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Carbohydrate metabolism
1Department of Endocrinology, Children's Hospital Medical Center, Cincinnati, OH 45229.
Insights
Newborns transition to energy autonomy using hormonal shifts and enzyme activity. Hormones like glucagon and epinephrine activate fuel mobilization, ensuring glucose homeostasis through glycogenolysis and gluconeogenesis.
Area of Science:
- Neonatal physiology
- Metabolic adaptation
- Endocrinology
Background:
- The transition from intrauterine to extrauterine life requires significant metabolic adjustments in newborns.
- Maintaining glucose homeostasis is critical for neonatal survival and development.
Purpose of the Study:
- To elucidate the hormonal and enzymatic mechanisms governing neonatal energy metabolism at birth.
- To explain the shift from maternal glucose dependence to endogenous fuel utilization.
Main Methods:
- Analysis of hormonal surges (glucagon, epinephrine, insulin) at birth.
- Examination of key enzyme activity patterns (phosphorylase, PEPCK) involved in glucose metabolism.
- Integration of lipolysis and fatty acid oxidation roles in gluconeogenesis.
Main Results:
- Hormonal changes (increased glucagon/epinephrine, decreased insulin) trigger specific enzyme activities.
- Phosphorylase and PEPCK activation facilitate rapid mobilization of endogenous fuel stores.
- Hepatic fatty acid oxidation provides essential cofactors, sustaining gluconeogenesis.
Conclusions:
- A coordinated hormonal and enzymatic framework enables newborn energy autonomy.
- This metabolic transition ensures glucose homeostasis via glycogenolysis and gluconeogenesis.
- Understanding these mechanisms aids in interpreting neonatal hypoglycemia and guiding future research.
Abstract:
In summary, the surges of glucagon and epinephrine at birth, coupled with the fall in insulin secretion, are in accord with appropriate receptor changes, as well as genetic ontogenic patterns of enzyme development. Enzyme activities are further stimulated by the hormonal changes at birth; phosphorylase is activated by glucagon and epinephrine, while PEPCK is activated by glucagon and its expression is facilitated by the fall in insulin. In concert, these changes permit rapid activation of catabolic processes and the mobilization and utilization of endogenous fuel stores. Glucose homeostasis is maintained by glycogenolysis and gluconeogenesis supported by the appropriate enzyme inductions. The free fatty acids released, via lipolysis, also serve to sustain gluconeogenesis, since hepatic fatty acid oxidation is necessary for gluconeogenesis by providing the essential cofactors. This framework permits a rational interpretation of the mechanisms underlying the remarkable transition from intrauterine dependence on maternal glucose to extrauterine autonomy of newborn energy integration. This framework can also explain several causes of neonatal hypoglycemia and act as a base for future investigations.