nsulin resistance in the likely cause of obesity. Dysfunction of the receptor signal pathway leads to an inability to oxidise fatty acids and glucose, and as a result ingested food is diverted away from skeletal muscle for oxidation and towards adipose tissue for storage. This is measurable scientifically as a blunted thermogenic response following the ingestion of food, caused by decreased sympathetic nervous system activation. This decrease in the thermic effect of food (TEF) is associated with adipose tissue accretion and abdominal obesity. In non-insulin resistant individuals of normal weight, ingestion of food causes a normal thermogenic response, initiated by catecholamines interacting with β-adrenergic receptors. As energy intakes rise above that required for metabolic needs, mechanism are upregulated to curtail excessive energy storage. Satiety is increased and food intake is reduced, but most importantly, excess energy is diverted for oxidation in skeletal muscle.
In obese individuals then, catecholamine release and thermogenesis are blunted and this causes weight gain. This explains the weight loss effects of caffeine and other methylxanthines, compounds that are known to stimulate the release of catecholamines and increase sympathetic nervous tone. In insulin resistance, the fat accumulation has a characteristic pattern, and as such this can be used as a loose clinical biomarker for the presence of metabolic dysfunction. Fat stored in the subcutaneous adipose tissue (SAT) directly under the skin tends to be uniform in distribution, and is not though to cause deleterious health effects. On the contrary, SAT provides insulation against cold, and is the primary repository of stored energy, thus preventing fat accumulation in other areas. In contrast, visceral adipose tissue (VAT) is a store of excess adipose tissue in and around organs, most notably the liver, which can lead to severe metabolic problems.
Researchers1 have investigated the association between visceral adipose tissue and the risk of cardiovascular disease in 4144 subjects, including those with type 2 diabetes. Visceral adipose tissue was estimated using cross-sectional computerised tomography and plasma biomarkers for cardiovascular disease were measured from a blood sample. The results showed that visceral adipose tissue was associated with biomarkers for insulin resistance, hepatic fat accumulation and the systemic inflammatory marker C-reactive protein. A more detrimental lipid profile characterised by higher ApoB (very-low, low and intermediate density lipoproteins and lipoprotein(a)), and lower high density lipoprotein (HDL) cholesterol was also associated with VAT. A positive correlation between VAT and type 2 diabetes in both men and women, independent of body mass index, was also evident. However, subcutaneous adipose tissue was inversely associated with type 2 diabetes in women, but not men.
Visceral adipose tissue, but not subcutaneous adipose tissue, is therefore associated with a number of metabolic risk factors for cardiovascular disease. These association were present in subjects irrespective of the presence of type 2 diabetes, suggesting that any individuals with abdominal obesity increases their risk of cardiovascular disease, even if apparently healthy. The association between lipoprotein changes and cardiovascular disease is explained by visceral adipose tissue accumulation, which results in hepatic liver dysfunction due to ectopic fat accumulation. The actual cause of the cardiovascular disease is more likely to be the inflammation that results from macrophage infiltration to the accumulated abdominal fat tissue. Such infiltration causes release of cytokines that lead to systemic inflammation and this may deplete antioxidant defences and increase susceptibility to cardiovascular disease. In particular, depletion of vitamin C would cause scurvy like bleeding from the endothelial lining of arteries that could initiate cardiovascular disease.
Research suggests that improving diet quality is more effective at reducing visceral fat, whereas exercise is more effective at reducing subcutaneous fat. This is logical, because subcutaneous fat is a store of energy for the purpose of providing skeletal muscle with the ability to perform work. Exercise then can harness this energy to increase force generation and at the same time the accumulated fat is reduced in quantity. However, visceral fat is the result of a metabolic abnormality caused by poor diet, particularly one high in refined carbohydrate. Such diets are thought to be a major cause of insulin resistance that leads to abdominal fat accumulation. Dietary alterations to remove or reduce refined carbohydrates and replace them with alternatives, are therefore necessary to reverse the insulin resistance and reduce visceral fat tissue. This explains why low carbohydrate diets reduce adiposity without the need for calorie restriction (here).
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