Influence of Transcortin on Degradation and Tissue Uptake of Corticosterone in the Infant Rat

Koch, Bernard; Lutz, B; Schmitt, G; Mialhe, C

doi:10.1055/s-0028-1095062

Cited by 15 publications

(2 citation statements)

References 3 publications

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“…Thus it would appear that if there is a decrease in MCR with age, it would be due to a corresponding decrease in V. Similarly, we would predict that the effects of thyroid status on corticosterone development could be accounted for by decreased V in hyperthyroid animals and increased V in hypothyroid animals. There is good precedent for this because in adult rats (32) and 6-day-old rats (29), the increased plasma concentrations of corticosterone following T4 treatment have been ascribed primarily to decreased V. Our further suggestion would be that decreasing values for V in response to both increasing age and increasing T4 are the result of the increase of CBG that occurs under these conditions (1, 3,8).…”

Section: Age (Days)mentioning

confidence: 88%

Circulating Corticosterone in the Infant Rat: The Mechanism of Age and Thyroxine Effects

1986

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ABSTRACT. Infant rats exhibit a marked rise in serum concentrations of corticosterone between postnatal days 12 and 24. As this rise appears to be cued by L-thyroxine, the aim of the current study was to determine the physiological bases of the effects of both age and thyroid status on serum corticosterone. The in vivo response to either adrenocorticotropic hormone (60 mU/g body weight) or dibutyryl 3',5'-cyclic adenylate (0.3 mg/g body weight) increased between 10 and 16 days and was advanced and delayed by hyper-and hypothyroidism, respectively. In contrast, in vitro studies with adrenals from rats aged 10 and 16 days showed no effect of age on either basal or adrenocorticotropic hormone-stimulated production of corticosterone. Chronic administration of exogenous corticosterone to hyperthyroid animals resulted in significantly higher concentrations of serum corticosterone than did an identical administration to hypothyroid animals. In the neonatal rat, circulating concentrations of corticosterone are extremely low on days 6 through 12, then they rise markedly beginning on day 14 and reaching a peak on days 24-25 (1-3). During this same period the circulating concentrations of ACTH do not change significantly (4). Thus, either the ontogenic increase of corticosterone is independent of ACTH or the system becomes increasingly responsive to the basal concentration of ACTH. There is conflicting evidence regarding the latter possibility (4-6) and the data are difficult to interpret because of the use of a fluorometric method for measuring corticosterone which is now recognized to be inappropriate in young rodents (1, 2, 7).

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Section: Age (Days)mentioning

confidence: 88%

Circulating Corticosterone in the Infant Rat: The Mechanism of Age and Thyroxine Effects

1986

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“…The circulating level of CBG indeed plays a crucial role in the extent to which the unbound moiety of glucocorticoids is transferred into the liver and hence in the biological activity of these steroids [43]. Moreover, the localization of receptors for CBG on cell membranes [13], and especially on hepatic membranes [44], together with the presence of CBG inside the cells (which is likely to interfere competitively with the glucocorticoid's access to the nucleus), confers additional degrees of complexity on the mechanisms of action of CBG at the cellular level. More work is clearly needed to clarify these issues.…”

Section: Figure 7 Schematic Model Showing the Putative Influence Of Cmentioning

confidence: 99%

Pituitary adenylate cyclase-activating polypeptide induces expression of corticosteroid-binding globulin in cultured fetal hepatocytes: synergy with tri-iodothyronine

Fahime

Lutz-Bucher

Felix

et al. 1996

Biochemical Journal

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The purpose of the present study was to determine whether functional receptors for pituitary adenylate cyclase-activating polypeptide (PACAP) are expressed in cultured rat fetal hepatocytes and eventually play a role in regulating gene expression of corticosteroid-binding globulin (CBG). We found PACAP38 and PACAP27 to elevate cAMP levels in hepatocytes in a dose-dependent manner, with a plateau being achieved at 10 nM and EC50 values of about 0.5–1 nM. PACAP failed to alter the turnover of inositol phosphates, whereas PACAP and VIP stimulated cAMP accumulation in an equipotent manner, suggesting the presence in these cells of type II receptor isoforms. As revealed by measurements of both CBG mRNA levels and concentrations of binding sites, long-term treatment of fetal cells with 10 nM PACAP, although resulting in partial desensitization of peptide-induced cAMP accumulation, caused a significant 3-fold elevation in CBG synthesis. This stimulatory influence of PACAP was mimicked by the cell permeant N6,2´-O-dibutyryladenosine 3´,5´-phosphate (dbcAMP). Treatment of hepatocytes with tri-iodothyronine (T3) enhanced CBG expression and, most interestingly, appeared to synergize with PACAP to elicit a 2–3-fold amplification of CBG synthesis. This study thus provides first evidence for the up-regulation by PACAP and cAMP of CBG expression in fetal hepatocytes and for T3's playing a synergistic role in enhancing PACAP-induced synthesis of the binder.

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Acquisition of submandibular gland nerve growth factor (SMG‐NGF) responsiveness to thyroxine administration in neonatal mice

Lakshmanan

Beri

Perheentupa

et al. 1984

J of Neuroscience Research

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The growth of the submandibular gland (SMG) was studied in newborn mice from birth to 15 days of age. Progressive changes in wet weight were observed to accompany changes in biochemical constituents such as RNA, protein, and lipid. Thyroxine (T4) administration from days 0-6 produced changes in SMG growth and SMG accumulation of RNA, protein, and lipid components relative to control pups treated with a similar volume of vehicle. This hormone regimen produced no measurable changes in SMG nerve growth factor (SMG-NGF) concentration. T4 responsiveness also was studied from days 0-15. Three patterns of T4 injection (from days 0-6, 7-14, and 0-14) were found to elicit a differential response in the three biochemical constituents measured, but treatment from days 7-14 and 0-14 elicited precocious increments in SMG-NGF concentrations on day 15. The effect of T4 injection from birth was more effective in augmenting SMG-NGF concentration than hormone treatment initiated from days 7-14. A persistent T4 effect on SMG-NGF also was observed on day 21 following hormone treatment from days 7-14 or 0-14. In summary, the acquisition of SMG-NGF responsiveness to T4 appears to develop during the neonatal period. The administration of T4 during this period also precociously stimulates the mechanisms that govern the normal ontogeny of SMG-NGF at the time of weaning.

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Influence of Transcortin on Degradation and Tissue Uptake of Corticosterone in the Infant Rat

Cited by 15 publications

References 3 publications

Circulating Corticosterone in the Infant Rat: The Mechanism of Age and Thyroxine Effects

Circulating Corticosterone in the Infant Rat: The Mechanism of Age and Thyroxine Effects

Pituitary adenylate cyclase-activating polypeptide induces expression of corticosteroid-binding globulin in cultured fetal hepatocytes: synergy with tri-iodothyronine

Acquisition of submandibular gland nerve growth factor (SMG‐NGF) responsiveness to thyroxine administration in neonatal mice

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