    CAS  PubMed  Google Scholar 

  17. Alagna S, Cossu ML, Gallo P, Tilocca PL, Pileri P, Alagna G, et al. Biliopancreatic diversion: long-term effects on gonadal function in severely obese men. Surg Obes Relat Dis. 2006;2:82–6.

    Article  PubMed  Google Scholar 

  18. Foster MT, Pagliassotti MJ. Metabolic alterations following visceral fat removal and expansion: beyond anatomic location. Adipocyte. 2012;1:192–9.

    Article  PubMed Central  PubMed  Google Scholar 

  19. Daniels SR, Morrison JA, Sprecher DL, Khoury P, Kimball TR. Association of body fat distribution and cardiovascular risk factors in children and adolescents. Circulation. 1999;99:541–5.

    Article  CAS  PubMed  Google Scholar 

  20. Van Pelt RE, Evans EM, Schechtman KB, Ehsani AA, Kohrt WM. Contributions of total and regional fat mass to risk for cardiovascular disease in older women. Am J Physiol Endocrinol Metab. 2002;282:E1023–8.

    PubMed  Google Scholar 

  21. Drapeau V, Lemieux I, Richard D, Bergeron J, Tremblay A, Biron S, et al. Metabolic profile in severely obese women is less deteriorated than expected when compared with moderately obese women. Obes Surg. 2006;16:501–9.

    Article  PubMed  Google Scholar 

  22. Wolf AM, Buffington C, Beisiegel U. Comparison of metabolic risk factors between severely and very severely obese patients. Obesity. 2006;14:2177–83.

    Article  PubMed  Google Scholar 

  23. Faintuch J, Marques PC, Bortolotto LA, Faintuch JJ, Cecconello I. Systemic inflammation and cardiovascular risk factors: are morbidly obese subjects different? Obes Surg. 2008;18:854–62.

    Article  PubMed  Google Scholar 

  24. •• Schindler TH, Schelbert HR, Quercioli A, Dilsizian V. Cardiac PET imaging for the detection and monitoring of coronary artery disease and microvascular health. JACC Cardiovasc Imaging. 2010;3:623–40. This review provides an excellent update on clinical and research possibilities of noninvasive MBF quantification with PET/CT.

    Article  PubMed  Google Scholar 

  25. Oliak D, Ballantyne GH, Davies RJ, Wasielewski A, Schmidt HJ. Short-term results of laparoscopic gastric bypass in patients with BMI> or =60. Obes Surg. 2002;12:643–7.

    Article  PubMed  Google Scholar 

  26. Marette A, Mauriège P, Marcotte B, Atgié C, Bouchard C, Thériault G, et al. Regional variation in adipose tissue insulin action and GLUT4 glucose transporter expression in severely obese premenopausal women. Diabetologia. 1997;40:590–8.

    Article  CAS  PubMed  Google Scholar 

  27. •• Quercioli A, Pataky Z, Vincenti G, Makoundou V, Di Marzo V, Montecucco F, et al. Elevated endocannabinoid plasma levels are associated with coronary circulatory dysfunction in obesity. Eur Heart J. 2011;32:1369–78. This study is the first to describe adverse effects of increases in endocannabinoid plasma levels on coronary circulatory function in obesity.

    Article  CAS  PubMed  Google Scholar 

  28. • Valenta I, Dilsizian V, Quercioli A, Schelbert HR, Schindler TH. The influence of insulin resistance, obesity, and diabetes mellitus on vascular tone and myocardial blood flow. Curr Cardiol Rep. 2012;14:217–25. Excellent review article describing the potential of PET flow quantification in the assessment of coronary circulatory dysfunction in the pre-diabetic and diabetic state.

    Article  PubMed  Google Scholar 

  29. • Goldstein BJ, Scalia RG, Ma XL. Protective vascular and myocardial effects of adiponectin. Nat Clin Pract Cardiovasc Med. 2009;6:27–35. Excellent overview article on the role of adiponectin in the cardiovascular system.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  30. •• Quercioli A, Pataky Z, Montecucco F, Carballo S, Thomas A, Staub C, et al. Coronary vasomotor control in obesity and morbid obesity: contrasting flow responses with endocannabinoids, leptin, and inflammation. JACC Cardiovasc Imaging. 2012;5:805–15. Important investigation, which identifies and characterizes obesity and morbid obesity as different disease entities affecting coronary circulatory function.

    Article  PubMed  Google Scholar 

  31. •• Quercioli A, Montecucco F, Pataky Z, Thomas A, Ambrosio G, Staub C, et al. Improvement in coronary circulatory function in morbidly obese individuals after gastric bypass-induced weight loss: relation to alterations in endocannabinoids and adipocytokines. Eur Heart J. 2013;34:2063–73. This investigation is the first to demonstrate a normalization of coronary circulatory function after gastric bypass-induced weight loss in initially morbidly obese individuals.

    Article  PubMed  Google Scholar 

  32. Benraouane F, Litwin SE. Reductions in cardiovascular risk after bariatric surgery. Curr Opin Cardiol. 2011;26:555–61.

    Article  PubMed  Google Scholar 

  33. • Valenta I, Dilsizian V, Quercioli A, Ruddy TD, Schindler TH. Quantitative PET/CT measures of myocardial flow reserve and atherosclerosis for cardiac risk assessment and predicting adverse patient outcomes. Curr Cardiol Rep. 2013;15:344. Thorough review on the potential of cardiac PET/CT in the detection and identification of CAD process and prognostic implications.

    Article  PubMed  Google Scholar 

  34. •• Gokce N, Vita JA, McDonnell M, Forse AR, Istfan N, Stoeckl M, et al. Effect of medical and surgical weight loss on endothelial vasomotor function in obese patients. Am J Cardiol. 2005;95:266–8. The study is first to denote the effects of bariatric surgery-induced weight loss on flow-mediated brachial artery function.

    Article  PubMed  Google Scholar 

  35. Watts K, Beye P, Siafarikas A, Davis EA, Jones TW, O’Driscoll G, et al. Exercise training normalizes vascular dysfunction and improves central adiposity in obese adolescents. J Amer Coll Cardiol. 2004;43:1823–7.

    Article  Google Scholar 

  36. •• Ziadi MC, Dekemp RA, Williams KA, Guo A, Chow BJW, Renaud JM, et al. Impaired myocardial flow reserve on rubidium-82 positron emission tomography imaging predicts adverse outcomes in patients assessed for myocardial ischemia. J Am Coll Cardiol. 2011;58:740–8. This study enrolled prospectively 704 patients with suspected and known CAD who underwent 82Rb- PET perfusion measurements and MFR calculation. The noninvasively calculated MFR predicted hard cardiac events and major adverse cardiac events independent of the presence of stress- induced myocardial perfusion defects and other parameters.

    Article  PubMed  Google Scholar 

  37. •• Herzog BA, Husmann L, Valenta I, Gaemperli O, Siegrist PT, Tay FM, et al. Long-term prognostic value of 13N-ammonia myocardial perfusion positron emission tomography added value of coronary flow reserve. J Am Coll Cardiol. 2009;54:150–6. This is a retrospectively performed study in 245 patients with suspicion for CAD. In patients with normal PET perfusion imaging the evaluation of the MFR proved to be a strong outcome predictor, whereas a reduced MFR in those with stress-induced perfusion defects improved the prediction of an adverse outcome.

    Article  PubMed  Google Scholar 

  38. Després JPLI. Abdominal obesity and metabolic syndrome. Nature. 2006;444:881–7.

    Article  PubMed  Google Scholar 

  39. Després JP, Lemieux I, Bergeron J, Pibarot P, Mathieu P, Larose E, et al. Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk. Arterioscler Thromb Vasc Biol. 2008;28:1039–49.

    Article  PubMed  Google Scholar 

  40. •• Gaborit B, Jacquier A, Kober F, Abdesselam I, Cuisset T, Boullu-Ciocca S, et al. Effects of bariatric surgery on cardiac ectopic fat: lesser decrease in epicardial fat compared with visceral fat loss and no change in myocardial triglyceride content. J Am Coll Cardiol. 2012;60:1381–9. Excellent investigation, which assessed the effects of bariatric surgery-induced weight loss on cardiac ectopic fat in comparison with visceral fat.

    Article  PubMed  Google Scholar 

  41. Karastergiou K, Evans I, Ogston N, Miheisi N, Nair D, Kaski JC, et al. Epicardial adipokines in obesity and coronary artery disease induce atherogenic changes in monocytes and endothelial cells. Arterioscler Thromb Vasc Biol. 2010;30:1340–6.

    Article  CAS  PubMed  Google Scholar 

  42. Mazurek T, Zhang L, Zalewski A, Mannion JD, Diehl JT, Arafat H, et al. Human epicardial adipose tissue is a source of inflammatory mediators. Circulation. 2003;108:2460–6.

    Article  PubMed  Google Scholar 

  43. Gaborit B, Kober F, Jacquier A, Moro PJ, Cuisset T, Boullu S, et al. Assessment of epicardial fat volume and myocardial triglyceride content in severely obese subjects: relationship to metabolic profile, cardiac function and visceral fat. Int J Obes. 2012;36:422–30.

    Article  CAS  Google Scholar 

  44. • Gaborit B, Kober F, Jacquier A, Moro PJ, Flavian A, Quilici J, et al. Epicardial fat volume is associated with coronary microvascular response in healthy subjects: a pilot study. Obesity. 2012;20:1200–5. This study provides the first evidence of direct effects of epicardial fat on coronary arteriolar function.

    Article  CAS  PubMed  Google Scholar 

  45. Venteclef N, Guglielmi V, Balse E, Gaborit B, Cotillard A, Atassi F, et al. Human epicardial adipose tissue induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines. Eur Heart J. 2013. [Epub ahead of print].

  46. Halberg N, Khan T, Trujillo ME, Wernstedt-Asterholm I, Attie AD, Sherwani S, et al. Hypoxia-inducible factor 1alpha induces fibrosis and insulin resistance in white adipose tissue. Mol Cell Biol. 2009;29:4467–83.

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  47. Hammer S, van der Meer RW, Lamb HJ, Schär M, de Roos A, Smit JW, Romijn JA. Progressive caloric restriction induces dose-dependent changes in myocardial triglyceride content and diastolic function in healthy men. J Clin Endocrinol Metab. 2008;93:497–503.

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgments

This work was supported by Research Grant 3200B0-122237 of the Swiss National Science Foundation (SNF), with contributions of the Clinical Research Center, University Hospital and Faculty of Medicine, Geneva, and the Louis-Jeantet Foundation, Gustave and Simone Prevot, and Swiss Heart Foundation, Switzerland.

Compliance with Ethics Guidelines

Conflict of Interest

Ines Valenta declares that she has no conflict of interest. Vasken Dilsizian declares that he has no conflict of interest. Alessandra Quercioli declares that she has no conflict of interest. Freimut D. Jüngling declares that he has no conflict of interest. Giuseppe Ambrosio is a member of the American College of Cardiology Committee on Cardiovascular Prevention. Richard Wahl declares that he has no conflict of interest. Thomas H. Schindler has received grant support from the Swiss National Research Foundation (SNF), the Swiss Heart Foundation, the Center of Clinical Research (Geneva), Prevot Foundation, and the Novartis Research Foundation.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Thomas H. Schindler.

Additional information

This article is part of the Topical Collection on Nuclear Cardiology

Rights and permissions

Reprints and permissions

About this article

Cite this article

Valenta, I., Dilsizian, V., Quercioli, A. et al. Impact of Obesity and Bariatric Surgery on Metabolism and Coronary Circulatory Function. Curr Cardiol Rep 16, 433 (2014). https://doi.org/10.1007/s11886-013-0433-8

Download citation

  • Published:

  • DOI: https://doi.org/10.1007/s11886-013-0433-8

Keywords

Navigation