**Neonatal Hypoglycemia**

**Neonatal Hypoglycemia**

Adauto Dutra Moraes Barbosa, Israel Figueiredo Júnior and Gláucia Macedo de Lima Israel Figueiredo Júnior and Gláucia Macedo de Lima Additional information is available at the end of the chapter

Adauto Dutra Moraes Barbosa,

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/intechopen.69676

#### **Abstract**

Hypoglycemia is the most frequent metabolic abnormality in the newborn, but no consensus exists on what level of blood glucose is able to protect the brain and influence the child's neural development and which is the best course of management in cases labeled as hypoglycemia. Early diagnosis, urgent treatment, and prevention of future episodes of hypoglycemia are the cornerstones of management, now supported by recent advances in molecular genetics and in our understanding of the pathophysiology of neonatal hypoglycemia, particularly the pathogenesis of congenital hyperinsulinemic hypoglycemia.

DOI: 10.5772/intechopen.69676

**Keywords:** hypoglycemia, newborn, molecular mechanisms, hyperinsulinemia, actual treatment

#### **1. Introduction**

Hypoglycemia is the most frequent metabolic abnormality in the newborn, and although it is the most common biochemical disorder in this age group [30], it is still a source of clinical concern and controversy, as no consensus exists on what level of blood glucose is able to protect the brain and influence the child's neural development [6, 22, 53] and which is the best course of management in cases labeled as hypoglycemia. Early diagnosis, urgent treatment, and prevention of future episodes of hypoglycemia are the cornerstones of management, now supported by recent advances in molecular genetics [48] and in our understanding of the pathophysiology of neonatal hypoglycemia, particularly the pathogenesis of congenital hyperinsulinemic hypoglycemia [12].

Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons

Hypoglycemia occurs in 1.3–4.4 per 1000 full-term newborns and 15–55 per 1000 preterm newborns. This suggests that gestational age has enormous influence on its onset; in certain groups, adaptive mechanisms are not adequately developed, which predisposes them to increased risk of hypoglycemia. According to current evidence, the prevalence of hypoglycemia is approximately 10% in full-term neonates [45]; 6.5% in appropriate for gestational age (AGA), 8% in large for gestational age (LGA), and 15% in small for gestational age (SGA) newborns; and 15.5% in late-preterm infants [7].

Most glucose in the fetus undergoes oxidation to supply its energy needs, while another part contributes significantly to a buildup of glycogen, protein, and fat in triglyceride form. Glucose is the most important source of energy for the fetus and the major substrate for brain

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http://dx.doi.org/10.5772/intechopen.69676

At birth, the fetus becomes dependent on itself to obtain energy and meet the metabolic needs of its vital organs, particularly the central nervous system (CNS). Each mole of oxidized glu-

Cerebral glucose transport takes place through a facilitated diffusion process, which is dependent on glycemia and is not regulated by insulin. Protection against hypoglycemia is coordinated by the autonomic nervous system by means of hormones that stimulate the production of glucose (through glycogenolysis and gluconeogenesis) and limit peripheral glucose utilization [54]. Glycogen is the only glucose storage medium in the body. Its deposits are found in the liver,

The fetal liver contains a complete enzyme system for the synthesis and breakdown of glycogen, levels of which are low in early pregnancy but rise slowly and steadily from gestational weeks 15–20, before peaking in the third trimester. At this time, fat deposition also increases. Thus, part of the energy and substrates used for fetal growth is redirected for storage, which

Hepatic glycogenolysis is the major mechanism of glucose release in the immediate neonatal period, which leads to depletion of glycogen stores. It is induced by an increase in glucagon and catecholamines and a reduction in insulin. This exhaustion of glycogen stores promotes activation of gluconeogenesis, which occurs largely as a result of free fatty acid oxidation in the liver. Glucose homeostasis will thus depend on glucose intake; gluconeogenesis; glycogen, protein,

Glucose produced from the breakdown of dietary lactose into galactose and glucose, for instance, is not taken up by the liver in the neonatal period; the newborn is thus dependent on

Once glycogen stores are low, gluconeogenesis induced by glucagon, catecholamines, cortisol, and growth hormone mobilizes fat and protein substrates. Insulin, thyroid hormone, cortisol, and glucagon systematically promote induction of specific enzymes, thus adapting the neonate to the abrupt cessation of the supply glucose that was provided continuously before birth. Upon clamping the umbilical cord, the maternal glucose supply, which was 54 mg/dL during pregnancy, ceases abruptly, and the neonate's blood glucose levels decline rapidly and precipitously—from a concentration similar to that of the mother to approximately 41 mg/dL within the first 6 h of life. Physiologically, glucose concentration decreases to approximately 30 mg/ dL in the first 2 h after birth, subsequently rises, and plateaus at approximately 45 mg/dL 12 h

striated muscle tissue (including cardiac muscle), kidneys, bowel, brain, and placenta.

will play an important role in the peripartum and postpartum periods.

and fat stores; and hormonal and neural factors.

hepatic gluconeogenesis to sustain glucose production.

metabolism.

after birth.

**2.2. Glucose uptake in the newborn**

cose provides 38 moles of adenosine triphosphate (ATP) [54].
