Effect of thyroid hormone on cerebral glucose metabolism in the infant rat

Tl, Moore; Lione, AP; Regen, DM

doi:10.1152/ajplegacy.1973.225.4.925

Cited by 23 publications

(8 citation statements)

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“…In postnatal rats, hypothyroidism diminishes, and T4 administration enhances, blood-brain glucose uptake (Moore et al 1973). Maternal iodine deficiency is also associated with reduced blood-brain glucose uptake in weanling progeny, which can be prevented by feeding an iodine-replete diet from parturition (Sunitha et al 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Thyroid hormone regulates glucose transport in astrocytes in culture (Roeder et al 1988) and postnatal rat brain in vivo (Moore et al 1973). Such findings are likely to be of relevance to maternal thyroid hormone action since the fetus is highly dependent upon glucose, both as an energy source and as a precursor for biosynthetic reactions intimately connected with tissue growth ( Jones & Rolph 1985).…”

Section: Introductionmentioning

confidence: 99%

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Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta

Pickard¹,

Sinha²,

Ogilvie³

et al. 1999

Journal of Endocrinology

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The influence of maternal hypothyroxinemia on the expression of the glucose transporters, GLUT1 and GLUT3, in rat fetal brain and placenta was investigated. Fetal growth was retarded in hypothyroxinemic pregnancies, but only before the onset of fetal thyroid hormone synthesis. Placental weights were normal, but placental total protein concentration was reduced at 19 days gestation (dg). Immunoblotting revealed a decreased abundance of GLUT1 in placental microsomes at 16 dg, whereas GLUT3 was increased. Fetal serum glucose levels were reduced at 16 dg. In fetal brain, the concentration of microsomal protein was deficient at 16 dg and the abundance of parenchymal forms of GLUT1 was further depressed, whereas GLUT3 was unaffected. Northern hybridization analysis demonstrated normal GLUT1 mRNA levels in placenta and fetal brain.In conclusion, maternal hypothyroxinemia results in fetal growth retardation and impaired brain development before the onset of fetal thyroid function. Glucose uptake in fetal brain parenchyma may be compromised directly, due to deficient GLUT1 expression in this tissue, and indirectly, as a result of reduced placental GLUT1 expression. Though corrected by the onset of fetal thyroid hormone synthesis, these deficits are present during the critical period of neuroblast proliferation and may contribute to long term changes in brain development and function seen in this model and in the progeny of hypothyroxinemic women.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta

Pickard¹,

Sinha²,

Ogilvie³

et al. 1999

Journal of Endocrinology

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“…The finding of such a marked increase during the 10-20 day interval is consistent with qualitative in vivo observations that [14C]glucose is progressively more rapidly incorporated into brain amino acids during maturation of suckling rats, the largest increases occurring later in the suckling period (Gaitonde and Richter, 1966;Cocks et al, 1970;Pate1 et al, 1974;DeVivo et al, 1975). Quantitative estimates of CMRG from brain uptake of 3Hz0, [ 1 4 C ] g l~~~~e , and [14C]methylglucose have indicated an increase in the rat from 0.02-0.04 pmoYmin/g in the neonate (Moore et al , 1971) to 0.34 pmol/min/g at 15 days (Moore et al, 1973).…”

Section: Cmrgmentioning

confidence: 99%

“…Some of the observations on developing compared with adult brain relevant to this question are: (1) Developing rat brain can derive a much larger proportion of its metabolic needs from ketone bodies (Hawkins et al, 1971; Sokoloff, 1973). (2) Developing rat brain utilizes glucose more slowly (Moore et al, 1973;Cremer and Heath, 1974; Dahlquist and Persson, 1976). (3) Developing mouse, rat, and dog brain have lower oxygen and energy requirements (Lowry et al, 1964;Duffy et al, 1975;Gregoire et al, 1978;Hernandez et al, 1978).…”

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confidence: 99%

Brain Carbohydrate Metabolism in Developing Rats During Hypercapnia

Miller

Corddry

1981

Journal of Neurochemistry

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Brain glucose metabolism was studied in developing rats at ages 10 and 20 days postnatal under normal and hypercapnic conditions. Brains were removed and frozen within 1 s with a freeze-blowing apparatus. Glucose utilization was measured with [2-14C]glucose and [3H]deoxyglucose as tracers. Metabolites were determined by standard enzymatic techniques. Data from [3H]deoxyglucose phosphorylation indicated that normal brain glucose utilization increased almost threefold between the 10th and 20th postnatal days. From the relative rates of utilization of the two isotopes in the 20-day-old control group, it appeared that about 25% of 14C label derived from metabolism of [2-14C]glucose was lost from brain (probably as lactate) rather than entering the Krebs cycle. Under hypercapnic conditions (20% CO2-21% O2-59% N2), rates of glucose utilization by brain were decreased by one-half at both ages and there were progressive decreases in the concentrations of many intermediary metabolites. The bases for concluding that these metabolites were used to supplement glucose as a fuel for respiration, rather than being lost by leakage into blood, are discussed. Despite the differences in brain glucose metabolism between 10-day-old and 20-day-old rats, their responses to hypercapnia are remarkably similar: Rates of glucose utilization are reduced to approximately the same proportion of the original rate by 20% CO2, and endogenous metabolites (particularly glutamate and lactate) appear to be oxidized as replacement fuels.

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“…This metabolic maturation includes the brain, accelerating lipid synthesis (14)(15)(16)(17), protein synthesis (10,18), and carbohydrate metabolism (19) in brain tissue. Furthermore, hyperthyroidism accelerates appearance of such behavioral phenomena as audiogenic seizure (20), maze learning (2 l), general locomotor activity (22), startle response (23,24), and swimming (25).…”

Section: Hyperthyroidism and Stress Responsementioning

confidence: 99%

Neonatal Hyperthyroidism and Maturation of the Rat Hypothalamo-Hypophyseal-Adrenal Axis

Meserve

Leathem

1974

Experimental Biology and Medicine

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The neonatal rat exhibits a refractory period of the hypothalamo-hypophyseal-adrenal axis in response to stress which encompasses days 3-1 2 of life, an interval called the stress nonresponsive period (SNR) (1). Then, at 15 days of age, the rat responds equally to ether stress and exogenous ACTH by an increased synthesis and release of corticosterone (2). However, hypothyroidism induced by thiouracil feeding during pregnancy and lactation prevented the hypothalamo-hypophyseal-adrenal axis response to ether stress possibly by extending the SNR period (3). What effect the feeding of desiccated thyroid would have on the maturation of this axis has not been reported. Thus the purpose of the present study was to examine the effect of thyroid feeding on the response of 12-day-old rats to ether stress and to exogenous ACTH by measuring adrenal corticosterone (B) (an index of hormone synthesis) and serum corticosterone (an index of hormone release). Materials and Methods.Female Sprague-Dawley rats weighing 150-175 g (Camm Research Institute, Wayne, NJ) were housed in a temperature (78" F) regulated room with a light-dark cycle of 12: 12 hr. The rats were fed Purina Lab Chow ad lib. until a body weight of 180-200 g was attained. The animals were then mated with proven males of the same strain.

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Effect of thyroid hormone on cerebral glucose metabolism in the infant rat

Cited by 23 publications

References 0 publications

Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta

Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta

Brain Carbohydrate Metabolism in Developing Rats During Hypercapnia

Neonatal Hyperthyroidism and Maturation of the Rat Hypothalamo-Hypophyseal-Adrenal Axis

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