Fueling the Brain—a New Role in Lactate Metabolism

Welling, Leonardo C.; Welling, Mariana S.; Teixeira, Manoel Jacobsen; Figueiredo, Eberval Gadelha

doi:10.1016/j.wneu.2015.07.063

Cited by 2 publications

(3 citation statements)

References 6 publications

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“…In addition, TTC staining indicated significant brain infarction following IRI. It is understood that the brain weight accounts for only 2% of body weight; however, the oxygen consumption of the brain accounts for 20% of the total body oxygen consumption (30). The brain is intensely sensitive to ischemia and hypoxia; therefore, ischemia following a prolonged period of time may lead to brain infarction (31).…”

Section: Discussionmentioning

confidence: 99%

Biliverdin administration ameliorates cerebral ischemia reperfusion injury in rats and is associated with proinflammatory factor downregulation

Zou

Liu

et al. 2017

Experimental and Therapeutic Medicine

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Biliverdin (BV), one of the heme oxygenase-1 (HO-1) catalytic products, has been demonstrated to have protective effects in liver ischemia reperfusion injury (IRI). The present study aimed to explore the effects of BV on cerebral IRI, and to investigate the potential mechanisms thereof. Adult male SD rats, weighing 200–240 g, were randomly divided into sham (group S), cerebral ischemia reperfusion control (group C) and BV (group BV) groups. Rats in group C underwent transient middle cerebral artery occlusion (tMCAO) and received 2 ml normal saline; rats in group BV received BV (35 mg/kg) intraperitoneally 15 min prior to reperfusion and 4 h after reperfusion, then twice a day thereafter for 5 days. Group S served as the control. Neurological Severity Scores (NSS) were evaluated at days 1–5 following reperfusion. Staining with 2, 3, 5-triphenyltetrazolium chloride was performed to determine the cerebral infarction at 48 h post reperfusion. mRNA expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, inducible nitric oxide synthase (iNOS) and HO-1 in the ischemic cerebral cortex were detected via reverse transcription-quantitative polymerase chain reaction at 3, 6, 12 and 24 h after reperfusion. Western blotting was used to detect the protein expression levels at 3 h after reperfusion. Compared with group S, the NSS, cerebral infarct volume, and the mRNA and protein expression levels of TNF-α, IL-6, IL-1β, iNOS and HO-1 of Group C were significantly increased (P<0.05). However, BV administration significantly improved and reduced these expression levels (P<0.01). The present study indicates that BV is able to ameliorate cerebral IRI in rats and that the mechanism may be associated with the downregulation of proinflammatory factors.

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Section: Discussionmentioning

confidence: 99%

Biliverdin administration ameliorates cerebral ischemia reperfusion injury in rats and is associated with proinflammatory factor downregulation

Zou

Liu

et al. 2017

Experimental and Therapeutic Medicine

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“…Brain cost 10 times higher than what should be expected from its weight alone ( 30 ). Lactate, transported by MCT1, is an indispensable energy source of neurons ( 31 ). Moreover, the developmental expression of oligodendrocyte MCT1 has a regulative effect on neuronal amounts in medial prefrontal cortex (mPFC) during 12 months ( 32 ).…”

Section: Mct1 Is Expressed In Glial Cells and Neuronsmentioning

confidence: 99%

“…In the CNS, MCT1 arouses much attention because of its unique localization, which is expressed in astrocytes and neurons ( 11 ). Meanwhile, MCT2 restrictively localizes to neurons ( 7 ) and MCT4 is mainly expressed by astrocytes ( 31 ). Such a cellular distribution of cerebral MCT1, MCT2, and MCT4 may associate with their functional characteristics.…”

Section: Mct1 Couples Astrocyte-to-neuron Lactate Flowmentioning

confidence: 99%

Monocarboxylate Transporter 1 May Benefit Cerebral Ischemia via Facilitating Lactate Transport From Glial Cells to Neurons

et al. 2022

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Monocarboxylate transporter 1 (MCT1) is expressed in glial cells and some populations of neurons. MCT1 facilitates astrocytes or oligodendrocytes (OLs) in the energy supplement of neurons, which is crucial for maintaining the neuronal activity and axonal function. It is suggested that MCT1 upregulation in cerebral ischemia is protective to ischemia/reperfusion (I/R) injury. Otherwise, its underlying mechanism has not been clearly discussed. In this review, it provides a novel insight that MCT1 may protect brain from I/R injury via facilitating lactate transport from glial cells (such as, astrocytes and OLs) to neurons. It extensively discusses (1) the structure and localization of MCT1; (2) the regulation of MCT1 in lactate transport among astrocytes, OLs, and neurons; and (3) the regulation of MCT1 in the cellular response of lactate accumulation under ischemic attack. At last, this review concludes that MCT1, in cerebral ischemia, may improve lactate transport from glial cells to neurons, which subsequently alleviates cellular damage induced by lactate accumulation (mostly in glial cells), and meets the energy metabolism of neurons.

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Fueling the Brain—a New Role in Lactate Metabolism

Cited by 2 publications

References 6 publications

Biliverdin administration ameliorates cerebral ischemia reperfusion injury in rats and is associated with proinflammatory factor downregulation

Biliverdin administration ameliorates cerebral ischemia reperfusion injury in rats and is associated with proinflammatory factor downregulation

Monocarboxylate Transporter 1 May Benefit Cerebral Ischemia via Facilitating Lactate Transport From Glial Cells to Neurons

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