Triglycerides are stored in two main repositories of white adipose tissue in humans. A subcutaneous store is present under the skin, and this constitutes the store of fat that it visible to the exterior. In addition, humans store fat around the organs abdominally, particularly the liver. Abdominal fat stores are labile and are used readily for energy production should an increased energy supply be required. However, subcutaneous fat is more stable and is not relinquished easily to supply energy needs. Research suggests that subcutaneous fat is not associated with disease whereas abdominal fat increases the risk of cardiovascular disease considerably. This is because excessive abdominal fat accumulation is the result of an underlying metabolic disorder characterised by insulin resistance. In fact, evidence suggests that the peripheral to abdominal adipose tissue is an effective marker for insulin resistance in humans.
For example, researchers1 have investigated the association between insulin resistance and fat distribution in non-diabetic overweight women. The subjects had their insulin sensitivity measured using an oral glucose tolerance test and the hyperinsulinaemic clamp method, and their body composition was assessed using computer tomography with respect to abdominal adipose tissue and dual energy x-ray absorptiometry with respect lean mass and peripheral fat mass. The results showed that those subjects with predominately abdominal fat mass had a significantly higher fasting insulin levels and insulin area under the curve as measured by the oral glucose tolerance test, when compared to those with predominately peripheral fat mass. In addition, those subjects with predominately abdominal fat mass had lower infusion rates for glucose when subjected to a hyperinsulinaemic clamp, compared to subjects with mainly peripheral fat mass. Therefore peripheral fat mass is associated with improved insulin sensitivity.
When the authors assessed the peripheral fat to abdominal fat ratio they found a negative correlation with fasting insulin and area under the curve for insulin and a positive correlation with fat free mass. Therefore the ratio of peripheral to abdominal fat mass is associated with the degree of insulin sensitivity. Insulin resistance is though to develop when the liver becomes overloaded by nutrients, particularly fructose. The oversupply of fructose increases fatty acid production and these fatty acids are stored in the liver and skeletal muscle. Stored fatty acids are thought to interfere with insulin signalling and lead to insulin resistance, which increases the storage of triglycerides centrally, particularly around the liver. These data support this contention by showing that abdominal adiposity correlates with insulin resistance. Abdominal obesity is thought to increase inflammation and oxidative stress, that subsequently increases the risk of cardiovascular disease.
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