Leptin is a metabolic signal to the reproductive system.

Leptin, a newly-discovered hormonal product of the obese (ob) gene, is expressed by adipocytes and thought to play a role in the regulation of food intake and metabolism. We tested the hypothesis that leptin signals metabolic information to the reproductive system by examining its effects on the reproductive system of ob/ob mice, which have a congenital deficiency in leptin and are infertile. We treated pair-fed males and females with leptin (50 microg twice daily, ip) or vehicle (n=10/group) for 14 days, after which the animals were bled and killed. Leptin-treated females had significantly elevated serum levels of LH, increased ovarian and uterine weights, and stimulated aspects of ovarian and uterine histology compared to controls. Leptin-treated males had significantly elevated serum levels of FSH, increased testicular and seminal vesicle weights, greater seminal vesicle epithelial cell height, and elevated sperm counts compared to controls. These results demonstrate that leptin stimulates the reproductive endocrine system in both sexes of ob/ob mice and suggest that leptin may serve as a permissive signal to the reproductive system of normal animals.

Nocturnal oxygen enrichment of room air at 3800 meter altitude improves sleep architecture.

Sleep is known to be impaired at high altitude, and this may be a factor contributing to reduced work efficiency, general malaise, and the development of acute mountain sickness (AMS). Nocturnal room oxygen enrichment at 3800 m has been shown to reduce the time spent in periodic breathing and the number of apneas, to improve subjective quality of sleep, and to reduce the AMS score. The present study was designed to evaluate the effect of oxygen enrichment to 24% at 3800 m (lowering the equivalent altitude to 2800 m) on sleep architecture. Full polysomnography and actigraphy were performed on 12 subjects who ascended in 1 day to 3800 m and slept in a specially constructed room that allowed oxygen enrichment or ambient air conditions in a randomized, crossover, double-blind study. The results showed that subjects spent a significantly greater percentage of time in deep sleep (stages III and IV combined, or slow wave sleep) with oxygen enrichment versus ambient air (17.2 +/- 10.0% and 13.9 +/- 6.7%, respectively; p < 0.05 in paired analysis). No differences between treatments were seen with subjective assessments of sleep quality or with subject's assessment of the extent to which they suffered from AMS. This study provides further objective evidence of improved sleep as a result of oxygen enrichment at 3800 m and suggests that alleviating hypoxia may improve sleep quality.

Rapid intravenous infusion of 20 mL/kg saline alters the distribution of perfusion in healthy supine humans.

Rapid intravenous saline infusion, a model meant to replicate the initial changes leading to pulmonary interstitial edema, increases pulmonary arterial pressure in humans. We hypothesized that this would alter lung perfusion distribution. Six healthy subjects (29 ± 6 years) underwent magnetic resonance imaging to quantify perfusion using arterial spin labeling. Regional proton density was measured using a fast-gradient echo sequence, allowing blood delivered to the slice to be normalized for density and quantified in mL/min/g. Contributions from flow in large conduit vessels were minimized using a flow cutoff value (blood delivered > 35% maximum in mL/min/cm(3)) in order to obtain an estimate of blood delivered to the capillary bed (perfusion). Images were acquired supine at baseline, after infusion of 20 mL/kg saline, and after a short upright recovery period for a single sagittal slice in the right lung during breath-holds at functional residual capacity. Thoracic fluid content measured by impedance cardiography was elevated post-infusion by up to 13% (p<0.0001). Forced expiratory volume in 1s was reduced by 5.1% post-20 mL/kg (p=0.007). Infusion increased perfusion in nondependent lung by up to 16% (6.4 ± 1.6 mL/min/g baseline, 7.3 ± 1.8 post, 7.4 ± 1.7 recovery, p=0.03). Including conduit vessels, blood delivered in dependent lung was unchanged post-infusion; however, was increased at recovery (9.4 ± 2.7 mL/min/g baseline, 9.7 ± 2.0 post, 11.3 ± 2.2 recovery, p=0.01). After accounting for changes in conduit vessels, there were no significant changes in perfusion in dependent lung following infusion (7.8 ± 1.9 mL/min/g baseline, 7.9 ± 2.0 post, 8.5 ± 2.1 recovery, p=0.36). There were no significant changes in lung density. These data suggest that saline infusion increased perfusion to nondependent lung, consistent with an increase in intravascular pressures. Dependent lung may have been "protected" from increases in perfusion following infusion due to gravitational compression of the pulmonary vasculature.