Effect of γ-Hydroxybutyrate on Local and Global Glucose Metabolism in the Anesthetized Cat Brain

Abstract

Summary: This study addresses three topics in the chlo ralose-anesthetized cat: (a) distribution of local CMRg 1 c : values ranging from 5 to 109 fl-molll00 glmin were found in 37 brain structures and the mean CMRgl C over all ex amined structures was 30.6 fl-mol/100 glmin; (b) effect of 'f-hydroxybutyrate (GHB, 250 mg/kg i. v.) on local CMRglc, which was significantly (p < 0.05) depressed in 16 of 37 structures, most prominently in the auditory sys tem, and the mean CMRglc over all structures after GHB was 20.4 fl-molll00 glmin; and (c) global values of CMRglc , CMR02, and CBP before and after GHB: in these exper iments, a modified Kety-Schmidt technique was em ployed measuring saturation/de saturation of inhaled H2 and concentrations of glucose and oxygen in aortic and

Sporadic Alzheimer's Disease: The Starving Brain

“…It has been found especially effective against ischemic reperfusion injury in the brain and other organs [22,62]. In pharmacological doses, GHB also reduces brain glucose utilization but, remarkably, not oxygen consumption, and it thus appears to have the capacity to serve as an alternate fuel [70].…”

“…Monocarboxylic acid transporters carry GHB across the blood brain barrier independently of glucose [131] and in preference to glucose. The application of GHB profoundly reduces the cerebral utilization of glucose but not its oxygen consumption and hence reveals GHB's capacity to serve as an alternate fuel [70]. Ketone bodies such as BHB are also carried across the blood brain barrier on monocarboxylic acid transporters [88] and also reduce cerebral glucose utilization without reducing oxygen consumption [132], and the brain's use of BHB as an alternate fuel has been well established in the newborn, in starvation, and in insulin resistance [133].…”

Sleep, Narcolepsy, and Sodium Oxybate

“…Recovery may occur in the absence of this depression. While SO, like other anesthetic agents, diffusely depresses neuronal activity in the brain, SO does not reduce cerebral oxygen consumption or cerebral blood flow [ 19 , 231 ]. SO reduces cerebral glucose utilization but supplies the brain with succinate in its stead.…”