Dexamethasone and colostrum feeding affect hepatic gluconeogenic enzymes differently in neonatal calves

Plasma glucose concentrations in neonates are influenced by colostrum feeding and by glucocorticoids. We have tested whether a high-glucocorticoid status after birth, as well as colostrum feeding, influences glucose metabolism in association with changes of hepatic expression and activities of gluconeogenic enzymes phosphoenolpyruvate carboxykinase (PEPCK; EC 4.1.1.32) and pyruvate carboxylase (PC; EC 6.4.1.1) in neonatal calves. Calves (n = 14 per group) were fed either colostrum or a milk-based formula with nutrient and energy contents similar to colostrum. Half the calves in each feeding group were treated with dexamethasone (DEXA; 30 microg/[kg BW x d]). Pre- and postprandial blood samples were taken on d 1, 2, 4, and 5 and liver samples were collected on d 5 of life. Dexamethasone treatment increased (P < or = 0.05) plasma concentrations of glucose, insulin, and glucagon more in colostrum-fed than in formula-fed calves but increased (P < or = 0.05) urea concentrations and decreased (P < or = 0.05) concentrations of NEFA, ACTH, and cortisol independent of colostrum vs. formula feeding. Colostrum feeding increased (P < 0.05) plasma glucose, but decreased (P < 0.05) plasma urea concentrations. Glucagon-to-insulin ratios in DEXA-treated and colostrum-fed calves were decreased (P < 0.05). Dexamethasone treatment decreased hepatic mRNA levels and activities of PC (P < 0.001 and P < 0.10) and activities of PEPCK (P < 0.001) but increased (P < 0.001) the glycogen content. Colostrum feeding increased (P < 0.05) mitochondrial PEPCK mRNA levels and PEPCK activities in calves not treated with DEXA but decreased (P < 0.1) amounts of PC mRNA. In conclusion, increased plasma glucose concentrations after DEXA treatment were not associated with a stimulation of hepatic gluconeogenic enzyme activities; however, colostrum feeding probably raised plasma glucose concentrations because of increased hepatic gluconeogenic activities.     

Ontogenesis of mRNA levels and binding sites of hepatic alpha-adrenoceptors in young cattle

Catecholamines affect hepatic glucose production through (alpha- and beta2-) adrenoceptors (AR). We studied mRNA abundance and binding of hepatic alpha-AR in pre-term (P0) calves and in full-term calves at day 0 (F0), day 5 (F5) and day 159 (F159) to test the hypothesis that gene expression and numbers of hepatic alpha-AR in calves are influenced by age and associated with beta2-AR and selected traits of glucose metabolism. mRNA levels of alpha1- and alpha2-AR were measured by real time RT-PCR. alpha1- and alpha2-AR numbers (maximal binding, Bmax) were determined by saturation binding of (3H)-prazosin and (3H)-RX821002, respectively. alpha1- and alpha2-AR subtypes were evaluated by competitive binding. alpha1A-AR mRNA levels were lower in P0 than in F0, F5 and F159 and alpha(2AD)-AR mRNA levels were lower in F159 than in P0, F0 and F5, while alpha2C-AR mRNA levels increased from P0 and F0 to F5 and F159. Bmax of alpha1-AR increased from P0 to F5, then decreased in F159. Bmax of alpha2-AR decreased from F0 to F159. Bmax of alpha1-AR was positively associated with mRNA levels of alpha1A-AR (r = 0.7), Bmax of beta2-AR (r = 0.5) and negatively with hepatic glycogen content (r = -0.6). Bmax of alpha2-AR was negatively associated with Bmax of beta2-AR (r = -0.4). In conclusion, mRNA levels and binding sites of alpha1- and alpha2-AR in calves exhibited developmental changes and were negatively associated with hepatic glycogen content.     

Effects of colostrum feeding and dexamethasone treatment on mRNA levels of insulin-like growth factors (IGF)-I and -II, IGF binding proteins-2 and -3, and on receptors for growth hormone, IGF-I, IGF-II, and insulin in the gastrointestinal tract of neonatal calves

The somatotropic axis regulates growth of the gastrointestinal tract (GIT). In addition, colostrum feeding and glucocorticoids affect maturation of the GIT around birth in mammals. We have measured mRNA levels of members of the somatotropic axis to test the hypothesis that colostrum intake and dexamethasone treatment affect respective gene expression in the GIT. Calves were fed either colostrum or an isoenergetic milk-based formula, and in each feeding group, half of the calves were treated with dexamethasone (DEXA; 30 microg/kg body weight per day). Individual parameters of the somatotropic axis differed (P < 0.05) among different GIT sections and formula feeding increased (P < 0.05) mRNA levels of individual parameters at various sites of the GIT. Effects of DEXA on the somatotropic axis in the GIT partly depended on different feeding. In colostrum-fed calves, DEXA decreased (P < 0.05) mRNA levels of IGF-I (esophagus, fundus, duodenum, and ileum), IGF-II (fundus), IGFBP-2 (fundus), IGFBP-3 (fundus), IGF1R (esophagus, ileum, and colon), IGF2R (fundus), GHR (fundus), and InsR (esophagus, fundus), but in formula-fed calves DEXA increased mRNA levels of IGF-I (esophagus, rumen, jejunum, and colon). Furthermore, DEXA increased (P < 0.05) mRNA levels of IGF-II (pylorus), IGFBP-3 (duodenum), IGF2R (pylorus), and GHR (ileum), but decreased mRNA levels of IGFBP-2 (ileum), and IGF1R (fundus). Whereas formula feeding had stimulating effects, effects of DEXA treatment on the gene expression of parameters of the somatotropic axis varied among GIT sites and partly depended on feeding.     

Ontogeny of mRNA abundance of nuclear receptors and nuclear receptor target genes in young cattle

After birth the development of appropriate detoxification mechanisms is important. Nuclear receptors (NR), such as constitutive androstane receptor (CAR), pregnane X receptor (PXR), peroxisome proliferator-activated receptor-alpha (PPARalpha), retinoid receptors (RAR, RXR), and NR target genes are involved in the detoxification of exogenous and endogenous substances. We quantified abundances of hepatic mRNA of NR and several NR target genes (cytochromes, CYP; cytochrome P450 reductase, CPR; UDP-glucuronosyl transferase, UDP) in calves at different ages. Gene expression was quantified by real-time RT-PCR. Abundance of mRNA of CAR and PXR increased from low levels at birth in pre-term calves (P0) and full-term calves (F0) to higher levels in 5-day-old calves (F5) and in 159-day-old veal calves (F159), whereas mRNA levels of PPARalpha did not exhibit significant ontogenetic changes. RARbeta mRNA levels were higher in F5 and F159 than in F0, whereas no age differences were observed for RARalpha levels. Levels of RXRalpha and RXRbeta mRNA were lower in F5 than in P0 and F0. Abundance of CYP2C8 and CYP3A4 increased from low levels in P0 and F0 to higher levels in F5 and to highest levels in F159. Abundance of CPR was transiently decreased in F0 and F5 calves. Levels of UGT1A1 mRNA increased from low levels in P0 and F0 to maximal level in F5 and F159. In conclusion, mRNA levels of NR and NR target genes exhibited ontogenetic changes that are likely of importance for handling of xeno- and endobiotics with increasing age.     

Differential response of cull cow muscles to the hypertrophic actions of ractopamine-hydrogen chloride

Ractopamine-HCl (RAC) is a beta-adrenergic agonist with variable effects on cattle performance and carcass variables. Cull cows fed RAC (200 mg . head(-1) . d(-1)) demonstrate an increased size of type I and II muscle fibers that does not translate into a larger ribeye area. The objective of this study was to examine the dose-dependent effects of RAC on cull cow muscle morphometrics. Eighty-eight cull beef cows representing 2 breed types (n = 44 each) were fed 0, 100, 200, and 300 mg . head(-1) . d(-1) of RAC for the last 28 d of a 54-d feeding period. On d 54, cows were slaughtered, and samples of the LM and semimembranosus muscle (SM) from 16 randomly selected carcasses (n = 4 per treatment) were taken for measurement of beta (2)-adrenergic receptors and type I, IIA, and IIX myosin heavy chain (MyHC) gene expression. Twenty-four hours postmortem, LM, SM, infraspinatus (INF), and vastus lateralis samples from 40 randomly selected carcasses (n = 10 per treatment) were obtained and frozen for immunohistochemical analysis. Muscle fiber cross-sectional area and diameter, MyHC isoform expression, and fiber-associated nuclei numbers were measured. Ractopamine dosage exhibited differential effects on muscle morphometrics and MyHC gene expression. Muscle fiber cross-sectional area and diameter were increased (P < 0.05) by RAC in INF type I and IIA fibers and SM type IIA fibers. Ractopamine increased (P < 0.05) MyHC type IIX mRNA and tended to increase (P < 0.10) beta(2)-adrenergic receptors in the SM; a change in mRNA abundance was not detected for either gene in the LM. Treatment with RAC decreased (P < 0.05) fiber-associated nuclei numbers in the INF, vastus lateralis, and LM but did not affect (P > 0.05) MyHC or beta-adrenergic receptor expression. These results indicate that cull cow feeding programs may consider supplementing RAC as a means of adding value to cuts within the chuck, such as the INF.     

Characterization of porcine beta1- and beta2-adrenergic receptors in heart, skeletal muscle, and adipose tissue, and the identification of an atypical beta-adrenergic binding site

The objective of this study was to characterize porcine beta1- and beta2-adrenergic receptors (beta1-AR and beta2-AR) in heart, skeletal muscle, and adipose tissue by measuring the binding of a radioligand to cell membrane fragments. In skeletal muscle (LM), [3H]CGP12177 labeled a homogeneous population of beta2-AR as evidenced by the rank order of affinity of catecholamines [(-)isoproterenol > (-)epinephrine > (-)norepinephrine], a high affinity of the binding site for the beta2-AR-agonist clenbuterol (equilibrium dissociation constant, Kd = 16 nM), and a low affinity of the binding site for the beta1-AR-antagonist CGP20712A (Kd = 21 microM). The affinity of ICI118551, a ligand selective for beta2-AR in other species, was uncharacteristically low in porcine LM (Kd = 441 nM), but was consistent with a value reported for the cloned porcine beta2-AR. In heart ventricle, ligand binding revealed a predominant population of beta1-AR, judged by the rank order of affinity of catecholamines [(-)isoproterenol > (-)epinephrine > or = (-)norepinephrine] and high-affinity binding to CGP20712A (Kd = 40 nM). The Kd for ICI118551 (731 nM) was close to that observed at beta2-AR in LM, confirming that ICI118551 is not subtype-selective in the pig. Displacement studies using (-)propranolol, clenbuterol, and (-)isoproterenol revealed a second high-affinity binding site in the heart that was not a beta2-AR and could not be eliminated by guanosine 5'-triphosphate or guanylyli-midodiphosphate. In adipose tissue, an equal number of beta1- and beta2-AR was identified through the binding of clenbuterol and CGP20712A, whereas ICI118551 could not discriminate between these sites. In further experiments, we used 10 microM CGP20712A to eliminate beta1-AR binding and allow accurate Kd values to be determined at beta2-AR for nonselective ligands. Under these conditions, another binding site was observed that had a high affinity for (-)propranolol (Kd = 20 pM), which is inconsistent with beta3- or beta4-AR binding reported elsewhere. Our results indicate that porcine adipose tissue contains beta1-AR, beta2-AR, and an atypical binding site in the proportions 50, 34, and 16%, respectively, of the total binding sites labeled by [3H]CGP12177.     

Ligand binding to the porcine adipose tissue beta-adrenergic receptor.

We measured ligand binding to the beta-adrenergic receptor from porcine adipocytes using tritiated radioligands, dihydroalprenolol (DHA) and CGP-12177 (CGP), and an iodinated radioligand, cyanopindolol (ICP). Binding was measured in a crude plasma membrane preparation. Equilibrium saturation binding was regular for all three ligands; the Kd were approximately 4,000 pM for DHA, 600 pM for CGP, and 100 pM for ICP. Binding was stereospecific with each radioligand. Association of each radioligand was relatively rapid; dissociation was rapid and complete for DHA, initially rapid but ultimately incomplete for CGP, and minimal for ICP. The Kd estimated from kinetic data were approximately 1,000 pM for DHA and 100 pM for CGP. The receptor did not bind phentolamine, an alpha-adrenergic antagonist, except at concentrations greater than 10(-5) M. Propranolol was bound to the receptor with a Ki of approximately 8 nM regardless of the radioligand used. Metoprolol, a purported beta 1-adrenergic specific antagonist, was bound to the receptor with a Ki of approximately 300 nM when the radioligands were CGP or ICP but with a Ki of approximately 1,000 nM when the radioligand was DHA. The Ki for ICI 118,551, a purported beta 2-adrenergic specific antagonist, were approximately 500 nM when the radioligands were DHA or CGP but 125 nM when the radioligand was ICP. Thus, the choice of radioligand can influence the characterization of the beta-adrenergic receptor being studied.     

Acute systemic anaphylaxis in adult domestic fowl: evidence for the protective role of H2-histaminergic and beta 2-adrenergic receptors

Pentobarbital-anesthetized and spontaneously breathing, bovine albumin (BA)-sensitized adult domestic fowl showed acute systemic anaphylaxis to IV injection of antigen (BA), which was characterized by arterial hypotension, central venous hypertension, and bradycardia. Large doses of pyrilamine maleate (/1-receptor antagonist) partially inhibited acute systemic anaphylaxis. On the other hand, metiamide (a specific H2-antagonist) and propranolol (beta-adrenergic antagonist) markedly enhanced the anaphylactic response. Terbutaline (beta 2-agonist), dimaprit (a highly selective H2-agonist), and compound FPL 55712 (a slow-reacting substance of anaphylaxis receptor antagonist) either significantly inhibited or reversed the anaphylactic response. Cimetidine (a newer H2-antagonist) enhanced only central venous pressor response to BA. This investigation appears to suggest a minor role of histamine and a major role of slow-reacting substance of anaphylaxis as chemical mediatiors of anaphylaxis. A protective role of beta 2-adrenergic and H2-histaminergic receptors seem to operate in immediate hypersensitivity reactions in adult domestic fowl.     

Beta-adrenergic receptor activity in ponies with recurrent obstructive pulmonary disease.

Pulmonary function measurements were made in control ponies and in ponies with recurrent obstructive pulmonary disease (principals) during clinical remission and during an attack of acute airway obstruction. The ponies were given beta-adrenergic antagonists and agonists to determine the role of beta receptors in recurrent obstructive pulmonary disease, and to determine the subtypes of beta receptors mediating bronchodilation in ponies. Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Intravenous administration of atropine reversed the effect of atenolol on Cdyn and RL, but was without effect on the decrease in Cdyn and increase in RL observed after butoxamine administration. The beta antagonists did not affect airway function in the control ponies. The effect of beta blockade on Cdyn and RL suggests beta-adrenergic activation in the central and peripheral airways of principal ponies, mediated through both beta 2- and beta 1-adrenergic receptors. The aerosol beta agonists, isoproterenol (beta 1 and beta 2), and clenbuterol (beta 2) attenuated histamine-induced airway obstruction to a similar extent in control ponies that were given histamine IV. In addition, the beta 1 antagonist, atenolol, did not attenuate the bronchodilation observed with isoproterenol. We concluded that, although beta 1- and beta 2-adrenergic receptors exist in pony airways and are activated during acute airway obstruction, bronchodilation in response to beta agonists in ponies seems to be mediated primarily by beta 2-adrenergic receptors.     

Response to ractopamine-hydrogen chloride is similar in yearling steers across days on feed

Yearling steers (n = 2,552; 314 kg of initial BW) were used to evaluate the effects of ractopamine-HCl (RAC) and days on feed on performance, carcass characteristics, and skeletal muscle gene expression in finishing steers. Treatment groups included serial slaughter dates of 150, 171, or 192 d on feed. Within each slaughter date, steers either received RAC (200 mg/steer) daily for the final 28 d or were not fed RAC. All steers were initially implanted with Revalor-IS and were reimplanted with Revalor-S after 75 d on feed. At slaughter, muscle samples from the semimembranosus were collected for mRNA analysis of the beta-adrenergic receptors (beta-AR). Ractopamine administration increased (P < 0.05) ADG, G:F, and HCW and increased (P = 0.08) LM area. Ractopamine did not affect the dressing percentage, USDA yield grade, or quality grade (P > 0.3). There was no change in overall feed intake across the entire feeding period; however, feed intake was increased during the 28-d period during which the steers were fed RAC (P < or = 0.05). Greater days on feed decreased (P < 0.05) ADG, G:F, DMI, and the number of yield grade 1 and 2 carcasses. Also, greater days on feed increased (P < 0.05) HCW, dressing percentage, and the number of prime and choice carcasses, as well as the number of yield grade 4 and 5 carcasses. Increasing days on feed decreased (P < 0.05) the abundance of beta(1)-AR and beta(3)-AR mRNA and increased (P < 0.05) the abundance of beta(2)-AR mRNA in skeletal muscle samples obtained at slaughter. Ractopamine had no effect (P > 0.10) on the abundance of beta(1)-AR or beta(3)-AR mRNA, but tended (P = 0.09) to increase beta(2)-AR mRNA. Additional time-course studies with primary muscle cell cultures revealed that advancing time in culture increased (P < 0.001) beta(2)-AR mRNA but had no effect (P > 0.10) on beta(1)-AR or beta(3)-AR mRNA. We conclude that days on feed and RAC are affecting beta-AR mRNA levels, which could, in turn, impact the biological response to RAC feeding in yearling steers.     

Muscarinic receptor subtypes, β-adrenoceptors and cAMP in the tracheal smooth muscle of conventional and double-muscled calves

The total muscarinic (M₁ + M₂ + M₃) and -adrenergic receptors in the tracheal smooth muscle of conventional and double-muscled calves were identified and characterized with the non-specific antagonists [³H]quinuclidinyl benzilate ([³H]QNB) and [³H]dihydroalprenolol ([³H]DHA) respectively.Although the quantity of -adrenoceptors in double-muscled calves was 25% lower (p<0.05) than in conventional calves (B _max=327±89 fmol/mg protein), adenylate cyclase assays indicated that the basal adenylate cyclase activity and the (–)-isopropylnoradrenaline (ISO)- and sodium fluoride (NaF)-stimulated values were not significantly different between these calves. However, the density of muscarinic receptors in double-muscled calves was 40% higher (p<0.01) than in conventional calves (B _max=2955±625 fmol/mg protein). Subtypes of muscarinic receptors were studied with [³H]telenzepine (M₁-receptors), [³H]AF-DX 384 (M₂-receptors) and [³H]4DAMP (M₁ and M₃-receptors). It was found that in both double-muscled and conventional calves about 40% of the receptors were of the M₃-subtype, the remaining 60% being M₂-receptors.From these results, it is suggested that inflammation of the respiratory tract in double-muscled calves may be complicated by an imbalance between the cholinergic bronchoconstrictor and the -adrenergic bronchodilator components of the autonomic nervous system.     

Abundance of message for insulin-like growth factors-I and -II and for receptors for growth hormone,insulin-like growth factors-I and -II,and insulin in the intestine and liver of pre- and full-term calves

The somatotropic axis and insulin are involved in pre- and postnatal development. In pre- and full-term calves (GrP0 and GrN0; born after 277 and 290 d of pregnancy, respectively) and in preterm calves on d 8 of life after being fed for 7 d (GrP8), we studied whether there are differences in the abundance of messenger RNA (mRNA) of IGF-I and IGF-II and of receptors for GH, IGF-I, IGF-II, and insulin among different intestinal sites (duodenum, jejunum, ileum, and colon) and whether there are ontogenetic differences during the perinatal period in intestine and liver. Intestinal site differences (P < 0.05) existed in mRNA levels of IGF-I and IGF-II and receptors for GH, IGF-I, IGF-II, and insulin. Abundance of mRNA of IGF-I and -II and of receptors for IGF-I and GH was highest (P < 0.05) in the colon, abundance of the receptor for IGF-II was comparably high in the colon and ileum, and that of the receptor for insulin was similarly high in colon, ileum, and jejunum. Among GrP0, GrN0, and GrP8 groups, there were differences (P < 0.05) in mRNA levels of IGF-I and IGF-II and of receptors for GH, IGF-I, IGF-II and insulin. Abundance of mRNA of IGF-I and IGF-II and of receptors for GH, IGF-I, IGF-II and insulin was highest (P < 0.05) in GrP0 calves immediately after birth and was primarily seen in the ileum. In liver, the mRNA levels differed (P < 0.05) among groups for IGF-II and receptors for IGF-I, IGF-II, and insulin, and were highest (P < 0.05) for IGF-II in GrP0, for receptors of IGF-I in GrN0, and were higher (P < 0.05) in GrP0 than GrP8 for receptors of IGF-II. In conclusion, mRNA levels of IGF-I and IGF-II and of receptors for GH, IGF-I, IGF-II, and insulin were different at different intestinal sites and in intestine and liver and changed during the perinatal period.     

Effects of temperature and plane of nutrition on beta-adrenergic receptors in heart, kidney, and liver of lambs

We determined the effects of temperature and feed intake on beta-adrenergic receptors (beta-adrenoceptors) in tissues of sheep. Twenty-four lambs were exposed during three 5-wk periods to either thermoneutral, control (W; 23+/-2 degrees C) or cold (C; 0+/-2 degrees C) temperatures and were fed either ad libitum (A) or restricted (R) levels of feed intake, resulting in four treatment groups: WA, WR, CA, and CR. Hearts, kidneys, and livers were harvested at slaughter and binding of [3H]dihydroalprenolol to plasma membrane extracts was used to determine densities (B(MAX)) and binding affinities (Kd) of beta1 and beta2 adrenoceptors. The B(MAX) values ranged from 12.10 to 201.26 and 3.38 to 12.30 fmol/mg protein for beta1 and beta2 adrenoceptors, respectively; heart and kidney had the highest and lowest values, respectively. Feed restriction reduced (P < .05) beta1 and beta2 receptor densities in heart but increased (P < .05) beta1 receptor density in kidney and liver. Cold temperature exposure reduced beta1 receptor density in heart tissue during feed restriction. The Kd values, ranging from 1.32 to 5.98 nM, were increased (P < .05) by cold exposure and feed restriction in kidney and liver. Because the effectiveness of hormones is a function of their concentrations, binding affinities, and their receptor densities, these results imply that cold temperature exposure and feed restriction could potentially reduce (in heart) and increase (in kidney and liver) metabolic responsiveness of tissues to catecholamines.     

Effect of nutrient intake on the development of the somatotropic axis and its responsiveness to GH in Holstein bull calves

We investigated the effect of increasing nutrient intake on the responsiveness of the GH/IGF-I system in calves fed a high-protein milk replacer. Fifty-four Holstein bull calves were fed one of three levels (low, medium, and high; n = 18 per treatment) of a 30% crude protein, 20% fat milk replacer to achieve target rates of gain of 0.50, 0.95, or 1.40 kg/d, respectively, for low, medium, and high. Six calves per treatment were slaughtered at approximately 65, 85, and 105 kg BW. Additionally, six calves were slaughtered at 1 d of age to provide baseline data. Plasma aliquots from blood samples collected weekly were analyzed for IGF-I, insulin, glucose, NEFA, and plasma urea nitrogen (PUN). Plasma IGF-I and insulin, measured weekly, increased (P < 0.001) with greater nutrient intake from wk 2 of life to slaughter. Plasma glucose and NEFA also increased (P < 0.05) with nutrient intake. In addition, each calf underwent a GH challenge beginning 4 d before the scheduled slaughter. Plasma from blood collected before the first GH injection and 14 and 24 h after the third injection was analyzed for IGF-I and PUN. Response to challenge, calculated as the absolute difference between the prechallenge and 14-h postchallenge plasma IGF-I concentrations, was significant in calves on all three treatments. Plasma urea nitrogen was not different among treatments as measured weekly but decreased (P < 0.001) following GH challenge in all calves. Results of ribonuclease protection assays showed increased expression of hepatic mRNA for GH receptor 1A and IGF-I with increased intake. The amounts of GH receptor and IGF-I mRNA in muscle and adipose, however, were not affected by intake. In summary, plasma IGF-I was elevated in calves with increased nutrient intake, and the elevations in plasma IGF-I following short-term administration of GH were significant in all calves by 65 kg BW. Data demonstrate that in well-managed milk-fed calves the somatotropic (GH/IGF-I) axis is functionally coordinated and sensitive to nutrient intake and GH.     

Paraventricular alpha1- and alpha2-adrenergic receptors mediate hindbrain lipoprivation-induced suppression of luteinizing hormone pulses in female rats

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, alpha1-, alpha2- or beta-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 alpha1- or alpha2-adrenergic antagonist into the PVN blocked the effect of the 4V MA injection on LH pulses. beta-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 alpha1- and alpha2-adrenergic receptor antagonists. These results suggest that alpha1- and alpha2-adrenergic receptors in the PVN mediate hindbrain lipoprivation-induced suppression of LH release and counter-regulatory increases in plasma glucose levels in female rats.