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Previous research has shown that ingestion of sucrose or injection of glucose following a learning experience can improve an animal's memory for that experience. The present work was directed towards elucidating the mechanisms by which sucrose and glucose produce this effect. Memory was tested by determining the effects of post-training injections of various substances on a conditioned emotional response. Glucose itself exerted a dose-dependent bidirectional action on retention. This action was shown not to depend on particular blood glucose levels. Insulin did not improve retention at any of the doses tested. Fructose, a sugar that does not cross the blood-brain barrier produced a dose-response effect on retention similar to that of glucose suggesting that fructose and glucose may act through a common peripheral mechanism. The observation of a memory improvement following injections of either 2-deoxyglucose or 3-O-methylgucose, two non-metabolized glucose analogs, suggested that the effect of glucose on retention may be due to an action on glucose transport and not to any metabolic effects of glucose. Two peripheral organs were examined for their possible involvement in the memory-improving action of glucose. This action was shown not to be dependent on the adrenal medulla which has been implicated in the action of other mnemoactive treatments. Partial denervation of the liver produced a partial attenuation of the effect of glucose on retention. The results are discussed in terms of the action of reinforcers on endogenous physiological mechanisms that modulate memory consolidation.

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The aim of this work was to establish the relative contribution of genetic regulation of the <I>PYK1</I>, <I>PFK1</I> and <I>PFK2</I> genes to the control of glycolysis. A series of isogenic mutant strains were constructed where the promoters and 5' untranslated sequences of the <I>PYK1, PFK1</I> and <I>PFK2</I> genes were replaced with those from <I>PGK1</I>. In addition , a second series of mutant strains were constructed where synthesis of Pyk1p and Pflkp was driven by the <I>PGK1_Δuas</I> promoter. These latter series of mutants were designed to contain weak expression of Pyklp and Pflkp. Analysis of UKC1 (<I>PGK::PYK1)</I> in shake flask cultures revealed similar growth rates on glucose and on lactate and similar rates of ethanol production and glucose consumption to those of the wild-type strain. This suggested that the native genetic regulation did not appear to play a significant role in the control of glycolysis. Nonetheless, analysis of this strain in the fermentor revealed that genetic regulation of <I>PYK1</I> may be important in co-ordinating Pyk1p synthesis, under the conditions studied. Analysis of YKC11 (<I>PGK_Δuas::PYK1)</I> in both shake flask and fermentor experiments showed that genetic control was important in maintaining Pyk1p levels in order to sustain glycolytic flux. Shake flask analysis of the single and double <I>PFK</I> mutants under the control of the <I>PGK1</I> promoter revealed that the genetic regulation of the <I>PFK1</I> and <I>PFK2</I> genes did not appear to be important in the control of glycolysis. Weak expression of the <I>PFK1</I> and <I>PFK2</I> genes, under the control of the <I>PGK_Δuas</I> promoter showed the importance of genetic regulation in maintaining Pflkp levels to support glycolytic flux, under the conditions studied.

To study maternal glucose tolerance in pregnancy and its effects on the fetus, a rapid 25g intravenous glucose tolerance test was performed at about 32 weeks gestation in a group of randomly selected women. Full glucose tolerance data was available in 815 cases. The results were withheld from the patients and their obstetricians and paediatricians, and no treatment or advice was offered. Fasting plasma glucose and indices of glucose disposal were distributed unimodally with no evidence of a separate pathological group towards the diabetic end of the distributions. Glucose disposal rate was not, however, signficantly associated with the fasting plasma glucose, suggesting that glucose intolerance associated with elevation of the fasting plasma glucose might be a more clearly defined entity. New reference standards for fasting plasma glucose in pregnancy, which differ from those currently in use, are presented. The major determinants of relatively impaired maternal glucose tolerance in pregnancy were maternal age and obesity. Nonetheless, many cases of relative glucose intolerance occurred in the absence of any preexisting clinical indication. Significant association were found between maternal glucose metabolism and various measures of neonatal size and morbidity, including the incidence of congenital malformations and the occurrence of perinatal asphyxia in post-term infants. These effects were graded through much of the range of maternal glucose tolerance and not of predictive value in individual cases. The available evidence did not indicate that these relationships were mediated by fetal hyperinsulinism. It is concluded that the adverse consequences of impaired glucose disposal with normal fasting plasma glucose in pregnancy do not justify exhaustive measures to identify the condition. Screening for glucose intolerance during pregnancy should seek to identify those cases in which glucose intolerance is associated with elevation of fasting plasma glucose.

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