Forebrain cellular bioenergetics in neonatal mice

Narchi, Hassib; Pramathan, Thachillath; Souid, Abdul‐Kader

doi:10.3233/npm-181737

Cited by 1 publication

(2 citation statements)

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“…Although the normal metabolic adaptation to extrauterine life also involves the use of ketone bodies as alternative substrates for cerebral oxidative metabolism, the newborn infant, however, has a limited ability to mobilize these nutrients [6]. Lactate is also a potential substitute substrate for energy metabolism [32], but it is insufficient to support metabolism as an alternate substrate to replace glucose [33].…”

Section: [Adp]/[atp] + [Adp] + [Amp]mentioning

confidence: 99%

“…As the administered insulin promotes glycogen storage and inhibits glycogenolysis, the prevalent ketogenesis in neonatal rodents, would also be suppressed as insulin suppresses lipolysis. Thus, the insulin-induced hypoglycemia cannot be explained only by decreases in circulating glucose as we have not measured nor controlled for the alternative cerebral fuels such as lactate and ketones [6,33]. Moreover, we did not control for the effect of pup sex, weight or litter size.…”

Section: Strengths and Limitationsmentioning

confidence: 99%

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Cellular adenylate energy charge and adenine nucleotides in brain tissue during hypoglycemia in newly born BALB/c mice pups

Narchi,

Yuvaraju,

George

et al. 2024

Exploration of Medicine

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Aim: Hypoglycemia occurs in the neonatal period but the exact pathophysiology of the resulting brain injury at the cellular level is not well known. Therefore, a neonatal murine model was developed with insulin-induced hypoglycemia, to analyze the in-vitro effects of hypoglycemia on brain nucleotides and adenylate energy charge (AEC) throughout the first ten days of life. Methods: Newly born BALB/c pups between one and ten days of age were used. In each age group, six pups were subjected to insulin-induced hypoglycemia and six others served as controls. In both groups, immediately after euthanasia, brain tissues were collected. The in-vitro effects of hypoglycemia on brain nucleotides [adenosine monophosphate (AMP), adenosine diphosphate (ADP), and adenosine triphosphate (ATP)] were analyzed using liquid chromatography with tandem mass spectrometry (LC-MS/MS) as well on AEC. Results: In the controls, the cellular AEC steadily decreased with age by at least 50% over the 10-day study period (P < 0.05) except in the parietal tissue (P = 0.30) where it remained stable throughout that period. The most marked decrease was observed in the occipital tissue (P < 0.001). In the hypoglycemic mice, AEC in both the parietal and occipital tissues decreased significantly more than in the controls, more rapidly and pronounced between day 2 and 5 in the occipital tissue, reaching very low levels from day 5 onward. Except in the occipital tissue, none of the adenine nucleotides on its own, including ATP, reflected the cellular AEC. Conclusions: Over the first ten days of life, hypoglycemia progressively depleted cellular AEC in the brain, unlike cellular ATP concentration which did not appropriately reflect cellular energy.

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Section: [Adp]/[atp] + [Adp] + [Amp]mentioning

confidence: 99%

Section: Strengths and Limitationsmentioning

confidence: 99%