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The impact of insulin resistance, gender, genes, glucocorticoids and ethnicity on body fat distribution


NJ Crowther
WF Ferris

Abstract

The metabolic consequences of obesity are highly dependent on body fat distribution and total body fat mass. Visceral adipose tissue in particular has been found to play an important aetiological role in obesity-related disorders. The contrasting fat distribution between genders, with gynoid and android obesity being characterised by increased subcutaneous and visceral fat deposition respectively, may be directly responsible for differences in obesity-related co-morbidities between the sexes. These differences in adiposity are likely to be directly due to the influence of the sex steroids. Glucocorticoids may further modify body fat distribution, as observed in Cushing’s syndrome in which hypercortisolaemia leads to increased visceral fat mass. Hereditary factors have also been found to be important, with studies demonstrating that up to 55% of the variance in visceral fat mass is genetically determined. Recently, it has been proposed that insulin sensitivity is a major factor that plays a role in determining fat distribution. Although it is accepted that excess adiposity results in insulin resistance, it has been suggested that insulin sensitivity at the level of the adipocyte may modulate the size of the subcutaneous and visceral fat depots. This occurs because insulin resistance retards triglyceride deposition in adipocytes and is therefore associated with reduced adipose tissue growth. It is thought that the subcutaneous depot is the prime site for triglyceride accumulation and, once this depot is lipid replete, triglycerides are diverted to the visceral tissue. The principal determinant of subcutaneous lipid storage capacity is the prevailing level of insulin resistance. This review will discuss all the factors that are thought to influence body fat distribution and will describe the possible role of insulin resistance in this process.

Keywords: visceral fat; subcutaneous fat; cortisol; oestrogen; testosterone


Journal Identifiers


eISSN: 2220-1009
print ISSN: 1608-9677