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Visceral fat deposits – not all fat deposits carry the same risk

28th July 2018, Dr Chee L Khoo

Visceral obesity is a better correlate with cardiometabolic risk, morbidity and mortality than general obesity. However, not all visceral fat depositions are the same. Some visceral fat depositions are worse than others in their contribution to atherosclerosis and cardiometabolic risk. The development of new imaging techniques has revolutionised the study of human body composition including measures of visceral fat. It has allowed us to measure ectopic fat deposits, deposits in areas of the body where fat is not physiologically stored – liver, pancreas, and heart.

Personal fat threshold

There was some confusion with interpreting earlier imaging data looking at contribution of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) to cardiometabolic risk (1). In different individuals, the SAT has a finite expansion capacity. SAT should be considered the metabolic sink for excess triglycerides. Once this sink is full, visceral and ectopic fat deposition occurs. The hypothesis is that the plasticity and expandability of SAT protects individuals from visceral and ectopic fat deposition and subsequent metabolic health consequences lead to the concept of a so-called personal fat threshold (2) which, if exceeded, increases the likelihood of developing metabolic disturbances such as type 2 diabetes, even when overall BMI is in the normal or mildly overweight range.

The VAT is drained by the portal vein. Visceral adiposity exposes the liver to high concentrations of free fatty acids and triglycerol leading to severe impairments in liver metabolisms such as reduced  insulin action, increased glucose production and increased production of triglyceride-rich-lipoproteins. This explains the link between VAT and glucose intolerance and lipid derangements we see in type 2 diabetes.

The expanded VAT becomes inflamed because of the infiltration of macrophages among hypertrophied adipocytes leads to increased production of inflammatory cytokines and reduced production of a protective adipokine, adiponectin. Epicardial adipose tissue (EAT) is a visceral fat deposit, located between the myocardial surface and the pericardium. Because of its proximity to the coronary arteries, there is evidence that epicardial fat exerts a more localized paracrine effect on the coronary arteries and heart, through local production and release of inflammatory cytokines into the coronary circulation (3).

The amount of EAT is reported to be associated with adverse cardiac structure and function and atrial fibrillation (AF). Severity of EAT accumulation also appears to be associated with stroke and MACEs in AF [4,5]. Pierdomenico et al. suggested that the EAT volume  was independently related to left ventricular hypertrophy after adjusting for confounding factors, including hypertension [6].

In a recent study, EAT thickness as determined by transthoracic echo, was found to be increased in CAD patients and is related to both presence and severity of CAD (7). In yet another study, EAT volume was linked to poorer outcomes three years post PCI independent of the usual cardiovascular risk factors (8).

How useful is this information?

If we reduce calorie intake, we should lose weight. There is evidence that any reduce calorie diet will lose both SAT and VAT.  In a 2-year dietary randomised controlled trial, and its 4-year follow-up (9) it was found that Mediterranean and low-carbohydrate diets were effective in improving cardiometabolic state and reversing carotid atherosclerosis (10). The PREDIMED study demonstrated reductions in cardiovascular events with the Mediterranean diet (11). It is also unclear whether defined clinical outcomes of such interventions can be directly attributed to losses of distinct fat depots beyond reduction in total body weight.

What about exercise? How important is it?

A meta-analysis by Sabag et al showed that aerobic type exercise was associated with a significant reduction in VAT in adults with type 2 diabetes (12). A meta-analysis of eight studies compared a hypocaloric diet with exercise (13) and found that although both strategies significant reduce VAT, a 5% loss in bodyweight led to a 21% reduction in VAT after exercise, whereas there was only a 13% reduction in VAT a hypocaloric diet. Hammond et al concludes in a review that moderate to high intensity exercises(50–70% VO2 peak) in adults is associated with substantial reductions in VAT and SAT (14).

A novel trial looking at sedentary adults with obesity or dyslipidaemia randomised subjects to either a low-calorie diet, low carbohydrate Mediterranean diet with or without added moderate intensity exercise (15). All groups lost weight but low carbohydrate, Mediterranean diet combined with being physically active lost more ectopic fat (pericardial and intrahepatic fat mass). More importantly, reduction in pericardial and intrahepatic fat were associated with improvement in lipid profile and insulin sensitivity compared with subcutaneous loss.

In summary, visceral fat has a stronger correlation with cardiometabolic risks than subcutaneous fat although some visceral fat deposits have a worse prognosis than others. With better imaging technology, we are now able to be more specific in where the visceral fat deposits are. Epicardial and intrahepatic fat deposits appears to be more correlated with elements of the metabolic syndrome and atherosclerotic cardiovascular disease. Weight loss with diet alone is insufficient to improve those cardiometabolic risks. Diet and exercise are needed.

References

  1. Abate N, Garg A, Peshock RM, Stray-Gundersen J, Grundy SM. Relationships of generalized and regional adiposity to insulin sensitivity in men. J Clin Invest 1995; 96: 88–
  2. Cuthbertson DJ, Steele T, Wilding JP, et al. What have human experimental overfeeding studies taught us about adipose tissue expansion and susceptibility to obesity and metabolic complications? Int J Obes (Lond) 2017; 41: 853–
  3. Xu Y, Cheng X, Hong K, Huang C, Wan L, authors. How to interpret epicardial adipose tissue as a cause of coronary artery disease: A meta-analysis. Coron Artery Dis. 2012;23:227–33
  4. RoeverE.S. ResendeA. DinizN. Penha-SilvaJ.L. O’ConnellP. Gomes (2018) Epicardial adipose tissue and carotid artery disease: protocol for systematic review and meta-analysis. Medicine 97, e0273 10.1097/MD.0000000000010273 29702973
  5. A. GoudisI.E. VasileiadisT. Liu (2018) Epicardial adipose tissue and atrial fibrillation: pathophysiological mechanisms, clinical implications, and potential therapies. Curr. Med. Res. Opin., 34, 1933–1943129625530
  6. D. PierdomenicoM. ManciniC. CuccurulloM.D. GuglielmiA.M. PierdomenicoM. Di Nicola (2013) Prediction of carotid plaques in hypertensive patients by risk factors, left ventricular hypertrophy, and epicardial adipose tissue thickness. Heart Vessels 28, 277–283 10.1007/s00380-012-0240-y 22427251
  7. Bhupendra Verma1, Deepak Katyal2, Akhilesh Patel3, Vivek Raj Singh4, Senthil Kumar. Relation of systolic and diastolic epicardial adipose tissue thickness with presence and severity of coronary artery disease (The EAT CAD study). Journal of Family Medicine and Primary Care. J Family Med Prim Care. 8(4): 1470-1475
  8. Changqing Lu, Helei Jia, Zhentao Wang. Association between epicardial adipose tissue and adverse outcomes in coronary heart disease patients with percutaneous coronary intervention. Biosci Rep. 39(5): BSR20182278
  9. Schwarzfuchs D, Golan R, Shai I. Four-year follow-up after two-year dietary interventions. N Engl J Med. 2012;367:1373–1374. doi: 10.1056/NEJMc1204792.
  10. Shai I, Spence JD, Schwarzfuchs D, Henkin Y, Parraga G, Rudich A, Fenster A, Mallett C, Liel-Cohen N, Tirosh A, Bolotin A, Thiery J, Fiedler GM, Blüher M, Stumvoll M, Stampfer MJ; DIRECT Group. Dietary intervention to reverse carotid atherosclerosis. Circulation. 2010;121:1200–1208. doi: 10.1161/CIRCULATIONAHA.109.879254.
  11. Estruch R, Ros E, Salas-Salvadó J, Covas MI, Corella D, Arós F, Gómez-Gracia E, Ruiz-Gutiérrez V, Fiol M, Lapetra J, Lamuela-Raventos RM, Serra-Majem L, Pintó X, Basora J, Muñoz MA, Sorlí JV, Martínez JA, Martínez-González MA; PREDIMED Study Investigators. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368:1279–1290. doi: 10.1056/NEJMoa1200303.
  12. Sabag A, Way KL, Keating SE, et al. Exercise and ectopic fat in type 2 diabetes: a systematic review and meta-analysis. Diabetes Metab 2017; 43: 195–
  13. Verheggen RJ, Maessen MF, Green DJ, Hermus AR, Hopman MT, Thijssen DH. A systematic review and meta-analysis on the effects of exercise training versus hypocaloric diet: distinct effects on body weight and visceral adipose tissue. Obes Rev 2016; 17: 664–
  14. Hammond BP, Brennan AM, Ross R. Exercise and adipose tissue redistribution in overweight and obese adults. In: Lukaski HC, ed. Body composition: health and performance in exercise and sport. Boca Raton: CRC Press, 2017: 109–
  15. Gepner Y, Shelef I, Schwarzfuchs D, et al. Effect of distinct lifestyle interventions on mobilization of fat storage pools: CENTRAL magnetic resonance imaging randomized controlled trial. Circulation 2018; 137: 1143–

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