TL;DR: In this article, the particle size and structure of zinc glutarates were determined by wide-angle X-ray diffraction, transmission electron microscopy, and the laser particle size analyzer technique.
TL;DR: Speculation that cerebral metabolism normally functions at close to its maximal capacity and cannot, therefore, be increased has been refuted by the findings of stimulation of cerebral oxygen consumption in vivo by epinephrine and related drugs.
Abstract: NUMEROUS studies have demonstrated that the mature brain, unlike most other tissues,' does not participate in the overall increase in total body metabolic rate in hyperthyroidism (GORDON and HEMING, 1944; SCHEINBERG, 1950; SOKOLOFF, WECHSLER, MANGOLD, BALLS and KETY, 1953 ; SENSENBACH, MADISON, EISENBERG and OCHS, 1954). Attempts to explain the lack of thyroxine effect on cerebral oxygen consumption have proved to be inadequate. Speculation that cerebral metabolism normally functions at close to its maximal capacity and cannot, therefore, be increased (SCHEINBERG, 1950; FAZEKAS, GRAVES and ALMAN, 1951) has been refuted by the findings of stimulation of cerebral oxygen consumption in vivo by epinephrine and related drugs (KING, SOKOLOFF and WECHSLER, 1952; RICHARDSON, FERGUSON and PATTERSON, 1957). The possibility that the blood-brain barrier limits the penetration of thyroxine into the cerebral tissues has been excluded by studies with 13Flabelled thyroxine which indicate that increased cerebral uptake follows increased circulating levels of thyroxine (FORD and GROSS, 1958~7, b; SOKOLOFF and DURELL, unpublished). In addition to the apparent lack of response to thyroxine, the metabolism of the mature brain manifests a number of other unique features. It normally exhibits a relatively high rate of oxygen consumption which in vivo can be supported only by the utilization of comparably high amounts of carbohydrate (KETY, 1957; SOKOLOFF, 1960). In fact, in vivo the brain utilizes oxygen and glucose in almost stoichiometric amounts, and the respiratory quotient approximates unity and furthermore, the brain fails to take up from the blood any substrate other than glucose in more than insignificant amounts (KETY, 1957; SOKOLOFF, 1960). All these features suggest that protein and lipid turnover are only negligibly reflected in the gross oxidative metabolism of the mature brain as compared to that of carbohydrate. It is noteworthy that of the three tissues, brain, testis, and spleen, in which oxidative metabolism has been reported to be unaffected in hyperthyroidism (GORDON and HEMING, 1944), two, the brain and testis, have a respiratory quotient of approximately one (HIMWICH and NAHUM, 1929; KETY, 1957; SOKOLOFF, 1960). On the other hand, in the immature or developing brain, in which the rates of protein (GAITONDE and RICHTER,
TL;DR: The previously reported 3-methylcrotonic acid was shown to be an artefact and is not a diagnostic metabolite for this defect, and the urinary organic acid profile of3-hydroxy-3-methylglutaric aciduria contains excessive amounts of 3- methylglutaconic acid.