Prolonged but Not Short Negative Energy Condition Restored Corticoadrenal Leptin Sensitivity in the Hypothalamic Obese Rat

PERELLO M; CASTROGIOVANNI D; GIOVAMBATTISTA A; GAILLARD RC; SPINEDI, E

NEUROENDOCRINOLOGY

Karger AG

Año: 2009 vol. 89 p. 276 - 287

0028-3835

Background/Aim. We have reported that neonatal treatment with monosodium L-glutamate (MSG), which causes damage to the arcuate nucleus leads to severe hyperleptinemia and reduced adrenal leptin receptor (ob-Rb) expression in adulthood. As a result, rats given MSG neonatally display corticoadrenal leptin-resistance, a defect that is overridden by normalization of corticoadrenal hyper-function. The aim of the present study was to determine whether negative energy conditions could correct corticoadrenal cell dysfunction in rats given MSG neonatally. Methods. Normal (CTR) and MSG-treated female rats were subjected to food removal for 1-5 days, or prolonged (24-61 days) food restriction (FR). Plasma levels of several biomarkers, and in vitro corticoadrenal function were evaluated following starvation or FR. Results. Fasting for 1-5 days reduced plasma leptin levels in CTR and MSG rats, compared to levels in the respective groups fed ad libitum (p < 0.05), but adrenal leptin-resistance was unchanged. With prolonged FR, isolated adrenal cells from MSG rats became sensitive to leptin, which lowered ACTH-induced glucocorticoid release. This restoration of leptin response was associated with normalization of adrenal ob-Rb gene expression. Conclusion. Dietary restriction in some leptin-resistant obese phenotypes may normalize adrenocortical function.