Catecholaminergic responses of neonatal adrenal gland to insulin

M, Souto; Piezzi, Ramón S.; Bianchi, Renzo

doi:10.1007/bf01243382

Cited by 3 publications

(4 citation statements)

References 17 publications

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“…Rat pups were treated with 20 U k g S.C. of regular insulin (Novolin, Novo Nordisk, NJ) or an equal volume of saline vehicle and placed back with their dams after 2 h as we previously described (22). This treatment resulted in significant neonatal hypoglycemia (12,16). The pups were decapitated 24 h after injection, adrenal medullae were microdissected, and total RNA was extracted.…”

Section: Methodsmentioning

confidence: 99%

“…2). Using this protocol (12,16), the level of hypoglycemia was well below the threshold described by Khalil (75 mg/dL). Thus, this late, nonneurogenic pathway may also be unresponsive or nonfunctional in the neonatal rat pup exposed to hypoglycemia.…”

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confidence: 99%

“…On the other hand, in the neonatal rat during the first week of life, hypoglycemic stress fails to result in significant CA release, as presynaptic nerve terminals are nonfunctional at that time (10)(11)(12)14,16). In contrast, at this same age neonatal hypoxia releases CA through a nonneurogenic mechanism, acting "directly7' on the adrenal medulla (11,14,(17)(18)(19).…”

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confidence: 99%

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Neonatal Stress: Effects of Hypoglycemia and Hypoxia on Adrenal Tyrosine Hydroxylase Gene Expression

DeCristofaro

LaGamma

1994

Pediatr Res

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Catecholamines (CA) are released from and resynthesized in the adrenal medulla in response to stress. In the mature animal, stimulus-secretion-synthesis coupling occurs through transsynaptic (neuronal) activity. In contrast, in the immature animal, before functional adrenal innervation, certain stressors (hypoglycemia and glycopenia) do not result in CA release. Additionally, it is not known whether release and biosynthesis remain coupled in the neonate as they are in the adult. Therefore, to evaluate whether neonatal stressors can induce CA biosynthesis at the genomic level "directly7' before function adrenal innervation, we studied the expression of the tyrosine hydroxylase (TH) gene, the rate-limiting enzyme in CA biosynthesis. Newborn rat pups were made either hypoxic, hypoglycemic, or cellularly glycopenic (2-deoxyglucose). Neither hypoxic stress nor insulin-induced hypoglycemic stress altered steady state levels of TH mRNA in the neonate. However, cellular glycopenia resulted in a significant 2-fold rise in TH mRNA levels ( p < 0.05). As expected, each of these stressors increased TH mRNA levels in the mature adult rat. Thus, neonatal hypoxia and hypoglycemia appear to require intact neurogenic impulse activity, whereas cellular glycopenia may "directly" induce TH RNA, perhaps through hormonal mechanisms. This developmental model allows for the analysis of mechanisms governing adrenal CA release separate from those governing biosynthesis at the level of TH RNA. Acute neonatal hypoxic stress results in adrenal CA release without increasing TH RNA. Intrauterine growth retardation from chronic prenatal hypoxemia results in neonatal CA depletion and decreased CA responsiveness. We speculate that chronic hypoxia alters CA pathways, increasing the susceptibility of these infants to later stressors. (Pediatr Res 36: 71F723, 1994) Abbreviations TH, tyrosine hydroxylase 2-DG, 2-deoxyglucose CA, catecholamine Adrenomedullary release of CA are important mediators of two common stressors that compromise the neonatal transition to extrauterine life: hypoxia and hypoglycemia (1-5). In the absence of the adrenal medulla, the fetus and newborn show maladaptive responses resulting in increased morbidity and mortality (6-8). Because functional innervation of the rat adrenal medulla occurs after the first postnatal week of life (9-ll), a developmental window exists whereby the direct effects of stressors can be examined, independent of neuronal impulse activity.Hypoxia, insulin-induced hypoglycemia, and 2-DGinduced glycopenia act transsynaptically to release adrenal C A in the adult (12-15). On the other hand, in the neonatal rat during the first week of life, hypoglycemic

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Section: Methodsmentioning

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Neonatal Stress: Effects of Hypoglycemia and Hypoxia on Adrenal Tyrosine Hydroxylase Gene Expression

DeCristofaro

LaGamma

1994

Pediatr Res

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“…Preweaning rats are naturally ketogenic and capable of utilizing ketone bodies for energy production [ 61 ]. Thus, they may be able to withstand low plasma glucose (<3.0 mmol/L (<54 mg/dL)) without mounting counterregulatory catecholamine response [ 62 ]. Conversely, healthy human children exhibit neurological dysfunction and counterregulatory hormonal response at higher blood glucose concentrations (3.6–4.2 mmol/L (65–75 mg/dL)) [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic-Pituitary-Adrenal Axis Programming after Recurrent Hypoglycemia during Development

Rao

2015

JCM

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Permanent brain injury is a complication of recurrent hypoglycemia during development. Recurrent hypoglycemia also has adverse consequences on the neuroendocrine system. Hypoglycemia-associated autonomic failure, characterized by ineffective glucose counterregulation during hypoglycemia, is well described in children and adults on insulin therapy for diabetes mellitus. Whether recurrent hypoglycemia also has a programming effect on the hypothalamus-pituitary-adrenal cortex (HPA) axis has not been well studied. Hypoglycemia is a potent stress that leads to increased glucocorticoid secretion in all age groups, including the perinatal period. Other conditions associated with exposure to excess glucocorticoid in the perinatal period have a programming effect on the HPA axis activity. Limited animal data suggest the possibility of similar programming effect after recurrent hypoglycemia in the postnatal period. The age at exposure to hypoglycemia likely determines the HPA axis response in adulthood. Recurrent hypoglycemia in the early postnatal period likely leads to a hyperresponsive HPA axis, whereas recurrent hypoglycemia in the late postnatal period lead to a hyporesponsive HPA axis in adulthood. The age-specific programming effects may determine the neuroendocrine response during hypoglycemia and other stressful events in individuals with history of recurrent hypoglycemia during development.

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Effects of acute stress on the contents of catecholamines and neuropeptides in chromaffin tissues of the newborn rabbit

Wikström

Rökaeus

Fried

1998

Regulatory Peptides

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Catecholaminergic responses of neonatal adrenal gland to insulin

Cited by 3 publications

References 17 publications

Neonatal Stress: Effects of Hypoglycemia and Hypoxia on Adrenal Tyrosine Hydroxylase Gene Expression

Neonatal Stress: Effects of Hypoglycemia and Hypoxia on Adrenal Tyrosine Hydroxylase Gene Expression

Hypothalamic-Pituitary-Adrenal Axis Programming after Recurrent Hypoglycemia during Development

Effects of acute stress on the contents of catecholamines and neuropeptides in chromaffin tissues of the newborn rabbit

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