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Effect of a High-Fat Diet on 24-Hour Pattern in Expression of Prolactin and Redox Pathway Enzymes in the Rat Adenohypophysis~!2009-06-24~!2009-10-09~!2010-06-09~!

The effect of a high-fat diet (35% fat) on 24-h changes in expression of prolactin and redox pathway enzyme genes was examined in the anterior pituitary of male rats. When body weight of high-fat fed rats attained values about 20- 25 % higher than controls (after 66 days of treatment) animals were sacrificed at 6 different time intervals throughout a 24-h cycle. Anterior pituitary mRNA levels were measured by real-time PCR analysis. In control rats expression of the prolactin gene peaked in anterior pituitary at early scotophase, 3 h in advance to the peak in plasma prolactin levels. In high-fat fed rats this correlation was lost. A disruption of 24-h rhythmicity of pituitary gene expression of heme oxygenase (HO)-2, Cu/Zn- superoxide dismutases (SOD), Mn-SOD, catalase, glutathione peroxidase (GPx) and glutathione reductase (GR) was apparent in high-fat fed rats. Anterior pituitary mRNA levels for nitric oxide synthase (NOS)-2 and HO-2, Cu/Zn- and Mn- SOD and catalase augmented in high-fat fed rats, whereas those of GPx and GR decreased. The results indicate a disrupted coordination between prolactin gene expression and prolactin release in high- fat fed rats that comes along with a disturbed expression of redox enzyme genes in the anterior pituitary.

Melatonin and diet-induced metabolic syndrome in rats: impact on the hypophysial-testicular axis

Abstract Combinations of fructose- and fat-rich diets in experimental animals can model the human metabolic syndrome (MS). In rats, the increase in blood pressure (BP) after diet manipulation is sex related and highly dependent on testosterone secretion. However, the extent of the impact of diet on rodent hypophysial-testicular axis remains undefined. In the present study, rats drinking a 10% fructose solution or fed a high-fat (35%) diet for 10 weeks had higher plasma levels of luteinizing hormone (LH) and lower plasma levels of testosterone, without significant changes in circulating follicle-stimulating hormone or the weight of most reproductive organs. Diet manipulation brought about a significant increase in body weight, systolic BP, area under the curve (AUC) of glycemia after an intraperitoneal glucose tolerance test (IPGTT), and plasma low-density lipoprotein cholesterol, cholesterol, triglycerides, and uric acid levels. The concomitant administration of melatonin (25 μg/mL of drinking water) normalized the abnormally high LH levels but did not affect the inhibited testosterone secretion found in fructose- or high-fat-fed rats. Rather, melatonin per se inhibited testosterone secretion. Melatonin significantly blunted the body weight and systolic BP increase, the increase in the AUC of glycemia after an IPGTT, and the changes in circulating lipid profile and uric acid found in both MS models. The results are compatible with a primary inhibition of testicular function in diet-induced MS in rats and with the partial effectiveness of melatonin to counteract the metabolic but not the testicular sequelae of rodent MS.

Interrelationships of GABAergic, serotoninergic and excitatory amino acid systems in its regulatory effect on prolactin secretion in prepubertal rats.

GABAergic, serotoninergic and excitatory amino acid systems (EAAs) regulate the prolactin (PROL) secretion in prepubertal female rats. The aim of the present paper was to determine the interrelationships of these systems on the control of this pituitary hormone. It was carried out through the following scheme: 1. The participation of the EAAs and serotonin in the effect of GABAergic system on PROL release, determined by evaluating the GABA A and GABA B receptor agonists. It was carried out on animals that were previously treated with AAEs receptor antagonist or p-chlorophenylamphetamine (PCA), this one depleting serotonin in the hypothalamus. 2. The participation of GABAergic system in the effect of serotonin and EAAs systems, determined by the evaluation of the effects of EAAs receptor agonists and of 5-HTP, a serotonin precursor. With this purpose the rats were previously treated with GABA A and GABA B receptor antagonists. 3. The interrelationships between the EAAs and the serotoninergic systems in the control of PROL secretion, determined (a) by using EAAs agonists (in rats depleted of serotonin by PCA) and (b) using EAAs antagonists (in rats treated with 5-HTP, a serotonin precursor). The administration of GABAergic agonists significantly increased PROL secretion in prepubertal female rats. Neither EAAs antagonists nor the depletion of serotonin in the brain, modified the stimulatory effects of the GABAergic system on PROL levels. This is a clear indication that the activity of the GABAergic system is independent of the serotoninergic and of the EAAs system effects on the pituitary hormone. The EAAs neurotransmitter system agonists significantly increase PROL levels. This effect was blocked by the GABAergic system antagonists but was not modified by serotonin depletion. Taking into account these facts it may be considered that the GABAergic system is involved in the stimulatory effect of EAAs on PROL secretion, this effect being independent of the serotoninergic system. 5-HTP significantly increased PROL plasma levels, and this effect was modified neither by the GABAergic nor by the EAAs receptor antagonists. These results indicate that the stimulatory effect of serotonin on PROL release is independent of the GABAergic and EAAs systems. In conclusion it may be considered that in prepubertal female rats, the GABAergic and serotoninergic systems stimulate PROL secretion by independent mechanisms that do not include EAAs. On the other hand, the effects of EAAs neurotransmission are exerted via the GABAergic system.