Manuel EF

Language: Spanish
References: 7
Page: 14-18
PDF size: 211.95 Kb.

ABSTRACT

The steroid hormones are lipid structures derived from cyclopentaneperhidrofenantren. They are synthesized by the transformation of cholesterol in steroid hormones, this is obtained because the chemical structure is modified in the cytoplasm and nucleus by many enzymatic reaction, with important cofactors, like Cithocrome P-450. The mechanism of action is mediated by receptors that are included in a superfamily of similar characteristics, which also includes estrogens, androgens, progesterone, glucocorticoids, aldosterone, retinoid acid, triiodothyronine, C-erb, etc. These receptors are transcription factors, who are activated by specific ligand. When this occurs, the complex hormone-receptor activates the synthesis of proteins in a very complex form, with a lot of regulations. The adipose tissue does not have the enzymes necessary for the synthesis of steroid hormones, although it could transform androstenedione into testosterone, estrone into estradiol or cortisol into cortisone. This interchange plus the different expression of the receptors and enzymes in visceral and peripheric adipose tissue, could help us to understand the different distribution of adipose tissue in men and women (android and gynoid) in normal and obese people. The regulation of the triglicerid deposit in adipose tissue depends on three mechanisms: the lipoprotein-lipase (LPL), the beta-adrenergic system and the alfa-2-adrenergic system. The glucocorticoids increase the gluteofemoral LPL activity. The progesterone has a competitive action on glucocorticoids receptors in the visceral adipose tissue, impairing the fat deposition in this place and this could explain why men have more central fat than fertile women. The opposite occurs when they become menopausal. In humans the sexual steroid receptors are few in number at the gluteofemoral adipose tissue, so a likely explanation for the action of sexual steroids is that they could interact with glucocorticoid receptors and perhaps also non genomic mechanisms.

REFERENCES

1. Bjontorp-Brodoff. Obesity. Lippincott ed. 2a ed. 1992

2. De Groot Leslie Endocrinology 3a Ed. Saunders 1995

3. Bruce Alberts y col. Biología molecular de la célula 3a edición Editorial Omega 1996.

4. Steven R Smith. The Endocrinology of Obesity. Endocrinology and Metabolism. Clinics of North America 1996; 25: 4.

5. Trent et al. Molecular Medicine. Churchill Livingston Ed. 2a ed. 1997.

6. Montero Julio César. Obesidad en el Adulto. d&p Ediciones Buenos Aires Argentina 1997.

7. Roberts Linsay et al. Estrogens and antiestrogens. Lippincott-Raven 1997.