Alterations in Adrenal Growth and Corticosteroid Content in Foetal and Neonatal Rats Developing at High Altitude

Abstract

To study the effects of chronic maternal hypoxia on the growth and functional development of foetal and neonatal adrenal glands, Long-Evans rats were acclimatized to high altitude (3800 m) before mating and were maintained at this height throughout gestation. The body growth of the progeny at high altitude was essentially normal during the perinatal period, but adrenal weight and adrenocortical function showed marked differences from those of control rats maintained at sea level. The adrenal glands were larger in foetuses but smaller in neonates, compared with the adrenal glands of control animals maintained at sea level. Differences in the protein content of the adrenal glands between the two groups paralleled differences in adrenal weight. The concentration and content of corticosterone in the adrenal glands of both foetuses and neonates kept at high altitude were markedly lower than values in animals kept at sea level. The lower adrenal corticosterone content was not reflected in the concentration of the hormone in the peripheral plasma, since this was essentially the same at high altitude and at sea level in both mothers and perinatal animals. The reduction in the adrenal corticosterone content was accompanied by and may have resulted from, a reduction in the concentration of cytochrome P-450 in the adrenal tissue of foetuses maintained at high altitude. Possible explanations for the dichotomous results are discussed.

Effect of chronic hypoxia on leptin, insulin, adiponectin, and ghrelin

“…The effect of hypoxia on the endocrine system was studied in men at high altitude [2][3][4][5] and in animals exposed to hypoxia [6][7][8][9][10]. This effect is not only limited to hormonal secretions, it can also extend to affect the morphology and histology of the endocrine glands [6,7,11].…”

Structural and functional ramifications of antigenic drift in recent SARS-CoV-2 variants

“…while others retain activity (e.g., 1-57, 2-7, mAb-222, S309, S2E12, COV2-2196, C669, etc.) ( 50 , 57 , 63 , 66 , 69 , 70 ). Here, we selected a representative panel of 17 human nAbs isolated from COVID-19 patients or humanized mice to study the escape mechanism.…”