Developmental disorders of glucose metabolism in infants

Abstract

An increase in plasma glucose of less than 4 mmol/L is considered abnormal in adults following administration of a fasting glucagon tolerance test. The responses of preterm infants and adults to glucagon are clearly different. The attenuated response to glucagon in the preterm infants is consistent with the low levels of hepatic glucose-6-phosphatase activity in premature infants as glucose-6-phosphatase is the terminal step of the two main pathways of liver glucose production.

Glucagon, cyclic AMP, and hepatic glucose mobilization: A half‐century of uncertainty

“…Neonates are at high risk of hypoglycemia, and are uniquely dependent on the nutritional provision of exogenous glucose or, failing that, of gluconeogenic substrates, to maintain glycemia (Decaux et al, 1986; Girard, 1986; Girard et al, 1973; Mehta et al, 1987; Stanley et al, 2015). In the early neonate, moderate hyperglycemia minimizes the risk of hypoglycemic damage, particularly to the developing central nervous system (Güemes et al, 2016; Hume et al, 2002). Whole‐body knockout of cytosolic PEPCK, for example, is lethal in the early postnatal period (Semakova et al, 2017).…”

“…Whole‐body knockout of cytosolic PEPCK, for example, is lethal in the early postnatal period (Semakova et al, 2017). Prematurely‐born infants appear to have abnormally low peak plasma glucagon levels, a blunted glucagon response to variable nutritional conditions (Bak et al, 2014; Hawdon et al, 1993; Hawdon et al, 1993; Hume et al, 2002; Jackson et al, 1997; Mehta et al, 1987; Molinari et al, 1982; Sunehag et al, 1994), and suppressed responses to exogenous glucagon (Hume et al, 2002). This helps to explain why premature infants are more vulnerable to damaging effects of fasting or restricted nutrient availability than are full‐term neonates (Table 4C, Figures 2d and 9a).…”

"Cardiotocografia computadorizada em gestantes com diabetes mellitus: efeitos da glicemia capilar materna na freqüência cardíaca fetal"

“…Em crianças prematuras, observa-se capacidade parcial de se obter suprimento de glicose pela produção endógena, ao ocorrer declínio da oferta exógena. A idade gestacional parece influenciar na maturação do metabolismo hepático da glicose e da atividade da glicose-6-fosfatase 37,38 . Prematuros nascidos com idade gestacional maior que 30 semanas parecem manter mais facilmente a concentração de glicose plasmática, com adaptação mais eficiente na utilização de glicose periférica 37 .…”