Obese (n = 8) and nonobese (n = 6) adult rhesus monkeys (Macaca mulatta) were assessed in terms of body size and distribution of body fat, glucose tolerance, and serum lipid, insulin, and androgen levels. The weights of the obese monkeys were more than 2 SD above the mean for their sex, while the nonobese monkeys averaged less than 0.25 SD from the mean. Obese males and females had excess body fat located predominantly in the abdominal region; abdominal circumference was highly correlated with total body fat, as estimated by the isotope dilution method (r = 0.98; P less than 0.001). Obese monkeys of both sexes had fasting hyperinsulinemia, greater insulin response to iv glucose administration, and marginally impaired glucose tolerance. Obese males had delayed maximal insulin response to glucose administration. Fasting serum triglycerides also were elevated in the obese monkeys (0.95 +/- 0.08 vs. 0.47 +/- 0.05 mmol/L; P less than 0.001). Obese males had lower serum dihydrotestosterone levels than nonobese males (3.1 +/- 0.7 vs. 5.6 +/- 0.4 nmol/L; P less than 0.01). Nonobese females had approximately 2-fold higher serum dehydroepiandrosterone sulfate levels than the other groups. We conclude that obese male and female rhesus monkeys have patterns of fat distribution and glucoregulatory abnormalities similar to those of humans with upper body obesity. The contribution of differences in androgen metabolism to the development of obesity and its complications in rhesus monkeys remain to be defined.
Absolute bioavailability and dose proportionality studies were performed with ceftiofur in horses. In the absolute bioavailability study, thirty animals received either an intravenous dose of ceftiofur sodium at 1.0 mg/kg or an intramuscular (i.m.) dose of ceftiofur crystalline-free acid (CCFA) at 6.6 mg/kg. In the dose proportionality study, 48 animals received daily i.m. ceftiofur sodium injections at 1.0 mg/kg for ten doses or two doses of CCFA separated by 96 h, with CCFA doses of 3.3, 6.6, or 13.2 mg/kg. Noncompartmental and mixed-effect modeling procedures were used to assess pharmacokinetics (PK). CCFA was well absorbed with a bioavailability of 100%. AUC(0-∞) and C(max) increased in a dose-related manner following administration of the two doses of CCFA at 3.3, 6.6, and 13.2 mg/kg. The least-squares mean terminal half-life (t(½) ) following the tenth daily i.m. injection of ceftiofur sodium at 2.2 mg/kg was 40.8 h, but the least-squares mean t(½) following the second i.m. injection of CCFA at 6.6 mg/kg was 100 h. The time that plasma ceftiofur equivalent concentrations remain above a threshold concentration of 0.2 μg/mL has been associated with efficacy, and following administration of two 6.6 mg/kg doses of CCFA, the mean time above 0.2 μg/mL was 262 h. Simulations with the nonlinear mixed-effect PK model predicted that more than 97.5% of horses will have plasma ceftiofur equivalent concentrations >0.2 μg/mL for 96 h after the second 6.6 mg/kg dose of CCFA.
Immunocytochemical procedures on thick, unembedded tissue sections were used to study the localization of LHRH neurons and fibers in the diencephalon and mesencephalon of rhesus and pigtailed macaques. Cell bodies were visualized in large numbers. Much of their dendritic arborization was also filled with reaction product. Cell bodies were present in the preoptic area, the periventricular hypothalamic zone from the level of the anterior hypothalamus to the premammillary nuclei, the infundibular nucleus, supraoptic nucleus, several septal nuclei, the nervus terminalis, and the amygdala. The localization of LHRH cells in several of these areas represents new observations. LHRH axons were observed to innervate the portal vessels in the median eminence, the organum vasculosum of the lamina terminalis, the median eminence, the organum vasculosum of the lamina terminalis, the medial mammillary nuclei, the epithalamus, and the amygdala. These observations are discussed in relationship to the regulation of gonadotropin secretion in the primate.
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