RT Book, Section
A1 Hay Jr., William W.
A2 Rudolph, Colin D.
A2 Rudolph, Abraham M.
A2 Lister, George E.
A2 First, Lewis R.
A2 Gershon, Anne A.
SR Print(0)
ID 6735163
T1 Chapter 51. Metabolic Abnormalities
T2 Rudolph's Pediatrics, 22e
YR 2011
FD 2011
PB The McGraw-Hill Companies
PP New York, NY
SN 978-0-07-149723-7
LK accesspediatrics.mhmedical.com/content.aspx?aid=6735163
RD 2024/04/19
AB Normal  postnatal  glucose  homeostasis  is  established  by  increased  glucose  production  and  glucose  utilization.1  Factors  that  promote  glucose  production  and  release  into  the  circulation  include  catecholamines  and  glucagon,  which  activate  glycogenolysis.  A  high  glucagon-to-insulin  ratio,  which  induces  synthesis  and  activity  of  the  enzymes,  is  required  for  gluconeogenesis.  Once  normal  feedings  are  established,  glycerol  and  amino  acids  continue  to  fuel  gluconeogenesis  while  dietary  fatty  acids  activate  the  enzymes  responsible  for  gluconeogenesis.  Additionally,  galactose  derived  from  hydrolysis  of  milk  sugar  (lactose)  in  the  gut  increases  hepatic  glycogen  production  for  sustained  between-feeding  hepatic  glucose  release  from  glycogen  breakdown.  Feedings  also  induce  production  of  intestinal  peptides,  or  incretins,  that  promote  insulin  secretion.  Insulin  decreases  hepatic  glucose  production  and  increases  glucose  utilization  for  energy  production  and  storage  as  glycogen.  These  opposing  conditions  of  glucose  production  and  utilization  continue  in  response  to  normal  feed-fast  cycles,  regulating  normal  plasma  glucose  concentrations.2