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 .
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.
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