» Articles » PMID: 36619556

Impact of Glucose Metabolism on the Developing Brain

Overview
Specialty Endocrinology
Date 2023 Jan 9
PMID 36619556
Authors
Affiliations
Soon will be listed here.
Abstract

Glucose is the most important substrate for proper brain functioning and development, with an increased glucose consumption in relation to the need of creating new brain structures and connections. Therefore, alterations in glucose homeostasis will inevitably be associated with changes in the development of the Nervous System. Several studies demonstrated how the alteration of glucose homeostasis - both hyper and hypoglycemia- may interfere with the development of brain structures and cognitivity, including deficits in intelligence quotient, anomalies in learning and memory, as well as differences in the executive functions. Importantly, differences in brain structure and functionality were found after a single episode of diabetic ketoacidosis suggesting the importance of glycemic control and stressing the need of screening programs for type 1 diabetes to protect children from this dramatic condition. The exciting progresses of the neuroimaging techniques such as diffusion tensor imaging, has helped to improve the understanding of the effects, outcomes and mechanisms underlying brain changes following dysglycemia, and will lead to more insights on the physio-pathological mechanisms and related neurological consequences about hyper and hypoglycemia.

Citing Articles

A rotenone organotypic whole hemisphere slice model of mitochondrial abnormalities in the neonatal brain.

Butler B, Renney M, Bennett K, Charpentier G, Nance E J Biol Eng. 2024; 18(1):67.

PMID: 39543609 PMC: 11566268. DOI: 10.1186/s13036-024-00465-w.


Maternal Nutrition during Pregnancy and Offspring Brain Development: Insights from Neuroimaging.

Na X, Mackean P, Cape G, Johnson J, Ou X Nutrients. 2024; 16(19).

PMID: 39408304 PMC: 11478768. DOI: 10.3390/nu16193337.


Altered metabolic profiles in male offspring conceived from intracytoplasmic sperm injection.

Zhang B, Ban M, Chen X, Hu J, Cui L, Chen Z BMC Med. 2024; 22(1):462.

PMID: 39402563 PMC: 11476986. DOI: 10.1186/s12916-024-03654-y.


Hindlimb immobilization induces insulin resistance and elevates mitochondrial ROS production in the hippocampus of female rats.

Kerr N, Mossman C, Chou C, Bunten J, Kelty T, Childs T J Appl Physiol (1985). 2024; 137(3):512-526.

PMID: 38961821 PMC: 11424180. DOI: 10.1152/japplphysiol.00234.2024.


Recommendations for recognizing, risk stratifying, treating, and managing children and adolescents with hypoglycemia.

Zucchini S, Tumini S, Scaramuzza A, Bonfanti R, Delvecchio M, Franceschi R Front Endocrinol (Lausanne). 2024; 15:1387537.

PMID: 38894740 PMC: 11183505. DOI: 10.3389/fendo.2024.1387537.


References
1.
Mitanchez-Mokhtari D, Lahlou N, Kieffer F, Magny J, Roger M, Voyer M . Both relative insulin resistance and defective islet beta-cell processing of proinsulin are responsible for transient hyperglycemia in extremely preterm infants. Pediatrics. 2004; 113(3 Pt 1):537-41. DOI: 10.1542/peds.113.3.537. View

2.
Tomlinson D, Gardiner N . Glucose neurotoxicity. Nat Rev Neurosci. 2007; 9(1):36-45. DOI: 10.1038/nrn2294. View

3.
Russo V, Higgins S, Werther G, Cameron F . Effects of fluctuating glucose levels on neuronal cells in vitro. Neurochem Res. 2012; 37(8):1768-82. DOI: 10.1007/s11064-012-0789-y. View

4.
Nevo-Shenker M, Shalitin S . The Impact of Hypo- and Hyperglycemia on Cognition and Brain Development in Young Children with Type 1 Diabetes. Horm Res Paediatr. 2021; 94(3-4):115-123. DOI: 10.1159/000517352. View

5.
Biessels G, Kerssen A, de Haan E, Kappelle L . Cognitive dysfunction and diabetes: implications for primary care. Prim Care Diabetes. 2008; 1(4):187-93. DOI: 10.1016/j.pcd.2007.10.002. View