Histomorphometric changes in the perirenal adipocytes of adrenalectomized rats treated with dexamethasone.

INTRODUCTION: Prolonged steroid treatment administered to any patient can cause visceral obesity, which is associated with metabolic disease and Cushing's syndrome. Glucocorticoids have a profound negative effect on adipose tissue mass, giving rise to obesity, which in turn is regulated by the 11ß-hydroxysteroid dehydrogenase type 1 enzyme. Adrenalectomized rats treated with dexamethasone exhibited an increase in visceral fat deposition but not in body weight. OBJECTIVES: The main aim of this study was to determine the effect of dexamethasone on the histomorphometric characteristics of perirenal adipocytes of adrenalectomized, dexamethasone-treated rats (ADR+Dexa) and the association of dexamethasone treatment with the expression and activity of 11 ß-hydroxysteroid dehydrogenase type 1 (11 ß-hydroxysteroid dehydrogenase type 1). METHODS: A total of 20 male Sprague Dawley rats were divided into 3 groups: a baseline control group (n = 6), a sham-operated group (n = 7) and an adrenalectomized group (n=7). The adrenalectomized group was given intramuscular dexamethasone (ADR+Dexa) 2 weeks post adrenalectomy, and the rats from the sham-operated group were administered intramuscular vehicle (olive oil). RESULTS: Treatment with 120 µg/kg intramuscular dexamethasone for 8 weeks resulted in a significant decrease in the diameter of the perirenal adipocytes (p<0.05) and a significant increase in the number of perirenal adipocytes (p<0.05). There was minimal weight gain but pronounced fat deposition in the dexamethasone-treated rats. These changes in the perirenal adipocytes were associated with high expression and dehydrogenase activity of 11ß-hydroxysteroid dehydrogenase type 1. CONCLUSIONS: In conclusion, dexamethasone increased the deposition of perirenal fat by hyperplasia, which causes increases in the expression and dehydrogenase activity of 11 ß-hydroxysteroid dehydrogenase type 1 in adrenalectomized rats.

Histomorphometric changes in the perirenal adipocytes of adrenalectomized rats treated with dexamethasone

INTRODUCTION: Prolonged steroid treatment administered to any patient can cause visceral obesity, which is associated with metabolic disease and Cushing's syndrome. Glucocorticoids have a profound negative effect on adipose tissue mass, giving rise to obesity, which in turn is regulated by the 11β-hydroxysteroid dehydrogenase type 1 enzyme. Adrenalectomized rats treated with dexamethasone exhibited an increase in visceral fat deposition but not in body weight. OBJECTIVES: The main aim of this study was to determine the effect of dexamethasone on the histomorphometric characteristics of perirenal adipocytes of adrenalectomized, dexamethasone-treated rats (ADR+Dexa) and the association of dexamethasone treatment with the expression and activity of 11 β-hydroxysteroid dehydrogenase type 1 (11 β-hydroxysteroid dehydrogenase type 1). METHODS: A total of 20 male Sprague Dawley rats were divided into 3 groups: a baseline control group (n = 6), a sham-operated group (n = 7) and an adrenalectomized group (n=7). The adrenalectomized group was given intramuscular dexamethasone (ADR+Dexa) 2 weeks post adrenalectomy, and the rats from the sham-operated group were administered intramuscular vehicle (olive oil). RESULTS: Treatment with 120 μg/kg intramuscular dexamethasone for 8 weeks resulted in a significant decrease in the diameter of the perirenal adipocytes (p<0.05) and a significant increase in the number of perirenal adipocytes (p<0.05). There was minimal weight gain but pronounced fat deposition in the dexamethasone-treated rats. These changes in the perirenal adipocytes were associated with high expression and dehydrogenase activity of 11β-hydroxysteroid dehydrogenase type 1. CONCLUSIONS: In conclusion, dexamethasone increased the deposition of perirenal fat by hyperplasia, which causes increases in the expression and dehydrogenase activity of 11 β-hydroxysteroid dehydrogenase type 1 in adrenalectomized rats.

Accessory sulci of the liver. An anatomical study with clinical implications.

OBJECTIVE: To study the presence of accessory sulcus (AS) in the embalmed cadaveric livers, and compare it with the normal liver. METHODS: The present study was conducted on 40 embalmed cadaveric livers in the Department of Anatomy, National University of Malaysia, Kuala Lumpur, Malaysia, from September to October 2007, in order to observe the presence and pattern of anomalous AS. RESULTS: Out of the 40 liver specimens studied, we observed the presence of AS in only 2 specimens 5%. The AS was located in the inferior and posterior surfaces of the right lobes in 2 specimens. CONCLUSION: The AS of the liver is a rare anomaly. Research studies had mainly described the diaphragmatic sulci in the liver, however there are no research reports on the presence of AS in the inferior surface of the right lobe of the liver. The presence of the AS may represent the deep course of the hepatic veins superficially, thus proving to be more beneficial to the hepatobiliary surgeons. The AS may be due to a developmental defect, or may be acquired as a result of pressure by any superficial structure. The precise anatomical knowledge of the AS may also be important for radiologists interpreting CT images of injected veins. The gross anatomical findings of anomalous AS in 2 liver specimens, and its clinical implications are being highlighted in the present study.