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Biomedical subjects

D H Polk

Publications and source records attributed to D H Polk.

At least 37 records · Page 2Linked to original sources
PubMed1995

Fetal corticosteroid and T4 treatment effects on lung function of surfactant-treated preterm lambs.

Three groups of sheep fetuses at 125 or 126 d gestational age randomly received a single ultrasound-guided intramuscular injection of saline, 0.5 mg/kg betamethasone, or 0.5 mg/kg betamethasone plus 50 micrograms/kg thyroxine (T4). Forty-eight hours later the fetuses were delivered, treated with a pulmonary surfactant preparation, and ventilated for 3 h. Corticosteroids alone and in combination with T4 increased FRC, compliance, and lung volumes, and decreased the protein leak into the airspace. Saturated phosphatidylcholine pool sizes recovered by alveolar washing were not changed after hormone treatment. To evaluate the function of surfactant recovered from the lambs in vivo, we treated preterm rabbits at 27 d gestational age with the large-aggregate surfactant from alveolar washes. Large-aggregate surfactants and the pulmonary surfactant preparation increased compliances and maximal lung volumes relative to those in untreated preterm rabbits. Large-aggregate surfactants improved compliance more than did the pulmonary surfactant preparation. We conclude that ultrasound-guided single fetal corticosteroid treatment followed by postnatal surfactant improved postnatal lung function in preterm lambs. Addition of T4 did not augment corticosteroid effects. The function of the exogenous surfactant was improved in premature lamb lungs independently of the fetal treatment modality.

Animals↗
PubMed1995

Postnatal lung function in lambs after fetal hormone treatment. Effects of gestational age.

We previously found that a single dose of betamethasone in combination with thyroxine given by intramuscular injection to fetal sheep 48 h before preterm delivery at 128 d gestation improved postnatal lung function. We have now asked how the combination of 0.5 mg/kg betamethasone and 15 micrograms/kg T4 given by a single fetal intramuscular injection changes lung response 48 h after treatment at 121 and 135 d gestation. At 121 d gestation the fetal hormone treatment significantly improved postnatal lung function. Compliance increased by 55%, arterial PO2 increased from 39 to 215 mm Hg, PCO2 decreased from 109 to 79 mm Hg, and maximal lung volumes increased by 112%. The hormone treatment decreased the severity of the respiratory failure, although these very preterm lambs still had severe respiratory failure. At 135 d gestation, the fetal hormone treatment decreased the ventilatory pressure requirements that were needed to normalize PCO2 values from 30 to 21 cm H2O. Compliance increased by 40%, and maximal lung volumes increased by 33%. Alveolar or lung tissue, saturated phosphatidylcholine, or alveolar SP-A pool sizes did not change with hormone treatment at 135 d gestation. We conclude that fetal hormone treatment significantly improved postnatal lung function at both gestational ages, although the characteristics of the responses were different.

Animals↗
PubMed1995

Postnatal cardiovascular and metabolic responses to a single intramuscular dose of betamethasone in fetal sheep born prematurely by cesarean section.

Although the benefits of antenatal hormone treatment are well accepted, most studies have reported only pulmonary effects. There is evidence of beneficial cardiovascular and metabolic effects in studies using chronically catheterized animals; however because of the route of administration, the results are not directly applicable to clinical strategies. We previously demonstrated significant pulmonary effects in animals treated antenatally with a single, direct fetal, intramuscular injection of glucocorticoids. This study was performed to determine the effects of a single fetal injection of betamethasone (BETA) alone or in combination with thyroxine (T4) on cardiovascular and metabolic responses after preterm birth. Hemodynamic and metabolic responses at birth were determined in fetuses (126-d gestation; term = 150 d) treated with ultrasound-guided intramuscular injections of 0.5 mg/kg BETA (n = 7), BETA plus 60 g/kg T4 (n = 7), or saline (SAL, n = 9). After 48 h, lambs were delivered by cesarean section and studied for 3 h. BETA treatment increased mean arterial blood pressure [56 +/- 6 (SEM) versus 42 +/- 3 mm Hg], heart rate (152 +/- 5 versus 123 +/- 4 beats/min), and cardiac output (467 +/- 17 versus 349 +/- 36 mL/min/kg) versus SAL. Responses of BETA+T4-treated animals were not different from animals treated with BETA alone. Glucose and FFA were similar among all groups. The increase in catecholamine levels normally seen at birth was significantly attenuated in both the BETA and BETA+T4-treated animals. A single, intramuscular injection of glucocorticoids 48 h before delivery improves cardiovascular responses to preterm birth. This effect is not augmented by concomitant administration of T4.

Animals↗
PubMed1994

Catecholamine response to ultrasonographically guided percutaneous blood sampling in fetal sheep.

OBJECTIVE: The purpose of this study was to investigate the fetal catecholamine and arterial blood gas responses to ultrasonographically guided percutaneous needle aspiration of blood from a fetal cardiac ventricle. STUDY DESIGN: A crossover trial design was used. Nine pregnant sheep of 120 to 130 days' gestation were stratified to either percutaneous fetal blood sampling or a sham experiment performed on the first day, and the alternative study on the following day. Arterial blood samples were withdrawn from chronically implanted catheters. RESULTS: Percutaneous fetal blood sampling caused small but statistically significant increases in mean plasma epinephrine and norepinephrine levels 5 seconds after the procedure. Levels thereafter were similar to baseline values. Arterial pH and PCO2 values were unaltered except in one fetus, where blood sampling was followed by bradycardia with acidosis and elevated catecholamine levels. CONCLUSIONS: Ultrasonographically guided percutaneous fetal blood sampling from a cardiac ventricle in sheep produces a rise in catecholamine levels that return to baseline values within 5 minutes. This technique provides an alternative to chronic catheterization for some experiments in which blood sampling or drug injection is required. The results also indicate that needle insertion produces only a modest and transient stress response in the fetus.

Animals↗
PubMed1994

Metabolism of sulfoconjugated thyroid hormone derivatives in developing sheep.

Although the production of thyroxine (T4) in the developing ovine fetus ranges from 20 to 50 micrograms.kg-1.day-1, production rates for 3,5,3'-triiodothyronine (T3) average only 1-2 micrograms.kg-1.day-1, whereas reverse T3 (rT3) production rates approach 5-6 micrograms.kg-1.day-1. Thus the fate of the majority of fetal T4 production is uncertain. Recently we have reported significant concentrations of various thyroid hormone sulfoconjugates in serum and other fetal compartments. In the present study, we used steady-state kinetic techniques in developing sheep to establish the clearance and production rates for T4, T3, and rT3 sulfates. These studies confirm that T4, T3, and rT3 sulfate are predominant metabolites of thyroid hormone in the developing ovine fetus. Plasma clearance rates for T3, T4, and rT3 sulfates are low in the fetus, averaging 0.67 +/- 0.07, 1.46 +/- 0.11, and 4.1 +/- 1 ml.kg-1.min-1, respectively. Clearance rates for these thyrosulfoconjugates increase two to fourfold postnatally, probably reflecting increased activity of 5'-monodeiodinase after birth. Moreover, fetal production rates for these sulfated thyroid hormone metabolites exceed those of 2-wk-old sheep 4- to 10-fold. The data suggest that a significant route of fetal T4 metabolism is sulfation followed by deiodination to rT3 sulfate.

Aging↗
PubMed1994

Time course of changes in lung mechanics following fetal steroid treatment.

We studied the effect of a single-dose, corticosteroid treatment on preterm lambs (gestational age: 128 d). A low, medium, or high betamethasone dose (0.1, 0.5, and 2.0 mg/kg) or saline control was administered directly to the fetus by ultrasound-guided intramuscular injection 48 h before delivery. A second group received either the high dose of betamethasome or saline 24 h before delivery. The lambs were delivered at 128 d gestation, anesthetized with ketamine, and ventilated for 50 min. Respiratory system elastance and resistance were measured at 10-min intervals using multiple linear regression analysis of pressure, flow, and volume. Similarly, estimates of lung mechanics were calculated from transpulmonary pressure. The viscoelastic time constant (tau) was calculated by fitting an exponential to the pressure changes occurring after occluding the airway during expiration. Excised lung volume at 40 cm H2O and lung weight were used to calculate specific elastance and resistance correcting for lung size using volume or weight, respectively. Of the 13 lambs in the 48-h high-dose betamethasone group, five developed pulmonary interstitial emphysema (PIE) as did 3 of 11 animals in the high-dose group treated 24 h before delivery. These animals were analyzed separately. The lambs receiving medium- or high-dose (24 and 48 h predelivery) betamethasone had significantly lower elastance and a trend toward lower resistance when compared with the control groups. Ten minutes after delivery, the animals that developed PIE all had elastance values comparable to that of the control animals despite corticosteroid treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

A 3,3'-diiodothyronine sulfate cross-reactive compound in serum from pregnant women.

Recently, we found high serum/urine concentrations of 3,3'-diiodothyronine sulfate (T2S) in both fetal and maternal sheep. In the present study, a RIA was employed to detect and measure serum T2S in women of different gestational ages and after delivery. Results were compared with values in nonpregnant women. In maternal serum, we identified a material that cross-reacts with T2S antibody, but is not T2S. Its concentration increased with the progression of pregnancy. The exact chemical structure of the T2S-like material (which we designated compound W) is unclear. It is immunologically (or chemically) similar to T2S, but does not cochromatograph with synthetic T2S in high pressure liquid chromatography. The serum concentrations of compound W were expressed as T2S equivalents (nanomoles per L +/- SE). Serum compound W concentrations were slightly elevated in women during the first trimester compared to those in nonpregnant women (0.73 +/- 0.04 vs. 0.17 +/- 0.02 nmol/L; P < 0.01). There was a moderate and progressive rise in the compound W concentration between 14-35 weeks gestation. The maternal serum compound W concentration then rapidly peaked before parturition (36-40 weeks gestation, 3.49 +/- 0.49 nmol/L; 27-35 weeks, 1.67 +/- 0.11 nmol/L; P < 0.01). After parturition, maternal serum levels of compound W decreased from 2.61 +/- 0.18 nmol/L (n = 25) to 1.47 +/- 0.12 nmol/L (n = 18) at 1 day, 0.89 +/- 0.07 nmol/L (n = 15) at 3 days, and 0.33 +/- 0.03 nmol/L (n = 8) at 7 days. hCG increased serum concentrations of T2S-cross-reactive material 6.2-fold (P < 0.01) in nonpregnant women. In summary, whereas hCG stimulation may account for some increase in maternal serum concentrations of this T2S-like material in the first trimester, the more rapid increase in maternal serum compound W concentrations during the late third trimester are probably related to changes that occur in fetal thyroid hormone economy. It is speculated that placental transfer and transformation of fetal T3 may be related to the rise in the level of T2S-like compound W in the serum of pregnant women.

Adolescent↗
PubMed1994

Diagnosis and management of altered fetal thyroid status.

Recent advances in the understanding of the normal process of maturation of fetal thyroid function now make possible the in utero diagnosis of fetal system abnormalities. The approach to the fetus at risk for altered thyroid function is discussed in the context of normal thyroid development and emphasis is given to the fetus presenting with goiter.

Female↗
PubMed1993

Sulfate conjugates of iodothyronines in developing sheep: effect of fetal hypothyroidism.

We recently showed that thyroxine sulfate (T4S) and 3,3',5-triiodothyronine sulfate (T3S) were major thyroid hormone metabolites in ovine fetuses and neonates. To further characterize the sulfation pathway in ovine fetuses, we measured 3,3',5'-triiodothyronine (rT3S) in serum and other body fluids in samples obtained from fetal (n = 23, 94-145 days of gestational age, term = 150 days), newborn (n = 6), and adult (n = 6) sheep. In addition, T3S, T4S, and rT3S levels were measured in tissue fluids and serum samples obtained from ovine fetuses 13 days after total thyroidectomy (Tx) conducted at gestational age of 110-113 days (n = 5). Sham-operated twin fetuses served as controls (n = 5). The relative order of mean rT3S concentration for various tissue fluids in fetuses were meconium > bile > serum > allantoic fluid > urine or amniotic fluid. Peak mean tissue fluid levels generally occurred at 110-130 days gestation. In hypothyroid fetuses, significant decreases in the mean serum concentrations of T4S and rT3S, but not T3S, were noted. The mean rT3S level also was decreased significantly in allantoic fluid, bile, and meconium, whereas T4S and T3S levels were reduced only in bile of the Tx fetuses. These data demonstrate that sulfation is a major pathway in thyroid hormone metabolism in both euthyroid and hypothyroid ovine fetuses.

Animals↗
PubMed1992

Respiratory disease in very-low-birthweight infants after prenatal thyrotropin-releasing hormone and glucocorticoid. TRH Study Group.

Although prenatal glucocorticoid treatment reduces neonatal respiratory morbidity, respiratory distress syndrome and chronic lung disease (CLD) develop in many very-low-birthweight infants despite therapy. To investigate the effect of additional prenatal treatment with thyrotropin-releasing hormone (TRH), we did a multicentre, blinded, randomised trial. 404 women with threatened preterm delivery at less than 32 weeks' gestation received betamethasone plus TRH (4 doses of 400 micrograms 8-hourly) or betamethasone plus placebo. 103 infants who were fully treated and of less than 1500 g birthweight were evaluated during the neonatal period. TRH treatment (55 infants) did not affect the total incidence of respiratory distress syndrome (47% vs 58% in controls) or of severe respiratory distress syndrome (13% vs 25% in controls, p = 0.11). CLD (defined as requirement for supplemental oxygen at 28 days after birth) developed in significantly fewer TRH-treated infants (18% vs 44% of controls, p less than 0.01). The unadjusted relative risk of CLD with TRH therapy was 0.40 (95% CI 0.26-0.80, p less than 0.05), and this was not materially changed after adjustment for potentially modifying variables. There were significantly fewer adverse outcomes, defined as death or continuing oxygen requirement, in the TRH group than in the steroid-alone group both at 28 days and when infants reached 36 weeks' postconceptional age. The incidence of other complications of prematurity was similar in the two groups. Prenatal TRH reduces the incidence of chronic lung disease among betamethasone-treated infants.

Betamethasone↗
PubMed1992

Plasma thyroid hormones and prolactin in premature infants and their mothers after prenatal treatment with thyrotropin-releasing hormone.

We assayed TSH, triiodothyronine, free thyroxine, and prolactin (PRL) in plasma of women and infants participating in a trial of prenatal thyrotropin-releasing hormone (TRH) treatment for prevention of newborn lung disease. Women in labor at 26-34 wk of gestation received 400 micrograms of TRH i.v. every 8 h (one to four doses) plus 12 mg betamethasone (one or two doses); controls received saline plus betamethasone. Mean cord concentrations in control infants were TSH 9.7 mU/L, triiodothyronine 0.6 nmol/L (40.2 ng/dL), free thyroxine 14.4 pmol/L (1.13 ng/dL), and PRL 67.6 micrograms/L. TRH increased maternal plasma TSH by 100% at 2-4 h after treatment and decreased levels by 28-34% at 5-36 h. In cord blood of treated infants delivered at 2-6 h, TSH, triiodothyronine, and PRL were all increased about 2-fold versus control, and free thyroxine was increased 19%; the response was similar after one, two, three, or four doses of TRH. In treated infants delivered at 13-36 h, cord TSH and triiodothyronine levels were decreased 62 and 54%, respectively, and all thyroid hormones were lower after birth at 2 h of age versus control. We conclude that prenatal TRH administration increases thyroid hormones and PRL in preterm fetuses to levels similar to those normally occurring at term. Pituitary-thyroid function is transiently suppressed after treatment to a greater extent in fetus than mother, and infants born during the early phase of suppression do not have the normal postnatal surge in thyroid hormones.

Betamethasone↗
PubMed1991

Thyrotropin-releasing hormone in ovine fetus: ontogeny and effect of thyroid hormone.

The ontogenesis of hypothalamic and extrahypothalamic thyrotropin-releasing hormone (TRH) and the effect of altered thyroid status on tissue TRH levels were studied in fetal sheep. At 62 days gestation (term = 145 days) TRH was detectable in serum and in hypothalamic, placental, and pancreatic tissues; pancreatic, placental, and serum levels exceeded hypothalamic levels two- to fivefold. Analysis of tissues obtained from 88-day gestation fetuses were comparable: TRH levels in placenta (54 +/- 15 pg/mg tissue protein), pancreas (34 +/- 5 pg/mg protein), and serum (93 +/- 9 pg/ml) exceeded those in hypothalamic extracts (15 +/- 9 pg/mg protein). By 120 days gestation, TRH values in the hypothalamus (610 +/- 52 pg/mg protein) exceeded those in extrahypothalamic sites; values were comparable at 140 days gestation. Fetal thyroidectomy resulted in a 2-fold elevation of hypothalamic TRH concentrations (1,030 +/- 139 vs. 522 +/- 29 pg/mg protein) and 2 to 20-fold elevations of TRH in the placenta (147 +/- 23 vs. 42 +/- 8 pg/mg protein), pancreas (195 +/- 11 vs. 29 +/- 7 pg/mg protein), duodenum (363 +/- 97 vs. 29 +/- 7 pg/mg protein), and serum (2,563 +/- 212 vs. 131 +/- 16 pg/ml). 3, 5, 3'-Triiodothyronine (T3) infusion in thyroidectomized fetuses resulted in elevated serum T3 values (480 +/- 80 ng/dl) and suppressed hypothalamic TRH (249 +/- 68 vs. 522 +/- 29 pg/mg protein) and serum TRH concentrations (30 +/- 4 vs. 131 +/- 156 pg/ml). Placental, pancreatic, and duodenal TRH concentrations in thyroidectomized T3-infused animals were below the level of detection of the assay (5 pg/mg tissue protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Ontogeny of thyrotropin releasing hormone and precursor peptide in the rat.

Thyrotropin releasing hormone (TRH) and its precursor peptide pGlu-His-Pro-Gly (TRH-Gly) were measured in serum and in a variety of tissues of developing rats using specific RIA. TRH and TRH-Gly immunoreactivities were detected in most tissues. TRH concentrations were highest in pancreas, in which mean (+/- SEM) TRH concentrations were 138 +/- 20 pmol/g wet tissue 2 d before birth and 644 +/- 80 and 586 +/- 86 pmol/g, respectively, 2 and 5 d after birth. Hypothalamic TRH levels gradually increased from 4 d before birth (12 +/- 2.5 pmol/g) to 77 d of postnatal age (348 +/- 33 pmol/g). Hypothalamic concentrations were lower than levels in pancreas until 13 d of age. The mean serum TRH level at 2 d was 80 +/- 20 pmol/L and fell to the adult range by 21 d. TRH-Gly concentrations were highest in small gut (371 +/- 64 pmol/g) during the neonatal period, falling gradually to adult levels (33 +/- 4.8 pmol/g) by 35 d. Mean hypothalamic TRH-Gly concentrations increased to a peak of 62 +/- 4.5 pmol/g at 13 d, falling thereafter. High TRH-Gly concentrations (greater than 100 pmol/g) also were observed in pancreas (at d 2), kidney, and pituitary gland (at d 21). Serum TRH-Gly concentrations were highest (mean 417 +/- 26 pmol/L) on the 2nd postnatal day and gradually decreased to the adult level by 35 d. Changes in the TRH-Gly/TRH ratio were inversely correlated with tissue TRH concentrations in hypothalamus, pancreas, and liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

Corticosteroids, thyrotropin-releasing hormone, and antioxidant enzymes in preterm lamb lungs.

Forty-three twin lamb fetuses of 121 +/- 1 d gestation were catheterized and received i.v. saline (n = 8), 0.75 mg/kg/h cortisol for 60 h (n = 15), 5 micrograms/kg thyrotropin-releasing hormone (TRH) every 12 h for five doses (n = 9), or cortisol and TRH (n = 11) before delivery at 128 +/- 1 d. After delivery, the lambs were randomized for natural sheep surfactant treatment or sham treatment, ventilated for 75 min, and killed. Superoxide dismutase, catalase, and glutathione peroxidase activities were measured in fetal lung tissue. Superoxide dismutase and catalase activities were increased in both the corticosteroid (p less than 0.001) and the corticosteroid with TRH (p less than 0.01) groups. Glutathione peroxidase activity was higher after prenatal corticosteroid treatment, but statistical significance was not reached (p = 0.06). Although prenatal exposure to corticosteroids increased superoxide dismutase, catalase, and glutathione peroxidase activities, TRH alone or TRH added to corticosteroids provided no additional benefit. Lambs treated with surfactant had higher lung catalase activities than lambs that did not receive surfactant, probably secondary to the presence of catalase activity in the surfactant preparation. Increased pulmonary antioxidant enzyme activity may be an additional feature of the overall beneficial effect of corticosteroids on fetal lung development.

Animals↗
PubMed1990

Pharmacokinetics of dopamine in critically ill newborn infants.

Dopamine pharmacokinetics was investigated in 14 critically ill newborn infants ranging from 27 to 43 weeks of gestational age and from 0.9 to greater than 4 kg birth weight. Plasma clearance rate was determined from dopamine levels during controlled infusions under actual clinical conditions. Dopamine was administered in stepwise increasing doses up to 8 micrograms/kg/min. Dopamine concentration and dopamine clearance rate were determined from duplicate samples drawn during each infusion in each patient. Steady-state plasma dopamine concentrations and plasma clearance rates were observed within 20 minutes at each infusion. Plasma dopamine concentration ranged from 0.5 ng/ml before infusion to almost 70 ng/ml at an infusion rate of 4 to 8 micrograms/kg/min. There was a linear correlation between infusion rate and plasma dopamine concentration (r = 0.68, p less than 0.001). Neither plasma dopamine concentration nor infusion rate had a significant effect on clearance rate. These data are consistent with first-order kinetics for administered dopamine in critically ill neonates over the range of concentrations studied.

Birth Weight↗
PubMed1990

Distribution and ontogeny of thyrotropin-releasing hormone degrading enzymes in rats.

The distribution and ontogeny of tissue prolyl endopeptidase and pyroglutamyl peptidase I activities were studied in the rat from the 7th day before birth to adulthood. While low levels of prolyl endopeptidase activity were demonstrable in many fetal tissues, activity in brain cortex, hypothalamus, lung, and kidney increased dramatically during the 2 wk after birth, gradually returning to adult levels. In adult rats, levels of tissue prolyl endopeptidase activity were highest in kidney, when compared with the intermediate levels in brain cortex, hypothalamus, and liver. Pyroglutamyl peptidase activity was widely distributed in adult rat tissues with high levels in kidney and liver that exceeded intermediate levels in brain cortex and hypothalamus. Pyroglutamyl peptidase activities in fetal gut, brain, and lung tissue were elevated above adult values. In contrast to the development changes in prolyl endopeptidase activities, pyroglutamyl peptidase activity remained elevated above adult levels only during the first week of life. These results indicate that both prolyl endopeptidase and pyroglutamyl peptidase activities in the rat are developmentally regulated.

Aging↗
PubMed1990

Two pathways for thyroxine 5'-monodeiodination in brown adipose tissue in fetal sheep: ontogenesis and divergent responses to hypothyroidism and 3,5,3'-triiodothyronine replacement.

Thermogenesis in rat brown adipose tissue (BAT) is thyroid hormone responsive. Rat BAT expresses a type II 5'-iodothyronine monodeiodinase (5'MDI) which mediates local T3 production from T4. Earlier studies show that BAT from fetal and newborn sheep contains a high Km type I, instead of type II, 5'MDI. To better characterize the 5'MDI of ovine fetal BAT, we studied the in vitro monodeiodination of [125I]T4 at a low substrate concentration (2 nM) and in the presence of 1 mM propylthiouracil in BAT homogenates of control and thyroidectomized fetuses at different gestational ages as well as in newborn lambs. Thyroidectomies were performed at three gestational ages: 99-107 days (group 1), 129-132 days (group 2), and 115-117 days (group 3A). Animals were studied 8-13 days after surgery. A significant increase in the activity of a low Km T4 5'MDI was noted in BAT from hypothyroid fetuses at all three gestational ages. This low Km activity was similar to the type II enzyme in rat BAT and brain in that the activity was also T3 resistant. A gradual rise in BAT type II 5'MDI activity was measured between 99 days gestation and term (150 days). These results indicate that ovine BAT contains two distinct iodothyronine 5'-monodeiodinating activities, one with a high Km and another with a low Km. The latter, resembling the type II 5'MDI in rat brain and BAT, is increased in ovine hypothyroid BAT. The former predominates in euthyroid tissue and is similar to the type I 5'MDI characterized in rat liver, kidney, and thyroid. We speculate that BAT type II 5'MDI may be important for neonatal BAT thermogenesis, while the type I enzyme may play a significant role in the increase in serum T3 concentration that occurs at birth.

Adipose Tissue, Brown↗