One theory proposes that once the storage capacity of subcutaneous adipose tissue (SAT) depots is exceeded under conditions of energy excess, either as a result of impaired expandability and / or excessive hypertrophic growth, fat deposition within visceral depots and non-adipose tissues including the liver, skeletal muscle and pancreas can ensue.93 This can subsequently lead to the
development of systemic IR and a series of associated cardiometabolic disorders including dyslipidaemia, dysglycaemia, hyperinsulinaemia and hypertension.3 Expression of pro-inflammatory mediators including interleukins 1 (IL - 1), 6 (IL - 6),
tumour necrosis factor alpha (TNF - α) and resistin, are also increased which can further potentiate IR and
promote atherosclerosis.