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Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
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Hypothalamic-Pituitary-Adrenal Axis Programming after Recurrent Hypoglycemia during Development.

Raghavendra Rao1,2

  • 1Department of Pediatrics, Division of Neonatology, University of Minnesota, Minneapolis, MN 55455, USA. raghurao@umn.edu.

Journal of Clinical Medicine
|September 8, 2015
PubMed
Summary
This summary is machine-generated.

Recurrent hypoglycemia during development can cause permanent brain injury and affect the neuroendocrine system. The timing of hypoglycemia exposure influences the adult hypothalamus-pituitary-adrenal cortex (HPA) axis response.

Keywords:
brain injurycorticosteronecortisoldevelopmenthypoglycemiahypoglycemia-associated autonomic failurehypothalamus-pituitary-adrenal axisprogrammingrecurrent hypoglycemia

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Area of Science:

  • Neuroendocrinology
  • Developmental neuroscience
  • Metabolic disorders

Background:

  • Recurrent hypoglycemia during development can lead to permanent brain injury and neuroendocrine dysfunction.
  • Hypoglycemia-associated autonomic failure is known in diabetes patients on insulin therapy.
  • The programming effect of recurrent hypoglycemia on the hypothalamus-pituitary-adrenal cortex (HPA) axis remains understudied.

Purpose of the Study:

  • To investigate the programming effect of recurrent hypoglycemia on the hypothalamus-pituitary-adrenal cortex (HPA) axis during development.
  • To determine if early-life recurrent hypoglycemia alters adult HPA axis activity.
  • To explore age-specific programming effects of hypoglycemia on neuroendocrine responses.

Main Methods:

  • Review of existing literature on hypoglycemia, brain injury, and HPA axis programming.
  • Analysis of animal data regarding postnatal hypoglycemia exposure and HPA axis function.
  • Correlation of age at hypoglycemia exposure with adult HPA axis responsiveness.

Main Results:

  • Recurrent hypoglycemia is a potent stressor, inducing glucocorticoid secretion.
  • Limited animal data suggest postnatal hypoglycemia can program the HPA axis.
  • Early postnatal hypoglycemia may lead to a hyperresponsive adult HPA axis, while late exposure may cause hyporesponsiveness.

Conclusions:

  • Recurrent hypoglycemia during development can have lasting programming effects on the HPA axis.
  • The age at which hypoglycemia occurs is critical in determining the long-term neuroendocrine consequences.
  • These age-specific programming effects may influence responses to stress and hypoglycemia in adulthood.