A survey with horses was conducted to determine whether plasma concentrations of triiodothyronine (T3), thyroxine (T4), insulin-like growth factor (IGF)-I and IGF binding proteins (IGFBP) change as horses grow, mature sexually, and age. Jugular blood was sampled from Standardbred fillies and mares at ages 0, 1, 7, and 14 d, at 1, 2, 4, 5, 6, and 9 mo, and at 5 to 8 and 16 to 22 yr (n = 5 to 18). In a second survey, we measured the same variables in eight breeds of horses with markedly different adult body sizes, from Miniatures to Friesians. Plasma T3, T4, and IGF-I were determined by radioimmunoassays validated for horses, and IGFBP were estimated from radioligand assay following separation of the IGFBP by SDS-PAGE electrophoresis. Plasma T3 decreased (P < .01) nearly continuously from 7.9 ng/mL on the day of birth to .9 ng/mL at 6 mo, and then changed little from .7 ng/mL at 9 mo to .5 ng/mL in mares 16 to 22 yr old. Similarly, T4 declined (P < .01) from 233 ng/mL on the day of birth to 49 ng/mL at 14 d and varied from 35 to 9 ng/mL among all of the older age groups. Plasma concentrations of IGF-I increased (P < .01) from 285 ng/mL on the day of birth to 572 ng/mL at 14 d, remained relatively constant until 9 mo of age (530 ng/mL), and then declined (P < .01) to low levels (295 ng/mL) in the oldest mares. We detected six IGFBP. The two smallest IGFBP (26 and 39 kDa) were highest during the first 14 d after birth and lowest (P < .01) in aged mares. The four larger IGFBP were lowest at birth and increased to the highest values during the most rapid growth period, but these changes were not significant (P > .20). In agreement with data for other species, our data suggest that IGF-I and IGFBP modulate growth in horses. Although there were impressive interbreed differences in circulating concentrations of T3, T4, IGF-I, and IGFBP, these were not related to differences in adult body size.
SummaryT o assess the functional maturity of adrenergic modulation of plasma concentration of glucose, a s well a s immunoreactive glucagon (IRC) and immunoreactive insulin (IRI) secretion in utero, adrenergic agonists with or without / 3 (propranolol) or a (phentolamine) antagonists were infused to the chronically catheterized sheep fetus (n = 35) late in the third trimester. Mean f S.E. days at study was 129.5 f 1.5; term is 150 days. In 9 separate studies at gestational age 129 f 1 days, the infusion of saline for 3 hr was not associated with significant changes in the basal levels of glucose, IRC, or IRI.With epinephrine, 6 pg/min (n = 6) glucose rose from 16.7 f 3.6 to 41.9 f 9.7 mg/dl, IRC rose from 75 f 8 to 219 f 45 pg/ml, and IRI fell from 22.6 + 1.7 t o 12.7 + 3.5 microunits/ml ( P < 0.05 for each). Propranolol alone (n = 4) did not alter basal glucose or IRC but significantly suppressed IRI. Propranolol did, however, markedly attentuate the rise in glucose and IRC while exaggerating the fall in IRI during epinephrine infusion. Qualitatively similar but smaller responses were obtained with epinephrine. 0.4 pg/min (n = 10). Similarly, elevation of glucose and suppression of IRI was obtained with norepinephrine, 2 gg/min (n = 5), but IRC levels did not rise significantly. a-Adrenergic blockade alone augmented IRI from 18 + 3 to 38 + 5 microunits/ml without affecting glucose or IRC concentrations; during a blockade, norepinephrine infusion failed to induce the rise in glucose, IRG remained unchanged, and IRI remained elevated (n = 5). 2-Deoxy-D-glucose, 200 mg IV over 30 min, did not affect glucose, IRG, or IRI (n = 5). Thus, appropriate adrenergic modulation of plasma concentrations of glucose, and of IRG and IR1 secretion is established in the third trimester.following placental separation and abrupt cessation of the transfer of nutrients from mother to fetus, thereby suggesting that hypoglycemia acts as the stimulus for the observed changes (15,-17). We have recently reported that in newborn lambs there is a similar 5-fold surge of IRG within minutes of delivery, whereas plasma IRI remains low and unchanged (17). In newborn lambs, however, there was no fall in plasma glucose concentration following delivery, so that unless curtailment of a different major nutrient for the lamb acts as the trigger for IRG secretion, hypoglycemia is not the stimulus for the observed surge in IRG. An abrupt increase in catecholamine secretion at birth could adequately explain the . .observed changes because catecholamines are-known to stimulate glucagon secretion, inhibit insulin secretion, and mobilize free fatty acids (9,12,19,23,26,29,32,38). A rise in circulating free fatty acid levels does occur shortly after delivery (1, 17). Moreover, catecholamines increase markedly and abruptly in the arterial plasma of newborns at delivery (10. 24), and urinary excretion of epinephrine increases in the initial hours of life (27). If this hypothesis regarding the role of catecholamines as the trigger for the observed neonatal cha...
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