Hypothermia: depression of tricarboxylic acid cycle flux and evidence for pentose phosphate shunt upregulation

Abstract

The results of this study suggest that an increased fraction of glucose metabolism was shunted through the pentose phosphate pathway in the presence of hypothermia.

Deep Hypothermia Markedly Activates the Small Ubiquitin-Like Modifier Conjugation Pathway; Implications for the Fate of Cells Exposed to Transient Deep Hypothermic Cardiopulmonary Bypass

“…One plausible explanation for the neuroprotective effects of hypothermia could be that it protects cells from ischemic damage by retarding the rate of energy depletion during ischemia. Hypothermia has indeed been found to depress the tricarboxylic acid flux (Kaibara et al, 1999) and, thus, to preserve cerebral energy metabolism during ischemia (Laptook et al, 1995), resulting in delayed anoxic depolarization (Kaminogo et al, 1999). These Figure 2 Deep hypothermic cardiopulmonary bypass (DHCPB) markedly modifies gene expression.…”

Increased Pentose Phosphate Pathway Flux after Clinical Traumatic Brain Injury: A [1,2-13C2]glucose Labeling Study in Humans

“…Several intermediates in the cycle are used for amino acid and neurotransmitter synthesis. These changes and demands on a cell's metabolism have been demonstrated in other forms of cellular stress (transformation and hypothermia), and thus may also be important after TBI (Ben-Yoseph et al, 1995;Boros et al, 2002;Kaibara et al, 1999;Lee et al, 1998).…”

“…Labeled-glucose administration is followed by detection of metabolites by nuclear magnetic resonance spectrometry or gas chromatography coupled to mass spectrometry (GC/MS). This technique has been described by many investigators in brain (Ben-Yoseph et al, 1995;Gruetter, 2002;Kaibara et al, 1999;Ross et al, 2003) and astrocyte culture (Lee et al, 1996) as well as many other organ systems and cell cultures. By administering glucose labeled with 13 C in the first and second carbon, the label can be effectively followed through its downstream metabolic products.…”

Persistent Neuroprotection with Prolonged Postischemic Hypothermia in Adult Rats Subjected to Transient Middle Cerebral Artery Occlusion

“…Shivering which, at least temporarily, accompanies hypothermia would elevate metabolism (16,41) and potentially diminish neuroprotection since lowered metabolism is probably one of the mechanisms by which hypothermia protects (1,10,23). Other neuroendocrine effects of unanesthetized hypothermia might also lessen protection.…”