Glucose Homeostasis in Newborns: An Endocrinology Perspective.

Physiologic adaptations in the postnatal period, along with gradual establishment of enteral feeding, help maintain plasma glucose concentrations in the neonatal period. The definition of normal plasma glucose in the neonatal period has been a subject of debate because of a lack of evidence linking a set plasma or blood glucose concentration to clinical symptoms or predictors of short- and long-term outcomes. However, there is consensus that maintaining plasma glucose in the normal range for age is important to prevent immediate and long-term neurodevelopmental consequences of hypoglycemia or hyperglycemia. The specific management strategy for abnormal glucose levels in neonates depends on the underlying etiology, and interventions could include nutritional changes, medications, hormone therapy, or even surgery. Here, we will review the physiological processes that help maintain plasma glucose in newborns and discuss the approach to a newborn with disordered glucose homeostasis, with an emphasis on the endocrine basis of abnormal glucose homeostasis.

Humanin is an endogenous activator of chaperone-mediated autophagy.

Chaperone-mediated autophagy (CMA) serves as quality control during stress conditions through selective degradation of cytosolic proteins in lysosomes. Humanin (HN) is a mitochondria-associated peptide that offers cytoprotective, cardioprotective, and neuroprotective effects in vivo and in vitro. In this study, we demonstrate that HN directly activates CMA by increasing substrate binding and translocation into lysosomes. The potent HN analogue HNG protects from stressor-induced cell death in fibroblasts, cardiomyoblasts, neuronal cells, and primary cardiomyocytes. The protective effects are lost in CMA-deficient cells, suggesting that they are mediated through the activation of CMA. We identified that a fraction of endogenous HN is present at the cytosolic side of the lysosomal membrane, where it interacts with heat shock protein 90 (HSP90) and stabilizes binding of this chaperone to CMA substrates as they bind to the membrane. Inhibition of HSP90 blocks the effect of HNG on substrate translocation and abolishes the cytoprotective effects. Our study provides a novel mechanism by which HN exerts its cardioprotective and neuroprotective effects.

Pericarditis as the Presenting Feature of Graves Disease in a Pediatric Patient.

Pericarditis is a rare presentation of thyrotoxicosis associated with Graves disease. This association has not been previously described in the pediatric literature. We report a 17-year-old male patient who presented with chest pain, dyspnea, and tachycardia. He was found to have diffuse ST-segment elevation consistent with pericarditis. At presentation, he was noted to have bilateral proptosis. Abnormal thyroid function studies and an elevated thyroid-stimulating hormone receptor antibody level confirmed the diagnosis of Graves thyrotoxicosis. The patient was treated with anti-inflammatory and antithyroid agents and improved in time. We discuss previously reported cases of Graves disease-associated pericarditis in adults, potential etiologies, and management strategies.