Reproductive cycle of northern largemouth bass Micropterus salmoides salmoides.

The seasonal dynamics of the northern largemouth bass (Micropterus salmoides salmoides) reproductive cycle was investigated in a Midwestern United States population. Mature largemouth bass (n = five males and five females) were collected each month over a one-year period. Environmental cues (water temperature and photoperiod) were recorded in situ using data loggers. Temporal changes in plasma sex steroid hormones (testosterone [T], 11-ketotestosterone [11-KT], and estradiol-17ß [E2 ]) and vitellogenin (Vtg), gamete development (histology), and organosomatic indices were highly associated with temporal water temperature and photoperiod dynamics. Female plasma concentrations of T and E2 and organosomatic indices exhibited similar temporal patterns, with peaks occurring in early summer. Gamete development in females was associated with increases in gonadosomatic index (GSI) and Vtg. In males, plasma concentrations of T and organosomatic indices exhibited bimodal peaks; high peaks occurred in the spring for T and GSI and in the fall for viscerosomatic and hepatosomatic indices. Male gamete development and GSI closely tracked temporal patterns in plasma T, with GSI lagging behind the T cycle by approximately one sampling period. Plasma concentrations of 11-KT were elevated in late winter and spring and were considerably higher than T throughout the reproductive cycle. Unlike the Florida largemouth bass (M. salmoides floridanus) advanced gamete development was observed in both sexes before winter, which may reduce the immediate energy required for gamete development in the spring. Results from this study also provide baseline information necessary for off-season spawning procedures and endocrine-disruption studies in northern largemouth bass.

Energy balance affects pulsatile secretion of luteinizing hormone from the adenohypophesis and expression of neurokinin B in the hypothalamus of ovariectomized gilts.

The pubertal transition of gonadotropin secretion in pigs is metabolically gated. Kisspeptin (KISS1) and neurokinin B (NKB) are coexpressed in neurons within the arcuate nucleus of the hypothalamus (ARC) and are thought to play an important role in the integration of nutrition and metabolic state with the reproductive neuroendocrine axis. The hypothesis that circulating concentrations of luteinizing hormone (LH) and expression of KISS1 and tachykinin 3(TAC3, encodes NKB) in the ARC of female pigs are reduced with negative energy balance was tested using ovariectomized, prepubertal gilts fed to either gain or lose body weight. Restricted feeding of ovariectomized gilts caused a rapid and sustained metabolic response characterized by reduced concentrations of plasma urea nitrogen, insulin, leptin, and insulin-like growth factor-1 and elevated concentrations of free fatty acids. The secretory pattern of LH shifted from one of low amplitude to one of high amplitude, which caused overall circulating concentrations of LH to be greater in restricted gilts. Nutrient-restricted gilts had greater expression of follicle-stimulating hormone and gonadotropin-releasing hormone receptor, but not LH in the anterior pituitary gland. Expression of KISS1 in the ARC was not affected by dietary treatment, but expression of TAC3 was greater in restricted gilts. These data are consistent with the idea that hypothalamic expression of KISS1 is correlated with the number of LH pulse in pig, and further indicate that amplitude of LH pulses may be regulated by NKB in the gilt.

Differential expression of the type I interferon pathway during persistent and transient bovine viral diarrhea virus infection.

Persistent infection with bovine viral diarrhea virus (BVDV) serves as a reservoir for the perpetuation of infection in cattle populations and causes a range of adverse effects on the health of the host. To study the interactions of the virus with the host, gene expression was compared in the blood of persistently infected (PI) and uninfected steer, and in the blood and tissues of PI fetuses, transiently infected (TI), and uninfected bovine fetuses. Microarray analysis of PI steer blood revealed differential gene expression indicative of an interferon (IFN) response including genes involved in cell cycle regulation, which may contribute to long-term adverse effects. Upregulation of IFN-stimulated genes (e.g., ISG15, PKR) and RNA helicases (RIG-I, LGP2, MDA-5) was identified in both PI fetal and steer blood in comparison to controls, indicating a continued stimulation of the innate antiviral response as a result of the persistent viremia. ISG15 was studied in further detail, implicating reticular cells as basal producers of ISG15 in the spleen, in addition to endothelial and macrophage-like cells in infected spleen. Consequences of chronic IFN pathway activation in PI cattle may include growth- and immunosuppression, the pathogenesis of which is still poorly understood. This study lends new insights into the interactions between BVDV and its host, and can serve as a model for studies of the role of the IFN system in persistent infections.

Effects of two different anaesthetics on serum concentrations of cortisol and luteinizing hormone in barrows and gilts.

To determine if administration of the anaesthetic cocktail, telazol-ketamine-xylazine (TKX) and pentothal (PEN) decreases serum concentrations of luteinizing hormone (LH) in pigs, the following experiment was performed. On day 1, eight gilts and six barrows of similar weight (75 kg) were anaesthetized with TKX (1 mL/22.5 kg body weight [BW] intramuscularly) and indwelling jugular catheters were inserted. On days 2, 6 and 8 blood samples were taken every 20 min, for 4 h before pigs were administered saline (day 2) or anaesthetized with TKX (day 6) and PEN (8.9 mg/kg BW intravenously, day 8). Blood samples were taken every 20 min for 4 h following administration of saline and anaesthetics. Mean serum concentrations of LH and cortisol did not differ (P > 0.05) within barrows or gilts from before administration of saline (day 2) to following saline administration. Mean serum concentrations of LH and cortisol were not different (P > 0.05) within barrows and gilts before administration of TKX (pre-TKX) or PEN compared with day 2 samples. Following administration of TKX (post-TKX), mean serum concentrations of LH decreased (P < 0.05) and remained decreased for 140 min, while mean serum concentrations of cortisol increased (P < 0.05) post-TKX and remained elevated for 140 min. In gilts, mean serum concentrations of LH did not differ (P > 0.05) from pre- to post-TKX. However, mean serum concentrations of cortisol increased (P < 0.05) post-TKX in gilts and remained elevated for 240 min. Following administration of PEN, mean serum concentrations of LH and cortisol within barrows and gilts were not different (P > 0.05) from concentrations before administration of PEN. Administration of TKX to barrows and gilts increased serum concentrations of cortisol, but transient decreases in serum concentrations of LH were observed only in barrows, indicating gonadal status and/or sex may influence the ability of TKX to alter circulating concentrations of LH in pigs.

The impact of varying dietary protein on serum IGF-I, IGFBP-1, and IGFBP-3 during 6 days of physical activity.

This study was designed to investigate the impact of dietary protein intake on serum concentrations of IGF-I and IGFBP-1 and relative amounts of serum IGFBP-3 during 6 d of physical activity. Ten men (23.8 +/- 2.0 y of age) were assigned to 1 of 3 trials in a random crossover design. Each trial was isocaloric but with varying amounts of dietary protein: 50 g, 100 g, or 200 g. Subjects expended 500 kcal through treadmill running or weightlifting on alternate days for 6 d. Fasting blood samples were obtained for measurement of IGF-I, IGFBP-1, and IGFBP-3. Pre-post 24-h urine was measured for urea nitrogen. 50 g/d of protein resulted in a negative nitrogen balance, whereas 100 g/d and 200 g/d resulted in a positive nitrogen balance--200 g greater (P < 0.05) than 50 g and 100 g. Baseline IGF-I, BP-1, and BP-3 were not different among treatments. IGF-I decreased (P = 0.002) during the 6 d. Postintervention IGFBP-I was greater (P = 0.03) than at baseline. Postintervention IGFBP-3 values were not different from baseline or between trials. A 6-d modification of protein intake, while in energy balance, during a strength and conditioning program does not appear to modify serum concentrations of IGF-I or IGFBP-1 or relative amounts of IGFBP-3.

Effect of protein supplementation during a 6-mo strength and conditioning program on insulin-like growth factor I and markers of bone turnover in young adults.

BACKGROUND: Exercise is beneficial for bone when adequate nutrition is provided. The role of protein consumption in bone health, however, is controversial. OBJECTIVE: The objective was to ascertain the effect of high protein intake on insulin-like growth factor I (IGF-I) and markers of bone turnover during 6 mo of exercise training. DESIGN: Fifty-one subjects aged 18-25 y (28 men, 23 women) received a protein supplement (42 g protein, 24 g carbohydrate, 2 g fat) or a carbohydrate supplement (70 g carbohydrate) twice daily. Exercise consisted of alternating resistance training and running 5 times/wk. Plasma concentrations of IGF-I, insulin-like growth factor-binding protein 3, serum bone alkaline phosphatase, and urinary N-telopeptide collagen crosslink (NTx) concentrations were measured at 0, 3, and 6 mo after 24 h without exercise and a 12-h fast. RESULTS: Three-day diet records indicated no difference in energy intake between the groups. Average protein intakes after supplementation began in the protein and carbohydrate groups were 2.2 +/- 0.1 and 1.1 +/- 0.1 g/kg, respectively (P < 0.001). The increase in plasma IGF-I was greater in the protein group than in the carbohydrate group (time x supplement interaction, P = 0.01). There were no significant changes over time or significant differences by supplement in plasma insulin-like growth factor-binding protein 3 (44 and 40 kDa). Serum bone alkaline phosphatase increased significantly over time (P = 0.04) and tended to be higher in the protein group than in the carbohydrate group (P = 0.06). NTx concentrations changed over time (time and time squared; P < 0.01 for both) and were greater in the protein group than in the carbohydrate group (P = 0.04). Men had higher NTx concentrations than did women (74.6 +/- 3.4 and 60.0 +/- 3.8 nmol/mmol creatinine; P = 0.005). CONCLUSION: Protein supplementation during a strength and conditioning program resulted in changes in IGF-I concentrations.

Hypoglycemia-induced suppression of luteinizing hormone (LH) secretion in intact female rhesus macaques: role of vasopressin and endogenous opioids.

The first objective of this study was to determine whether insulin-induced hypoglycemia (IIH) inhibits LH secretion in unrestrained female macaques during the follicular phase of the menstrual cycle. There was a consistent inhibitory effect of hypoglycemia on LH secretion within 3 h in these females. This inhibition was likely an indirect effect since low glucose levels did not inhibit GnRH secretion from GT1-1 neurones in vitro. We next investigated whether administration of a vasopressin antagonist (AVPa) either alone, or with naloxone could reverse the IIH-induced inhibition of LH release. Females were studied in the follicular phase during 10 h periods with blood samples collected every 10 min. Experimental groups were IIH (n=6), IIH+AVPa (n=5) and IIH+AVPa+naloxone (n=4). The first 5 h of each study served as a control and hypoglycemia was then induced with insulin. The AVPa was given as a bolus (180 microg) just before the insulin and was followed by a continuous infusion (180 microg/h) for 5 h. Naloxone (5 mg/kg) was given with the AVPa and followed by a continuous infusion (5 mg/kg/h) for 5 h. In the IIH group, LH reached its lowest value 3-4 h after insulin. Neither AVPa nor AVPa+naloxone infusion reversed the inhibitory action of hypoglycemia on LH release. These data suggest that if there are inhibitory actions of vasopressin and endogenous opioids on GnRH release induced by hypoglycemia, they are not sufficient to explain the suppression of GnRH/LH release in intact female primates.