The present study aims to clarify the role of fatty acids in regulating pulsatile LH secretion in rats. To produce an acute central lipoprivic condition, mercaptoacetate (MA), an inhibitor of fatty acids oxidation, was administered into the fourth cerebroventricle (4V) in ad libitum fed ovariectomized (OVX) rats (0.4, 2, and 10 micromol/rat) with or without an estradiol (E2) implant producing diestrus plasma E2 levels. Pulsatile LH secretion was suppressed by 4V MA administration in a dose-dependent manner in both OVX and OVX plus E2 rats. Mean LH levels and LH pulse frequency and amplitude were significantly reduced by the highest dose of MA in OVX rats, and by the middle and highest dose of MA in E2-treated rats, suggesting that estrogen enhanced LH suppression. Blood glucose levels increased immediately after the highest dose of MA in both groups. Fourth ventricular injection of trimetazidine (2 and 3 micromol/rat), another inhibitor of fatty acids oxidation, also inhibited pulsatile LH release, resulting in significant and dose-dependent suppression of LH pulse frequency and an increase in blood glucose levels in OVX plus E2 rats. In contrast, peripheral injection of the highest 4V dose of MA (10 micromol/rat) did not alter LH release or blood glucose levels. Microdialysis of the hypothalamic paraventricular nucleus (PVN) revealed that norepinephrine release in the region was increased by 4V MA administration. Preinjection of alpha-methyl-p-tyrosine, a catecholamine synthesis inhibitor, into the PVN completely blocked the lipoprivic inhibition of LH and the counter-regulatory increase in blood glucose levels in OVX plus E2 rats. Together, these studies indicate that fatty acid availability may be sensed by a central detector, located in the lower brainstem to maintain reproduction, and that noradrenergic inputs to the PVN mediate this lipoprivic-induced suppression of LH release.

Abstract. The present study examined the effect of acute lipoprivation on pulsatile luteinizing hormone (LH) secretion in both normal-fat diet, ad libitum-fed and fasted female rats. To produce an acute lipoprivic condition, mercaptoacetate (MA), an inhibitor of fatty acid oxidation, was administered intraperitoneally to ad libitum-fed or 24-h fasted ovariectomized (OVX) rats with or without an estradiol (E2) implant, that produces a negative feedback effect on LH pulses. The steroid treatment was performed to determine the effect of estrogen on lipoprivic changes in LH release, because estrogen enhances fasting-or glucoprivation-induced suppression of LH pulses. Pulsatile LH secretion was suppressed by MA administration in a dose-dependent manner in the ad libitum-fed OVX and OVX+E2 rats. LH pulses were more severely suppressed in the 24-h-fasted OVX and OVX+E2 rats compared to the ad libitum-fed rats. Estrogen slightly enhanced lipoprivic suppression but the effect was not significant. In the present study, increased plasma glucose and free-fatty acid concentrations may indicate a blockade of fatty acid metabolism by the MA treatment, but food intake was not affected by any of the MA doses. Acute vagotomy did not block lipoprivic suppression of LH pulses. Thus, the present study indicates that lipid metabolism is important for maintenance of normal reproductive function even in rats fed a normal-fat diet and lipoprivation may be more critical in fasted animals that probably rely more heavily on fatty acid oxidation to maintain appropriate metabolic fuel levels. In addition, failure of blockade of lipoprivic LH inhibition by vagotomy suggests that lipoprivic information resulting in LH suppression is not transmitted to the brain via the vagus nerve. Key words: Fatty acids, Mercaptoacetate, Gonadotropin, Vagotomy (J. Reprod. Dev. 52: [763][764][765][766][767][768][769][770][771][772] 2006) nergy availability has been considered to be a critical factor maintaining gonadal functions [1] at various reproductive stages in mammalian species, not only in the adult animal [2], but also at the onset of puberty [3,4] and during lactation [5]. Experimentally, food restriction [3,6] or acute food deprivation [7] inhibits pulsatile luteinizing hormone (LH) secretion in rats through central mechanisms [8] and causes suppression of gonadal function. Pulsatile LH release is sensitive to the

Abstract. Acute central lipoprivation suppresses pulsatile luteinizing hormone (LH) release and increases blood glucose levels through noradrenergic input to the hypothalamic paraventricular nucleus (PVN) in female rats. The present study was conducted to identify adrenergic receptor subtypes involved in central lipoprivation-induced suppression of pulsatile LH secretion and increases in plasma glucose levels in female rats. Acute hindbrain lipoprivation was produced by injection into the fourth cerebroventricle (4V) of 2-mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in estradiol-implanted ovariectomized rats. Two min before MA injection, α1-, α2-or β-adrenergic receptor antagonist was injected into the PVN. Injection of MA into the 4V suppresses pulsatile LH release in PVN vehicle-treated rats, whereas pretreatment of animals with injection of α1-or α2-adrenergic antagonist into the PVN blocked the effect of the 4V MA injection on LH pulses. β-Adrenergic antagonist did not affect MA-induced suppression of LH pulses. The counter-regulatory increase in plasma glucose levels after 4V MA injection was also partially blocked by pretreatment with α1-and α2-adrenergic receptor antagonists. These results suggest that α1-and α2-adrenergic receptors in the PVN mediate hindbrain lipoprivation-induced suppression of LH release and counterregulatory increases in plasma glucose levels in female rats. Key words: Adrenergic receptor, Energy sensing, Free fatty acid, Lipoprivation, Mercaptoacetate, Rat (J. Reprod. Dev. 54 : 198-202, 2008) nergy availability is one of the critical factors regulating gonadal function through control of gonadotropin release in mammals at various phases of reproduction, such as the onset of puberty and lactational anestrus [1][2][3][4]. Pulsatile luteinizing hormone (LH) release is suppressed by food restriction or acute food deprivation in rats [1,5,6]. Acute glucoprivation induced by peripheral injection of 2-deoxyglucose (2DG) also results in suppression of LH pulses [7].Glucose availability has been reported to be monitored by a specific sensor(s) located in the brain to regulate food intake [8]. The hindbrain may monitor glucose availability in rats to control food intake and LH release because 2DG injection into the fourth cerebroventricle (4V) increases food intake and suppresses LH release [9]. Glucokinase-immunoreactive ependymocytes in the hindbrain show an in vitro increase in intracellular Ca 2+ levels in response to altered extracellular glucose levels [10], suggesting that ependymocytes in the hindbrain play a role in glucose sensing. In addition, information concerning the glucose availability may partly be conveyed by noradrenergic ascending input into the hypothalamic paraventricular nucleus (PVN) [11].Peripheral and central inhibition of β-oxidation of fatty acids, another metabolic fuel, also suppresses pulsatile LH release in female rats [12,13], suggesting that the fatty acid is a metabolic signal controlling LH release. Our previous study demonstrated that fat...

Galanin-like peptide (GALP), a ligand for three types of galanin receptor, is reported to have a role in regulating luteinising hormone (LH) release in male rodents and primates, but its role in LH release in female rodents remains controversial. The present study was conducted to test whether GALP has a stimulatory role in regulating LH secretion in female rats. The effect of i.c.v. infusion of GALP (5 nmol) on pulsatile LH release was investigated in Wistar-Imamichi strain female rats, or lean and obese Zucker rats. In oestradiol-17beta (oestradiol)-primed ovariectomised (OVX) Wistar-Imamichi female rats, i.c.v. infusion of GALP caused a gradual increase in LH release for the first 1.5 h after the infusion followed by an increased LH pulse frequency during the next 1.5 h, resulting in a significant increase in the mean LH concentrations and baseline levels of LH pulses throughout the sampling period and in the frequency of LH pulses at the last half of the period compared to vehicle-treated controls. The stimulatory effect of GALP was oestrogen-dependent because the same GALP treatment did not affect LH release in OVX rats in the absence of oestradiol. In lean Zucker rats, LH pulses were found in oestradiol-primed OVX individuals and central GALP infusion increased mean LH concentrations in the last half of the period. By contrast, few LH pulses were found in oestradiol-primed OVX obese Zucker rats reportedly with lower hypothalamic GALP expression. Central GALP infusion caused an apparent but transient increase in LH release, resulting in the significant increase in all pulse parameters of LH pulses compared to vehicle-treated controls in the first half of the sampling period. These results suggest that hypothalamic GALP is likely involved in stimulating GnRH/LH release, and that the stimulatory effect of GALP on LH release is oestrogen-dependent in female rats.

Background and Aim: Swine enteric colibacillosis caused by Escherichia coli is a major problem in the swine industry, causing diarrhea among swine and resulting in substantial financial losses. However, efforts to counter this disease are impeded by the increase in antimicrobial resistance (AMR) worldwide, so intensive research is being conducted to identify alternative treatments. This study isolated, characterized, and evaluated the efficacy of bacteriophages to control pathogens causative of swine enteric colibacillosis. Materials and Methods: Five sewage samples were collected from different areas of a swine farm in Suphanburi province, Thailand and the bacteriophages were enriched and isolated, followed by purification by the agar overlay method using E. coli RENR as the host strain. The selected phages were characterized by evaluating their morphology, while their specificity was verified by the host range test. The efficiency of plating and multiplicity of infection (MOI) were also determined. Results: Four selected phages, namely, vB_Eco-RPNE4i3, vB_Eco-RPNE6i4, vB_Eco-RPNE7i1, and vB_Eco-RPNE8i3, demonstrated different patterns of host range and phage efficiency. They significantly decreased E. coli concentration at the tested MOIs (0.01–100) from 1 h onward. However, bacterial regrowth was observed in all phage treatments. Conclusion: This study shows the potential of using phages as an alternative treatment for swine enteric colibacillosis. The obtained results demonstrated that the selected phages had a therapeutic effect against pathogens causative of swine enteric colibacillosis. Therefore, phages could be applied as an alternative treatment to control specific bacterial strains and reduce AMR arising from the overuse of antibiotics.