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Effect of chronic ethanol consumption on the response of parathyroid hormone to hypocalcemia in the pregnant rat Duggal, Shalu

Abstract

Drinking alcohol during pregnancy is known to have adverse effects on the offspring. Little is known, however, about the effects of drinking on the health of the pregnant female. Chronic ethanol consumption in the pregnant rat has been shown to alter the level of maternal blood calcium (Ca) and the major Ca-regulating hormone, parathyroid hormone (PTH). Specifically, ethanol decreases maternal blood ionized Ca (iCa) levels and, in spite of this decrease, PTH levels are unchanged or even decreased in ethanol-exposed dams. It is unknown if ethanol impairs the ability of PTH to respond to hypocalcemia, or if the ethanol-exposed dam can still regulate her serum Ca levels, but ethanol lowers the level of iCa that is maintained. The objective of my thesis was to determine the effect of chronic ethanol consumption on the response of maternal serum PTH levels to an acute decrease in blood iCa level. Rats were fed a liquid diet with ethanol (36% ethanol derived calories, Ethanol, E rats) or without ethanol (Pair-Fed, PF or Control, C rats), 3 weeks prior to and throughout 21 days gestation. On day 21 gestation, the E and PF dams received an intraperitoneal (ip) injection of the Ca-chelating agent ethylene glycol-bis(beta-aminoethyl ether)-N,N,N’,N’- tetraacetic acid (EGTA) at a dose of 300 or 500 μmol/kg body weight (300-EGTA or 500-EGTA group, respectively), an equal volume of saline (Saline group), or no injection (Baseline group). The C rats received all treatments except the 300-EGTA dose. Maternal blood was collected from the Baseline group (0 min), and at 30 and 60 min post-injection in the Saline and EGTA groups. Blood was analyzed for iCa, pH, blood ethanol concentration (BEC), PTH, and corticosterone levels. Saline injection had no effect on blood iCa and serum PTH levels. Injection of EGTA resulted in a significant decrease (vs. Saline) in blood iCa levels, which varied with both dose of EGTA and time post-injection, but did not vary with dietary treatment. Importantly, ethanol consumption did not prevent PTH from increasing in response to the EGTA-induced hypocalcemia, and PTH levels were significantly increased in all diet groups at 30 min post-injection. Ethanol did, however, appear to decrease the maximum PTH levels achievable in blood (vs. PF dams). This difference in maximum PTH levels between E and PF rats could not be explained by an increased response of the PF rats to stress, as measured by serum corticosterone levels. These data suggest that chronic ethanol consumption does not impair the ability of the pregnant rat to raise serum PTH levels in response to acute hypocalcemia, but may decrease the maximum level of PTH achieved. Ethanol’s effect on the maximal PTH level could potentially impair the ability of the pregnant female to sustain high PTH levels in response to a more chronic hypocalcemia, as might occur during consumption of a low Ca diet. Effects of ethanol on the ability to maintain Ca homeostasis during pregnancy could have adverse effects on both maternal and fetal health.

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