Barbara M. Jankowski

The effect of hypoxia on plasma leptin and insulin in newborn and juvenile rats.

Hypoxia leads to a decrease in food intake and attenuated weight gain in rats. The purpose of this study was to measure plasma leptin and insulin in young rats exposed to hypoxia for 7 d as compared to a normoxic control group of the same age. One group was exposed from birth to 7 d of age; the other was exposed from 28 to 35 d of age (weaned at 21 d of age). As expected, body weight was significantly lower in rats of either age exposed to hypoxia for 7 d. Plasma leptin was significantly lower in hypoxic (2.0±0.2 ng/mL; n=41) compared with normoxic (2.6±0.3 ng/mL; n=30) 7-d-old rats. Plasma leptin was also significantly lower in hypoxic (1.1±0.1 ng/mL; n=20) as compared to normoxic (1.5±0.1 ng/mL; n=20) 35-d-old rats. Seven-day-old rats exposed to hypoxia demonstrated significant increases in plasma glucose and insulin whereas 35-d-old rats exhibited a decrease inboth variables. We conclude that exposure to hypoxia for 7 d leads to a decrease in body weight and plasma leptin in infant and juvenile rats. The decrease in leptin may be an attempt to reverse hypoxia-induced anorexia.

The effect of fetal hypoxia on adrenocortical function in the 7-day-old rat.

Fetal hypoxia in late gestation is a common cause of postnatal morbidity. The purpose of the present study was to evaluate adrenal function in vivo and in vitro in 7-d-old rat pups previously exposed to normoxia or hypoxia (12% O2) during the last 2–3 d of gestation. Seven-day-old rats exposed to fetal hypoxia had a small, but significant decrease in plasma aldosterone despite no decreases in plasma ACTH or renin activity. There was a small (approx 20%) but significant decrease in the aldosterone and corticosterone response to cAMP in vitro in dispersed cells from 7-d-old pups exposed to fetal hypoxia. The aldosterone, corticosterone, and cAMP response to ACTH, however, was not altered by prior fetal hypoxia. There was also no effect of fetal hypoxia on steroidogenic enzyme expression or zonal dimension in 7-d-old rats. We conclude that fetal hypoxia in late gestation results in a subtle decrease in cAMP-stimulated steroidogenesis. Fetal hypoxia appears to have minimal effects on subsequent adrenal function in the neonatal rat.

VASOPRESSIN RESPONSE TO HAEMORRHAGE IN RATS: EFFECT OF HYPOXIA AND WATER RESTRICTION

1. The aim of the present study was to determine the effect of water restriction and/or hypoxia on the vasopressin response to haemorrhage in conscious rats.

Growth Hormone Therapy During Neonatal Hypoxia in Rats Body Composition, Bone Mineral Density, and Insulin-like Growth Factor-1 Expression

Hypoxia from birth results in a decrease in body weight gain, body size, and bone mineral density (BMD). The purpose of the present study was to determine whether short-term administration of growth hormone (GH) (rat GH; 100 µg/d) could attenuate some of these effects of neonatal hypoxia. Rat pups (with their lactating dams) were exposed to hypoxia (vs normoxic control) from birth. Hypoxia was continued until 14 d of age, with rat GH (vs vehicle control) administered daily. Hypoxia significantly inhibited body weight gain; GH therapy did not reverse this effect. GH therapy did reverse the inhibitory effect of hypoxia on tail length but not on body length. Hypoxia decreased BMD analyzed by dual X-ray absorptiometry (DXA); this effect was not reversed by GH therapy. Both GH therapy and hypoxia decreased the percentage of body fat analyzed by DXA, the effects of which were additive when combined. There were minimal effects of hypoxia and GH therapy on plasma insulin-like growth factor-1 (IGF-1), IGF-binding protein-3, and hepatic IGF-1 mRNA expression. We conclude that some of the effects of hypoxia on body habitus are reversed by GH therapy, but that short-term GH therapy did not prevent a loss of BMD. GH therapy for more than 14 days may be necessary to appreciate fully its potential in the treatment of the sequelae of neonatal hypoxia.