Regulators of Lipolysis and Fat Storage

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The processes of lipolysis and fat storage are regulated by hormonal factors, which either enhance or suppress the activities of HSL and LPL. Through the action of glucocorticoid receptors, glucocorticoids enhance LPL activity and promote abdominal deposition of fat. The density of glucocorticoid receptors is greater in the visceral abdominal depot than in the subcutaneous abdominal depot. Therefore, an increase in glucocorticoid secretion is associated with increases in abdominal fat deposition compared to other fat depots.

Insulin favors fat storage by increasing LPL and decreasing HSL activity. Insulin has stronger antily-polytic effects in adipose located in the abdominal region compared to the femoral regions in both men and women. Paradoxically, insulin binding is stronger in the gluteal-femoral region than the abdominal region. Therefore, it has been hypothesized that insulin regulates lipolysis at the postreceptor level.

Catecholamines regulate lipolysis through a2- and /3-adrenoreceptors. The /3-adrenoreceptors increase lipolysis, whereas the a2-adrenoreceptor inhibits it. Although both the a2- and the /3-adrenoreceptors coexist in adipose tissue, they are regionally specific such that there may be an excess of one type of receptor relative to the other in various adipose regions. The lipolytic effect of catecholamines is 10-20 times greater in the abdominal region than in the gluteal-femoral region, as marked by a twofold increase in the number of /3-adrenoreceptors in both sexes. The lipolytic action of catecholamines is more pronounced intraabdominally than in the abdominal subcutaneous tissue. Sex differences are displayed with the a-adrenoreceptor. Although the number of receptors is similar in both sexes, the sensitivity of the receptors is reduced by a factor of 10-15 in the abdominal compared with the gluteal-femoral region.

Sex hormones, such as estrogen, testosterone, and progesterone, also affect the balance of fat accumulation/mobilization, although their effects vary in men and women and the mechanisms are not clearly understood. Studies show that estrogen decreases LPL expression and activity in adipose tissue. It has been shown that testosterone stimulates lipolysis by increasing the number of /3-adrenoreceptors. Estrogen and progesterone, on the other hand, stimulate fat storage and inhibit lipolysis, preferentially in the gluteal-femoral area compared to the abdominal area.

An increased androgenic profile is associated with upper body fat accumulation in women, but studies on men are conflicting. Significant inverse associations between fat distribution and testosterone have been found in population studies on men. Reduced visceral fat has also been observed when testosterone treatment was administered to men. These findings challenge the hypothesis that an androgenic hormone profile contributes to a more 'male type' of fat pattern and the associated metabolic sequelae.

The controversy over the effect of sex hormones on fat distribution is complicated by the metabolism of sex hormones. Sex hormone-binding globulin (SHBG) binds circulating testosterone and estrogen. Decreased SHBG concentration may be associated with an android shape. Therefore, studies need to distinguish between total circulating and unbound sex hormones and SHBG.

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