Journal articles: 'Memory – Effect of glucose on'

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Smith, Michael A., Leigh M. Riby, J. Anke M. van Eekelen, and Jonathan K. Foster. "Glucose enhancement of human memory: A comprehensive research review of the glucose memory facilitation effect." Neuroscience & Biobehavioral Reviews 35, no. 3 (January 2011): 770–83. http://dx.doi.org/10.1016/j.neubiorev.2010.09.008.

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FOX, COSETTE, and SABRINA PAJOR. "The Effect of Sucrose and Stress on Male Participants' Memory." Michigan Academician 47, no. 2 (January 1, 2021): 162–72. http://dx.doi.org/10.7245/0026-2005-47.2.162.

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ABSTRACT Glucose has been shown to have a memory facilitating effect. The goal of this study is to test if sucrose, a carbohydrate consumed on a daily basis, would also enhance memory in male college students. Subjects were given either a sucrose (50 g) or a placebo drink (50.6 mg of saccharine). Subjects filled the Stress Indicator Questionnaire that measures five stress indicators: physical, sleep, behavioral, emotional, and personal habits. A slideshow of 52 IAPS pictures were then shown to the subjects followed by immediate and delayed recall tests and a recognition test. Even though we found no direct effect of sucrose on memory, the results showed that high fasting blood glucose level is associated with lower recognition memory. Furthermore, high sleep stress enhanced memory for immediate recall. On the other hand, high behavioral stress was detrimental for delayed recall and recognition. The differential effects of the different indicators of stress on memory is discussed in relation to changes in cortisol levels that may result in modulation of blood glucose levels which in turn can affect memory. The results of this study shed light on the effect of different types of stress and fasting glucose levels on memory.

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Gancheva, Silvia M., and Maria D. Zhelyazkova-Savova. "Vitamin K2 Improves Anxiety and Depression but not Cognition in Rats with Metabolic Syndrome: a Role of Blood Glucose?" Folia Medica 58, no. 4 (December 1, 2016): 264–72. http://dx.doi.org/10.1515/folmed-2016-0032.

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AbstractBackground:The metabolic syndrome is a socially important disorder of energy utilization and storage, recognized as a factor predisposing to the development of depression, anxiety and cognitive impairment in humans.Aim:In the present study we examined the effects of vitamin K2 on the behavior of rats with metabolic syndrome and looked for relationships with the effects on blood sugar.Materials and methods:Male Wistar rats were divided in four groups: a control group on a regular rat chow, a metabolic syndrome (MS) group fed a high-fat high-fructose diet, a control group treated with vitamin K2 and a MS group treated with vitamin K2. Vitamin K2 was given by gavage. At the end of the study (after 10 weeks) behavioral tests were performed and fasting blood glucose was measured. Anxiety was determined using the social interaction test and depression was assessed by the Porsolt test. Memory effects were estimated by the object recognition test. Correlations between fasting blood glucose and behavioral performance were analyzed.Results:The rats from the MS group had elevated blood glucose. They had anxiety, depression and memory deficit. Vitamin K2 normalized blood glucose, reduced anxiety and depression, but did not improve memory. Time of social interaction (inverse index of anxiety) and memory recognition were negatively correlated with blood glucose in the untreated rats but the immobility time (measure of depression) was not. When vitamin K2-treated rats were added, the correlation of blood glucose with the time of social interaction was kept, but the one with the recognition memory was lost. It might be that the anxiolytic effect of vitamin K2 in this setting is at least partly due to its effects on blood glucose, while the anti-depressant effect is glucose-independent.Conclusion:The present study demonstrated that vitamin K2 prevented the development of anxiety and depression, but did not improve the memory deficit caused by the dietary manipulation in an experimental model of metabolic syndrome. It might be that the anxiolytic effect of vitamin K2 is at least partly due to its effects on blood glucose, while the antidepressant effect is glucose-independent.

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Messier, C. "Effect of Glucose and Peripheral Glucose Regulation on Memory in the Elderly." Neurobiology of Aging 18, no. 3 (May 6, 1997): 297–304. http://dx.doi.org/10.1016/s0197-4580(97)80311-9.

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Messier, Claude, Alain Desrochers, and Michèle Gagnon. "Effect of glucose, glucose regulation, and word imagery value on human memory." Behavioral Neuroscience 113, no. 3 (1999): 431–38. http://dx.doi.org/10.1037/0735-7044.113.3.431.

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Meikle, Andrew, Leigh M. Riby, and Brian Stollery. "Memory processing and the glucose facilitation effect: The effects of stimulus difficulty and memory load." Nutritional Neuroscience 8, no. 4 (August 2005): 227–32. http://dx.doi.org/10.1080/10284150500193833.

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Riby, Leigh M., Jennifer McLaughlin, and Deborah M. Riby. "Lifestyle, glucose regulation and the cognitive effects of glucose load in middle-aged adults." British Journal of Nutrition 100, no. 5 (November 2008): 1128–34. http://dx.doi.org/10.1017/s0007114508971324.

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Interventions aimed at improving glucose regulatory mechanisms have been suggested as a possible source of cognitive enhancement in the elderly. In particular, previous research has identified episodic memory as a target for facilitation after either moderate increases in glycaemia (after a glucose drink) or after improvements in glucose regulation. The present study aimed to extend this research by examining the joint effects of glucose ingestion and glucose regulation on cognition. In addition, risk factors associated with the development of poor glucose regulation in middle-aged adults were considered. In a repeated measures design, thirty-three middle-aged adults (aged 35–55 years) performed a battery of memory and non-memory tasks after either 25 g or 50 g glucose or a sweetness matched placebo drink. To assess the impact of individual differences in glucose regulation, blood glucose measurements were taken on four occasions during testing. A lifestyle and diet questionnaire was also administered. Consistent with previous research, episodic memory ability benefited from glucose ingestion when task demands were high. Blood glucose concentration was also found to predict performance across a number of cognitive domains. Interestingly, the risk factors associated with poor glucose regulation were linked to dietary impacts traditionally associated with poor health, e.g. the consumption of high-sugar sweets and drinks. The research replicates earlier work suggesting that task demands are critical to the glucose facilitation effect. Importantly, the data demonstrate clear associations between elevated glycaemia and relatively poor cognitive performance, which may be partly due to the effect of dietary and lifestyle factors.

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Messier, Claude, and Norman M. White. "Memory improvement by glucose, fructose, and two glucose analogs: A possible effect on peripheral glucose transport." Behavioral and Neural Biology 48, no. 1 (July 1987): 104–27. http://dx.doi.org/10.1016/s0163-1047(87)90634-0.

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Wu, Lung-Yuan, Wang-Chuan Chen, Fan-Shiu Tsai, Chin-Chuan Tsai, Chi-Rei Wu, and Li-Wei Lin. "p-Hydroxybenzyl Alcohol, an Active Phenolic Ingredient of Gastrodia elata, Reverses the Cycloheximide-Induced Memory Deficit by Activating the Adrenal Gland in Rats." American Journal of Chinese Medicine 43, no. 08 (January 2015): 1593–604. http://dx.doi.org/10.1142/s0192415x15500901.

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The present study investigated the ameliorating effects of p-hydroxybenzyl alcohol (HBA), an active phenolic ingredient of Gastrodia elata, on cycloheximide (CXM)-induced impairment of passive avoidance response and clarified the role of adrenal glands on the effect of HBA in rats. An adrenalectomy (ADX) caused the memory deficit from 1 to 3 days after surgery. Administration of corticosterone (CORT) plus glucose completely recovered the memory deficit caused by ADX, and this effect was better than that of glucose or CORT alone. HBA ameliorated the memory deficit induced by CXM in sham and ADX rats, but ADX partially blocked it. Furthermore, plasma glucose, epinephrine and adrenal steroid levels of ADX rats significantly decreased. Sham rats who received HBA had an increase in plasma glucose and adrenal steroid levels. Therefore, we suggest that the reversal of CXM-induced memory deficit by HBA was partially dependent on adrenal glands through the increase of the levels of plasma adrenal steroids.

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Riby, Leigh M., Hazel McMurtrie, Jonathan Smallwood, Carrie Ballantyne, Andrew Meikle, and Emily Smith. "The facilitative effects of glucose ingestion on memory retrieval in younger and older adults: is task difficulty or task domain critical?" British Journal of Nutrition 95, no. 2 (February 2006): 414–20. http://dx.doi.org/10.1079/bjn20051649.

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The ingestion of a glucose-containing drink has been shown to improve cognitive performance, particularly memory functioning. However, it remains unclear as to the extent to which task domain and task difficulty moderate the glucose enhancement effect. The aim of this research was to determine whether boosts in performance are restricted to particular classes of memory (episodic v. semantic) or to tasks of considerable cognitive load. A repeated measures (25g glucose v saccharin), counterbalanced, double-blind design was used with younger and older adults. Participants performed a battery of episodic (e.g. paired associate learning) and semantic memory (e.g. category verification) tasks under low and high cognitive load. Electrophysiological measures (heart rate and galvanic skin response) of arousal and mental effort were also gathered. The results indicated that whilst glucose appeared to aid episodic remembering, cognitive load did not exaggerate the facilitative effect. For semantic memory, there was little evidence to suggest that glucose can boost semantic memory retrieval even when the load was manipulated. One exception was that glucose facilitated performance during the difficult category fluency task. Regardless, the present findings are consistent with the domain-specific account in which glucose acts primarily on the hippocampal region, which is known to support episodic memory. The possible contribution of the hippocampus in semantic memory processing is also discussed.

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Lim, Ilhan, Hye-Young Joung, A. Ram Yu, Insop Shim, and Jin Su Kim. "PET Evidence of the Effect of Donepezil on Cognitive Performance in an Animal Model of Chemobrain." BioMed Research International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/6945415.

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A considerable number of patients with breast cancer complain of cognitive impairment after chemotherapy. In this study, we showed that donepezil enhanced memory function and increased brain glucose metabolism in a rat model of cognitive impairment after chemotherapy using behavioral analysis and positron emission tomography (PET). We found that chemotherapy affected spatial learning ability, reference memory, and working memory and that donepezil improved these cognitive impairments. According to PET analysis, chemotherapy reduced glucose metabolism in the medial prefrontal cortex and hippocampus, and donepezil increased glucose metabolism in the bilateral frontal lobe, parietal lobe, and hippocampus. Reduced glucose metabolism was more prominent after treatment with doxorubicin than cyclophosphamide. Our results demonstrated the neural mechanisms for cognitive impairment after chemotherapy and show that cognition was improved after donepezil intervention using both behavioral and imaging methods. Our results suggested that donepezil can be employed clinically for the treatment of cognitive deficits after chemotherapy.

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Alharbi, Ibrahim, Hindi Alharbi, Yasser Almogbel, Abdullah Alalwan, and Ahmad Alhowail. "Effect of Metformin on Doxorubicin-Induced Memory Dysfunction." Brain Sciences 10, no. 3 (March 7, 2020): 152. http://dx.doi.org/10.3390/brainsci10030152.

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Doxorubicin (DOX) is widely used to treat many types of cancer; however, it is associated with chemotherapy-related complications such as cognitive dysfunction, known as chemobrain. Chemobrain affects up to 75% of cancer survivors, and there are currently no available therapeutic options. This study aims to examine whether metformin (MET) can protect against the neurotoxicity caused by DOX treatment. Forty male rats were divided into four groups (10 rats/group): control, DOX, DOX + MET, and MET. Rats treated with DOX received five doses of 4 mg/kg DOX weekly (cumulative dose: 20 mg/kg). For the DOX-MET and MET groups, MET (3 mg/mL) was dissolved in drinking water. Behavioral and glucose tests were performed one day after treatment was completed. We found DOX (4 mg/kg/week, 5 weeks) caused learning and memory impairment in the Y-maze, novel object recognition, and elevated plus maze behavioral tests. MET did not rescue these DOX-induced memory impairments. Neither DOX nor MET nor MET + DOX altered glucose levels following the treatment. In summary, DOX treatment is associated with memory impairment in rats, but MET does not rescue this cognitive dysfunction.

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Brandt, Karen R., Sandra I. Sünram-Lea, and Kirsty Qualtrough. "The effect of glucose administration on the emotional enhancement effect in recognition memory." Biological Psychology 73, no. 2 (August 2006): 199–208. http://dx.doi.org/10.1016/j.biopsycho.2006.04.001.

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Riby, Leigh M. "The Impact of Age and Task Domain on Cognitive Performance: A Meta-Analytic Review of the Glucose Facilitation Effect." Brain Impairment 5, no. 2 (December 1, 2004): 145–65. http://dx.doi.org/10.1375/brim.5.2.145.58253.

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AbstractConsiderable research has been devoted to the issue of whether the ingestion of glucose enhances cognitive performance in both younger and older adults. However, it has proven difficult to draw firm conclusions from this literature due to the diversity of methodologies that have been used, and it is therefore still unclear what factors might moderate the facilitative effect. The present study investigates methodological variations and their impact on the magnitude of the glucose enhancement effect. In particular, age group (young vs. old) and task domain (memory vs. nonmemory tasks) were considered as moderator variables. In addition, differences in experimental design, glucose dose and fasting regime were examined. The effect size d was extracted from studies comparing cognitive performance after the ingestion of either a glucose or control solution. Subsequent meta-analyses were conducted (using the procedures outlined by Hedges & Olkin, 1985) to examine potential moderators. A moderate overall effect size was found (d = 0.56), which clearly demonstrated the value of glucose ingestion as a cognitive enhancer. However, this effect size was not representative of the 104 individual effect sizes reported. Secondary analyses found larger effect sizes for memory compared to nonmemory tasks. Unexpectedly, no evidence was provided for greater beneficial effects of glucose on cognitive performance for older compared to younger adults. The impact of other methodological variables and the need for further exploration in an elderly population are discussed.

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Foster, J. K., P. G. Lidder, and S. I. Sünram. "Glucose and memory: fractionation of enhancement effects?" Psychopharmacology 137, no. 3 (June 2, 1998): 259–70. http://dx.doi.org/10.1007/s002130050619.

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Brindal, Emily, Danielle Baird, Amy Slater, Vanessa Danthiir, Carlene Wilson, Jane Bowen, and Manny Noakes. "The effect of beverages varying in glycaemic load on postprandial glucose responses, appetite and cognition in 10–12-year-old school children." British Journal of Nutrition 110, no. 3 (December 19, 2012): 529–37. http://dx.doi.org/10.1017/s0007114512005296.

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Reducing glycaemic index (GI) and glycaemic load (GL) inconsistently improves aspects of cognitive function and appetite in children. Whether altering the GL by lowering carbohydrate relative to protein and fat has a role in these effects is unknown. Therefore, we assessed the differential effects of beverages varying in GL and dairy composition on appetite, energy intake and cognitive function in children. A total of forty children (10–12 years) completed a double-blind, randomised, crossover trial, receiving three isoenergetic drinks (approximately 1100 kJ): a glucose beverage (GI 100, GL 65), a full milk beverage (GI 27, GL 5) and a half milk/glucose beverage (GI 84, GL 35). For 3 h post-consumption, subjective appetite and cognitive performance (speed of processing, memory, attention and perceptual speed) were measured hourly. At completion, each child was provided a buffet-style lunch and energy intake was calculated. Blood glucose was objectively measured using the Continuous Glucose Monitoring System. Blood glucose AUC values were significantly different between the drinks (P< 0·001), but did not sustain above the baseline for 3 h for any drink. Mixed modelling revealed no effect of beverage on subjective appetite or energy intake. Participant sex and drink GL significantly interacted for short-term memory (P< 0·001). When girls consumed either milk-containing beverage, they recalled 0·7–0·8 more words compared with 0·5 less words after the glucose drink (P≤ 0·014). Altering GL of drinks by reducing carbohydrate and increasing protein did not affect appetite or cognition in children. Girls may demonstrate improved short-term memory after consuming beverages with higher protein and lower GL.

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Gold, Paul E., JoAnn Vogt, and Jeremy L. Hall. "Glucose effects on memory: Behavioral and pharmacological characteristics." Behavioral and Neural Biology 46, no. 2 (September 1986): 145–55. http://dx.doi.org/10.1016/s0163-1047(86)90626-6.

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Sünram-Lea, Sandra I., Jonathan K. Foster, Paula Durlach, and Catalina Perez. "The Influence of Fat Co-administration on the Glucose Memory Facilitation Effect." Nutritional Neuroscience 7, no. 1 (February 2004): 21–32. http://dx.doi.org/10.1080/1028415042000198816.

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Chung, Yong‐Chan, Yong Shik Shim, and Byoung Chul Chun. "Effect of glucose crosslinking on thermomechanical properties and shape memory effect of PET‐PEG copolymers." Journal of Applied Polymer Science 109, no. 6 (September 15, 2008): 3533–39. http://dx.doi.org/10.1002/app.28489.

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DiNuzzo, Mauro. "How glycogen sustains brain function: A plausible allosteric signaling pathway mediated by glucose phosphates." Journal of Cerebral Blood Flow & Metabolism 39, no. 8 (June 17, 2019): 1452–59. http://dx.doi.org/10.1177/0271678x19856713.

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Astrocytic glycogen is the sole glucose reserve of the brain. Both glycogen and glucose are necessary for basic neurophysiology and in turn for higher brain functions. In spite of low concentration, turnover and stimulation-induced degradation, any interference with normal glycogen metabolism in the brain severely affects neuronal excitability and disrupts memory formation. Here, I briefly discuss the glycogenolysis-induced glucose-sparing effect, which involves glucose phosphates as key allosteric effectors in the modulation of astrocytic and neuronal glucose uptake and phosphorylation. I further advance a novel and thus far unexplored effect of glycogenolysis that might be mediated by glucose phosphates.

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Khoruzhenko, Stanislav, Chunfa Jie, and Scheherazade Sadegh-Nasseri. "Long-term memory CD4+ T cells - a survival network (47.12)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 47.12. http://dx.doi.org/10.4049/jimmunol.188.supp.47.12.

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Abstract Memory CD4+ T cells specific for a particular antigen can survive for a lifetime of an individual through undefined mechanisms. Previously we have demonstrated that memory CD4+ T cells undergo a state of dormancy during the resolution of infection, and dormant memory T cells survive for the life of mice. To gain an understanding of the genetic programs involved, we examined gene expression profile of memory DO11.10 CD4+ T cells in mice infected with Vaccinia-OVA virus 10.5 months post infection and compared it with gene expression in age-matched old mice. Extensive literature search allowed reverse engineering of genetic network of differentially expressed genes in long-term memory T cells. Pattern of gene expression pointed to the induction of anti-apoptotic and genomic stability pathways. We found that in long term memory CD4+ T cells a shift from glucose to lipid metabolism occurs, along with upregulation of ceramide synthesis and utilization that may favor memory T cell survival. Insulin resistance appears to play a major role in downregulation of glucose metabolism. In conclusion, our data show that in long-term memory CD4+ T cells several major regulatory genes that regulate anti-apoptotic, genomic stability, glucose and lipid metabolism pathways are upregulated and possibly coordinate an overall pro-survival effect.

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Gao, Li-Mo, Shun Fu, Fen Liu, Han-Bing Wu, and Wen-Jie Li. "Astragalus Polysaccharide Regulates miR-182/Bcl-2 Axis to Relieve Metabolic Memory through Suppressing Mitochondrial Damage-Mediated Apoptosis in Retinal Pigment Epithelial Cells." Pharmacology 106, no. 9-10 (2021): 520–33. http://dx.doi.org/10.1159/000515901.

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Introduction: Metabolic memory is one of the causes of diabetic retinopathy, and astragalus polysaccharide (APS) has great advantages in the treatment of diabetes. However, the effect of APS on metabolic memory remains to be investigated. Methods: Retinal pigment epithelial cell line ARPE-19 and primary retinal pigment epithelial cells were used to verify the effect of APS on mitochondria damage and apoptosis induced by high glucose-induced metabolic memory. The relationship between miR-182 and Bcl-2 was confirmed by a luciferase activity assay. Western blotting and quantitative reverse-transcriptase polymerase chain reaction were conducted to investigate the changes in mitochondrial damage- and apoptosis-associated markers. The cell mitochondrial membrane potential was assessed by JC-1 fluorescence. Terminal deoxynucleotidyl transferase dUTP nick end labelling staining and flow cytometry assays were performed to determine the occurrence of apoptosis. Results: Treatment with high glucose followed by normal glucose significantly upregulated the expression of miR-182 and downregulated the expression of its target Bcl-2, and APS treatment reversed the above effects. Additionally, APS treatment restored mitochondrial function and inhibited apoptosis in cells in a state of metabolic memory. The effects of APS against mitochondrial damage and apoptosis were partially inhibited after miR-182 overexpression. Conclusion: APS alleviated mitochondrial damage and apoptosis induced by metabolic memory by regulating the miR-182/Bcl-2 axis, which might serve as a new strategy for the treatment of diabetic retinopathy.

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Kim, Esther S., Fumiko Isoda, Irwin Kurland, and Charles V. Mobbs. "Glucose-Induced Metabolic Memory in Schwann Cells: Prevention by PPAR Agonists." Endocrinology 154, no. 9 (May 24, 2013): 3054–66. http://dx.doi.org/10.1210/en.2013-1097.

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A major barrier in reversing diabetic complications is that molecular and pathologic effects of elevated glucose persist despite normalization of glucose, a phenomenon referred to as metabolic memory. In the present studies we have investigated the effects of elevated glucose on Schwann cells, which are implicated in diabetic neuropathy. Using quantitative PCR arrays for glucose and fatty acid metabolism, we have found that chronic (>8 wk) 25 mM high glucose induces a persistent increase in genes that promote glycolysis, while inhibiting those that oppose glycolysis and alternate metabolic pathways such as fatty acid metabolism, the pentose phosphate pathway, and trichloroacetic acid cycle. These sustained effects were associated with decreased peroxisome proliferator-activated receptor (PPAR)γ binding and persistently increased reactive oxygen species, cellular NADH, and altered DNA methylation. Agonists of PPARγ and PPARα prevented select effects of glucose-induced gene expression. These observations suggest that Schwann cells exhibit features of metabolic memory that may be regulated at the transcriptional level. Furthermore, targeting PPAR may prevent metabolic memory and the development of diabetic complications.

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van der Kooij, Michael A., Tanja Jene, Giulia Treccani, Isabelle Miederer, Annika Hasch, Nadine Voelxen, Stefan Walenta, and Marianne B. Müller. "Chronic social stress-induced hyperglycemia in mice couples individual stress susceptibility to impaired spatial memory." Proceedings of the National Academy of Sciences 115, no. 43 (October 9, 2018): E10187—E10196. http://dx.doi.org/10.1073/pnas.1804412115.

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Stringent glucose demands render the brain susceptible to disturbances in the supply of this main source of energy, and chronic stress may constitute such a disruption. However, whether stress-associated cognitive impairments may arise from disturbed glucose regulation remains unclear. Here we show that chronic social defeat (CSD) stress in adult male mice induces hyperglycemia and directly affects spatial memory performance. Stressed mice developed hyperglycemia and impaired glucose metabolism peripherally as well as in the brain (demonstrated by PET and induced metabolic bioluminescence imaging), which was accompanied by hippocampus-related spatial memory impairments. Importantly, the cognitive and metabolic phenotype pertained to a subset of stressed mice and could be linked to early hyperglycemia 2 days post-CSD. Based on this criterion, ∼40% of the stressed mice had a high-glucose (glucose >150 mg/dL), stress-susceptible phenotype. The relevance of this biomarker emerges from the effects of the glucose-lowering sodium glucose cotransporter 2 inhibitor empagliflozin, because upon dietary treatment, mice identified as having high glucose demonstrated restored spatial memory and normalized glucose metabolism. Conversely, reducing glucose levels by empagliflozin in mice that did not display stress-induced hyperglycemia (resilient mice) impaired their default-intact spatial memory performance. We conclude that hyperglycemia developing early after chronic stress threatens long-term glucose homeostasis and causes spatial memory dysfunction. Our findings may explain the comorbidity between stress-related and metabolic disorders, such as depression and diabetes, and suggest that cognitive impairments in both types of disorders could originate from excessive cerebral glucose accumulation.

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Niki, Ichiro, Tatsuo Tamagawa, Hatsumi Niki, Atsushi Niki, Tadataka Koide, and Nobuo Sakamoto. "Possible involvement of diacylglycerol-activated, Ca2+-dependent protein kinase in glucose memory of the rat pancreatic B-cell." Acta Endocrinologica 118, no. 2 (June 1988): 204–8. http://dx.doi.org/10.1530/acta.0.1180204.

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Abstract. Exposure to high concentrations of glucose potentiates insulin release from the pancreatic B-cell stimulated by various secretagogues after an interval under basal condition. We studied the role of diacylglycerol-activated, Ca2+-dependent protein kinase (protein kinase C) in this priming effect of glucose in rat pancreatic islets, using 12-O-tetradecanoyl phorbol-13-acetate (TPA), 1 -(5- isoquinolinesulfonyl)-2- methylpiperazine (H-7),N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004) and forskolin. The priming effect of glucose was mimiced by 10 nmol/l of TPA, an activator of protein kinase C, but not by 5 μmol/l of forskolin, which increases cAMP via activating adenylate cyclase. When pancreatic islets were exposed to glucose (10 mmol/l) together with 50 μmol/l of H-7, an inhibitor of protein kinase C, the secretory response to glucose (10 mmol/l) after a 30-min interval was significantly reduced compared with that in the islets previously exposed to 10 mmol/l glucose alone. In contrast, this was not the case for HA-1004, its inhibitory activity against protein kinase C being less potent than H-7. These findings suggest that protein kinase C may play an important role in the priming effect of glucose on the pancreatic B-cell.

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Gonder-Frederick, L., J. L. Hall, J. Vogt, D. J. Cox, J. Green, and P. E. Gold. "Memory enhancement in elderly humans: Effects of glucose ingestion." Physiology & Behavior 41, no. 5 (January 1987): 503–4. http://dx.doi.org/10.1016/0031-9384(87)90087-4.

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Azari, Nina P. "Effects of glucose on memory processes in young adults." Psychopharmacology 105, no. 4 (December 1991): 521–24. http://dx.doi.org/10.1007/bf02244373.

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Owen, Lauren, Andrew Scholey, Yvonne Finnegan, and Sandra I. Sünram-Lea. "Response variability to glucose facilitation of cognitive enhancement." British Journal of Nutrition 110, no. 10 (June 21, 2013): 1873–84. http://dx.doi.org/10.1017/s0007114513001141.

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Glucose facilitation of cognitive function has been widely reported in previous studies (including our own). However, several studies have also failed to detect glucose facilitation. There is sparsity of research examining the factors that modify the effect of glucose on cognition. The aims of the present study were to (1) demonstrate the previously observed enhancement of cognition through glucose administration and (2) investigate some of the factors that may exert moderating roles on the behavioural response to glucose, including glucose regulation, body composition (BC) and hypothalamic–pituitary–adrenal axis response. A total of twenty-four participants took part in a double-blind, placebo-controlled, randomised, repeated-measures study, which examined the effect of 25 and 60 g glucose compared with placebo on cognitive function. At 1 week before the study commencement, all participants underwent an oral glucose tolerance test. Glucose facilitated performance on tasks of numeric and spatial working memory, verbal declarative memory and speed of recognition. Moderating variables were examined using several indices of glucoregulation and BC. Poorer glucoregulation predicted improved immediate word recall accuracy following the administration of 25 g glucose compared with placebo. Those with better glucoregulation showed performance decrements on word recall accuracy following the administration of 25 g glucose compared with placebo. These findings are in line with accumulating evidence that glucose load may preferentially enhance cognition in those with poorer glucoregulation. Furthermore, the finding that individuals with better glucoregulation may suffer impaired performance following a glucose load is novel and requires further substantiation.

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Gaylor, Chantelle, Hayley Young, and David Benton. "The Impact of Glycemic Load on Cognitive Performance in Adults: A Systematic Review and Meta-Analysis." Current Developments in Nutrition 5, Supplement_2 (June 2021): 905. http://dx.doi.org/10.1093/cdn/nzab049_018.

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Abstract Objectives A systematic review and meta-analysis compared the effects of high (HGL) and low glycemic load (LGL) breakfasts on the cognitive performance of adults. In particular, the time after eating that cognition was assessed and the influence of pre-existing glucose tolerance (GT) were considered. Methods A systematic search for randomized and non-randomized acute breakfast studies was conducted using PubMed, Scopus, and Cochrane Library. Data were available from 15 studies (1,100 participants, age 20–80 years). Episodic memory (e.g., word list recall), working memory (e.g., Serial Sevens), and attention/vigilance (e.g., Trails Part A) were examined. Better and poorer GT were defined as fasting glucose < or > 6.1 mmol/L (110 mg/dL) and/or two-hour postprandial glucose < or > 7 mmol/L (126 mg/dL). All analyses were performed using RevMan 5.3 (Cochrane) and a random-effects model. Results Five to 110 minutes after eating a HGL or LGL breakfast there were no differences cognition. However, between 120 and 195 minutes, immediate episodic memory was significantly better following a LGL breakfast (SMD = 0.16, 95% confidence interval [CI] = –0.00–0.32, P = 0.05, I2 = 0%). Pre-existing glucose tolerance (GT) status moderated this effect. In those with better GT, immediate episodic memory was significantly better following a LGL breakfast (SMD = 0.26, 95% CI = 0.00–0.52, P = 0.05, I2 = 0%), whereas there was no difference in those with poorer GT (SMD = 0.12, 95% CI = –0.21–0.45, P = 0.47, I2 = 0%). Conclusions A LGL breakfast improved memory later in the morning, especially in those with better GT. The phenomenon is unlikely to occur in pre-diabetics or type 2 diabetics and as such there are no clinical implications. There is, however, a possibility of exploring the nature of breakfast, or developing functional foods, to improve memory and work performance. If a similar phenomenon was found in children, there could be positive consequences for school performance. Funding Sources This study was not funded.

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Zawalich, W. S., V. A. Diaz, and K. C. Zawalich. "Role of phosphoinositide metabolism in induction of memory in isolated perifused rat islets." American Journal of Physiology-Endocrinology and Metabolism 254, no. 5 (May 1, 1988): E609—E616. http://dx.doi.org/10.1152/ajpendo.1988.254.5.e609.

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Prior exposure of isolated perifused rat islets to 20 mM glucose or 10 mM glyceraldehyde amplifies their subsequent insulin secretory response to 10 mM glucose. The involvement of phosphoinositide turnover in the induction of this "time-dependent potentiation" (TDP) was investigated. In islets in which inositol-containing phospholipids were prelabeled with myo-[2-3H]inositol, the addition of 20 mM glucose augments the efflux of 3H. This effect persists for approximately 50 min after the cessation of stimulation. Direct measurements of labeled inositol phosphate accumulation confirmed that this increase in 3H efflux is primarily the result of a persistent increase in phosphoinositide (PI) hydrolysis and not due to the slow efflux and/or degradation of performed [3H]inositol phosphates. The duration of the increase in 3H efflux parallels the duration of TDP. Mannoheptulose abolishes both the increase in 3H efflux evoked by 20 mM glucose and TDP. The omission of extracellular calcium plus 0.5 mM ethylene glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid also abolishes both of these effects of high glucose. D-Glyceraldehyde (10 mM) addition to 3H-inositol-prelabeled islets results in an acute efflux of 3H, a persistent efflux after removal of the D-glyceraldehyde from the perifusion medium, and the induction of TDP. Similar to the results obtained with high glucose, the return of 3H efflux rates to prestimulatory values is accompanied by the abolition of TDP. These results suggest that events associated with persistent stimulant-induced increases in phosphoinositide hydrolysis may participate in the induction and maintenance of TDP.

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Joshi, Archita C., Chetna R. Patel, and Naresh D. Kantharia. "Effect of leptin on spatial learning, memory and blood glucose level in streptozotocin induced diabetes mellitus in male wistar albino rats." International Journal of Basic & Clinical Pharmacology 9, no. 1 (December 24, 2019): 24. http://dx.doi.org/10.18203/2319-2003.ijbcp20195594.

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Background: Diabetes mellitus is known to cause cognitive impairment that can be possibly attributed to deficient levels of leptin in diabetic animals. This study was undertaken to study the effect of administration of leptin on spatial learning, memory and blood glucose levels in diabetic rats.Methods: Rats were divided into three groups. The first group was the control group. Diabetes was induced in groups 2 and 3 by streptozotocin (STZ) injection (60 mg/kg) intraperitoneally. Group 2 received saline while group 3 received leptin (0.1 mg/kg) subcutaneously for 10 days from 4th day of STZ administration. Behavioural assessment was done in T maze after 21 days of the last injection of leptin. Blood glucose levels were also analysed.Results: The number of correct arm entries decreased while time spent being immobile and time spent to reach the correct arm increased in the diabetic group when compared to the control group and correct arm entries increased while time spent immobile and time spent to reach the correct arm decreased with leptin treatment when compared to the diabetic control rats. Blood glucose levels increased in the diabetic rats while leptin administration reduced blood glucose levels in the group 3.Conclusions: Our study suggests that leptin can improve learning and memory while also producing a slight reduction in the blood glucose levels in diabetic rats.

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Munoz-Pacheco, Jesus M., Cornelio Posadas-Castillo, and Ernesto Zambrano-Serrano. "The Effect of a Non-Local Fractional Operator in an Asymmetrical Glucose-Insulin Regulatory System: Analysis, Synchronization and Electronic Implementation." Symmetry 12, no. 9 (August 21, 2020): 1395. http://dx.doi.org/10.3390/sym12091395.

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For studying biological conditions with higher precision, the memory characteristics defined by the fractional-order versions of living dynamical systems have been pointed out as a meaningful approach. Therefore, we analyze the dynamics of a glucose-insulin regulatory system by applying a non-local fractional operator in order to represent the memory of the underlying system, and whose state-variables define the population densities of insulin, glucose, and β-cells, respectively. We focus mainly on four parameters that are associated with different disorders (type 1 and type 2 diabetes mellitus, hypoglycemia, and hyperinsulinemia) to determine their observation ranges as a relation to the fractional-order. Like many preceding works in biosystems, the resulting analysis showed chaotic behaviors related to the fractional-order and system parameters. Subsequently, we propose an active control scheme for forcing the chaotic regime (an illness) to follow a periodic oscillatory state, i.e., a disorder-free equilibrium. Finally, we also present the electronic realization of the fractional glucose-insulin regulatory model to prove the conceptual findings.

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Bhatt, Mahendra Prasad, Yeon-Ju Lee, Se-Hui Jung, Yong Ho Kim, Jong Yun Hwang, Eun-Taek Han, Won Sun Park, Seok-Ho Hong, Young-Myeong Kim, and Kwon-Soo Ha. "C-peptide protects against hyperglycemic memory and vascular endothelial cell apoptosis." Journal of Endocrinology 231, no. 1 (October 2016): 97–108. http://dx.doi.org/10.1530/joe-16-0349.

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C-peptide exerts protective effects against diabetic complications; however, its role in inhibiting hyperglycemic memory (HGM) has not been elucidated. We investigated the beneficial effect of C-peptide on HGM-induced vascular damage in vitro and in vivo using human umbilical vein endothelial cells and diabetic mice. HGM induced apoptosis by persistent generation of intracellular ROS and sustained formation of ONOO− and nitrotyrosine. These HGM-induced intracellular events were normalized by treatment with C-peptide, but not insulin, in endothelial cells. C-peptide also inhibited persistent upregulation of p53 and activation of mitochondrial adaptor p66shc after glucose normalization. Further, C-peptide replacement therapy prevented persistent generation of ROS and ONOO− in the aorta of diabetic mice whose glucose levels were normalized by the administration of insulin. C-peptide, but not insulin, also prevented HGM-induced endothelial apoptosis in the murine diabetic aorta. This study highlights a promising role for C-peptide in preventing HGM-induced intracellular events and diabetic vascular damage.

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Matyi, Stephanie, Jordan Jackson, Karla Garrett, Sathyaseelan S. Deepa, and Archana Unnikrishnan. "The effect of different levels of dietary restriction on glucose homeostasis and metabolic memory." GeroScience 40, no. 2 (February 17, 2018): 139–49. http://dx.doi.org/10.1007/s11357-018-0011-5.

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Sünram-Lea, Sandra I., Stephen A. Dewhurst, and Jonathan K. Foster. "The effect of glucose administration on the recollection and familiarity components of recognition memory." Biological Psychology 77, no. 1 (January 2008): 69–75. http://dx.doi.org/10.1016/j.biopsycho.2007.09.006.

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Wang, R. "Change of learning and memory ability and IGF-1 level in type 3 diabetes rats and effect of analog P165 of APP 5-mer peptide." European Psychiatry 26, S2 (March 2011): 503. http://dx.doi.org/10.1016/s0924-9338(11)72210-6.

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ObjectiveTo investigate the effect of Analog P165 of APP5-mer peptide on change of learning and memory ability in type 3 diabetes rats.MethodHealthy adult male rats were randomly divided into 3 groups: Control group; type 3 diabetes (T3DM) group; T3DM administrated P165 group. T3DM models were induced by intracerebroventricular injection of Streptozotocin (STZ, 3 mg/kg) bilaterally. P165 groups were treated with gastric P165 (355 μg/kg) Then, learning and memory ability was detected by Morris water maze test. Body weight and serum glucose were recorded. The rat serum Insulin, Gluocagon, insulin-like growth factor-1 (IFG-1) was detected by ELISA method.ResultsIn the Morris water maze test, compared with control group, the escape latency increased significantly (p < 0.05) in model group at the 3rd day. Compared with model group, the escape latency decreased significantly (p < 0.05) in the models administrated P165 group at the 3rd day. Although there was no significant difference, the escape latency decreased in P165 group at the 4th and 5th day. From the result of rats blood serum detection, the serum IGF-1 level decreased significantly in the model group (p < 0.01) than the control group. The serum IGF-1 level increased significantly in P165 treated group(p < 0.05).The body weight and the serum glucose, insulin, gluocagon had no significant difference among the groups in the period of experiment.ConclusionThere is learning and memory impairment in the T3DM rats. P165 can raise the rats blood serum IGF-1 level, ameliorate learning and memory ability but don’t influence the serum glucose.

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Mana, Lulu, Huili Feng, Yunfang Dong, Yahan Wang, Jing Shi, Jinzhou Tian, and Pengwen Wang. "Effect of Chinese herbal compound GAPT on the early brain glucose metabolism of APP/PS1 transgenic mice." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841984148. http://dx.doi.org/10.1177/2058738419841482.

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A number of studies have shown that early-stage Alzheimer’s disease (AD) is associated with abnormal brain glucose metabolism before cognitive decline, which may be the key pathological change of asymptomatic AD. The pathogenesis of AD in traditional Chinese medicine is kidney deficiency and turbid phlegm. Based on this, GAPT (a mixture of herbal extracts) was made to invigorate kidney Yang and eliminate phlegm. Previous studies have shown that GAPT can improve and delay the memory decline, but the specific therapeutic target of AD in an early stage has not been studied. The aim of this study was to investigate the effect of GAPT on glucose metabolism in the early stage of AD. Eighty-eight 3-month-old male APP/PS1 transgenic mice were randomly divided into model group; donepezil group; and low, middle and high GAPT dosage groups. Twelve 3-month-old C57BL/6J mice were used as a control group. The Morris water maze test and the Step-Down Passive-Avoidance test were used to evaluate learning and memory ability. Cerebral extraction and the accumulation of glucose were scanned with a micro-positron-emission tomography (PET) imaging system. Immunohistochemistry, western blot analysis and polymerase chain reaction (PCR) were used to detect the expression of the PI3K/AKT-mTOR signalling pathway–related proteins and messenger RNAs (mRNAs) in hippocampus of APP/PS1 transgenic mice after 3 months of drug administration. GAPT can shorten the escape latency and error numbers compared to the model group. In micro-PET imaging analysis, GAPT can increase the glucose uptake average rate in the frontal lobe, temporal lobe, parietal lobe and hippocampus. The immunohistochemistry, western blot analysis and PCR results indicated that GAPT can increase the expression of PI3K, AKT, GLUT1 and GLUT3 in the hippocampus of APP/PS1 transgenic mice. In summary, GAPT can improve brain glucose metabolism damage in APP/PS1 transgenic mice, mainly by increasing brain glucose uptake, increasing glucose transport and improving the insulin signalling pathway.

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Jiang, Tingting, Junxiang Gu, Wenwen Chen, and Qing Chang. "Resveratrol inhibits high-glucose-induced inflammatory “metabolic memory” in human retinal vascular endothelial cells through SIRT1-dependent signaling." Canadian Journal of Physiology and Pharmacology 97, no. 12 (December 2019): 1141–51. http://dx.doi.org/10.1139/cjpp-2019-0201.

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Diabetes induces vascular endothelial damage and this study investigated high-glucose-induced inflammation “metabolic memory” of human retinal vascular endothelial cells (HRVECs), the effects of resveratrol on HRVECs, and the underlying signaling. HRVECs were grown under various conditions and assayed for levels of sirtuin 1 (SIRT1); acetylated nuclear factor κB (Ac-NF-κB); NOD-like receptor family, pyrin domain containing 3 (NLRP3); and other inflammatory cytokines; and cell viability. A high glucose concentration induced HRVEC inflammation metabolic memory by decreasing SIRT1 and increasing Ac-NF-κB, NLRP3, caspase 1, interleukin-1β, inducible nitric oxide synthase, and tumor necrosis factor α, whereas exposure of HRVECs to a high glucose medium for 4 days, followed by a normal glucose concentration for an additional 4 days, failed to reverse these changes. A high glucose concentration also significantly reduced HRVEC viability. In contrast, resveratrol, a selective SIRT1 activator, markedly enhanced HRVEC viability and reduced the inflammatory cytokines expressions. In addition, high glucose reduced AMP-activated protein kinase (AMPK) phosphorylation and retained during the 4 days of the reversal period of culture. The effects of resveratrol were abrogated after co-treatment with the SIRT1 inhibitor nicotinamide and the AMPK inhibitor compound C. In conclusion, resveratrol was able to reverse high-glucose-induced inflammation “metabolic memory” of HRVECs by activation of the SIRT1/AMPK/NF-κB pathway.

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Haley, Michael J., Siddharth Krishnan, David Burrows, Leon de Hoog, Jamie Thakrar, Ingo Schiessl, Stuart M. Allan, and Catherine B. Lawrence. "Acute high-fat feeding leads to disruptions in glucose homeostasis and worsens stroke outcome." Journal of Cerebral Blood Flow & Metabolism 39, no. 6 (November 24, 2017): 1026–37. http://dx.doi.org/10.1177/0271678x17744718.

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Chronic consumption of diets high in fat leads to obesity and can negatively affect brain function. Rodents made obese by long-term maintenance on a high-fat diet have worse outcome after experimental stroke. High-fat consumption for only three days does not induce obesity but has rapid effects on the brain including memory impairment. However, the effect of brief periods of high-fat feeding or high-fat consumption in the absence of obesity on stroke is unknown. We therefore tested the effect of an acute period of high-fat feeding (three days) in C57B/6 mice on outcome after middle cerebral artery occlusion (MCAo). In contrast to a chronic high-fat diet (7.5 months), an acute high-fat diet had no effect on body weight, adipose tissue, lipid profile or inflammatory markers (in periphery and the brain). Three days of high-fat feeding impaired glucose tolerance, increased plasma glucose and insulin and brain expression of the glucose transporter GLUT-1. Ischaemic damage was increased (48%) in mice fed an acute high-fat diet, and was associated with a further reduction in GLUT-1 in the ischaemic hemisphere. These data demonstrate that only a brief period of high-fat consumption has a negative effect on glucose homeostasis and worsens outcome after ischaemic stroke.

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Jensen, Nicole Jacqueline, Malin Nilsson, Jonas Schultz Ingerslev, Dorte Aalund Olsen, Mogens Fenger, Mads Svart, Niels Møller, Mette Zander, Kamilla Woznica Miskowiak, and Jørgen Rungby. "Effects of β-hydroxybutyrate on cognition in patients with type 2 diabetes." European Journal of Endocrinology 182, no. 2 (February 2020): 233–42. http://dx.doi.org/10.1530/eje-19-0710.

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Objective Cognitive impairment in type 2 diabetes is associated with cerebral glucose hypometabolism. Providing a glucose substitute such as ketone bodies might restore metabolic balance in glucose-compromised neurones and improve cognitive performance. We aimed to investigate if β-hydroxybutyrate (ketone body) infusion acutely affects cognitive performance, measured by a neuropsychological test battery, in patients with type 2 diabetes. Design Randomised, placebo-controlled, double-blind cross-over trial. Methods Eighteen patients with type 2 diabetes received i.v. ketone body (β-hydroxybutyrate) and placebo (saline) infusion in a randomised order on two separate occasions. On both days of examination, blood glucose was clamped at 7.5 mmol/L and a neuropsychological test battery was used to assess global cognitive performance (primary outcome) and specialized cognitive measures of verbal memory, working memory, executive function, psychomotor speed, and sustained attention. Results During neurocognitive testing, β-hydroxybutyrate concentrations were 2.4 vs 0.1 mmol/L. Working memory assessed by Wechsler Adult Intelligence Scale letter-number-sequencing significantly improved by 1.6 points (95% CI: 0.7, 2.4; non-adjusted P < 0.001) corresponding to a 17% increase in performance during ketone infusion compared to placebo. There was no change for global cognitive performance or any other cognitive measure after adjusting for multiple comparisons. Blood concentrations of β-hydroxybutyrate and glycaemic status did not associate with test performance; however, insulin resistance measured by HOMA was related to improved working memory performance during ketone infusion (β = 4%; 95% CI: 1.1, 7.7; P = 0.012). Conclusions Ketone infusion specifically improved working memory performance in patients with type 2 diabetes in the absence of changes in global cognition.

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Amin, Shaimaa Nasr, Shaimaa Abdalaleem Abdalgeleel, Mubarak Ali Algahtany, Sherif Ahmed Shaltout, Walaa Bayoumie El Gazzar, and Dalia Azmy Elberry. "Effect of Allopregnanolone on Spatial Memory and Synaptic Proteins in Animal Model of Metabolic Syndrome." Brain Sciences 11, no. 5 (May 15, 2021): 644. http://dx.doi.org/10.3390/brainsci11050644.

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Metabolic Syndrome (MetS) is considered a common disorder, especially with a sedentary lifestyle and unhealthy food consumption. Cognitive impairment is one of the MetS consequences that worsens the quality of life of the patients. The study aimed to assess the therapeutic effect of the neurosteroid Allopregnalonone on spatial memory and, therefore, the expression of two synaptic plasticity markers in the hippocampus. Thirty-two male rats were divided into four groups: control groups, MetS, and MetS + Allopregnalone. Spatial memory has been evaluated by the Y-maze task and blood pressure measured by the rat tail method. Biochemical evaluation of serum glucose, insulin, lipid profile, and hippocampal expression of Synaptophysin and Associated Protein 43 (GAP-43) were performed for assessing Allopregnanolone on serum and hippocampal markers. Allopregnanolone therapy improved working spatial memory, hypertension, and biochemical markers measured in the serum and hippocampus.

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Bedi, Upneet, and Bavneet Kaur Dang. "Association of duration of type 2 diabetes with short term and working memory." International Journal of Research in Medical Sciences 5, no. 11 (October 27, 2017): 4724. http://dx.doi.org/10.18203/2320-6012.ijrms20174643.

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Background: Type 2 diabetes mellitus has deleterious effects on brain resulting in loss of short term memory and working memory in elderly and poorly controlled diabetic patients. Less attention has been given to the effect of diabetes on cognitive functions. Hence, the study was undertaken to study the status of short term and working memory in type 2 diabetes mellitus and to correlate it with the duration of diabetes.Methods: Study was conducted in Punjab Institute of Medical Sciences, Jalandhar, India, on 100 diabetic patients in the age group of 40-60 years. Short term memory and working memory was assessed using 4 memory tests. AVLT and VFT for short term memory and WDST and VST for working memory. The results expressed in average of total scores. One-way ANOVA followed by post hoc (t) test were used for statistical analysis.Results: Short term memory and working memory status was negatively correlated with duration of diabetes. Diabetics more than 55 years showed greater cognitive decline compared to younger age group.Conclusions: The short term and the working memory status decreased significantly in diabetic patients, which may be due to age of onset, duration, vascular dementia, hyperglycemia or hypoglycemia. These effects observed that duration, sex, age and blood glucose levels are of clinical importance as short term and working memory loss could have important practical implications for daily activities.

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Kukula, Osman, and Caner Günaydın. "Atorvastatin reduces alloxan-induced impairment of aversive stimulus memory in mice." Asian Biomedicine 16, no. 2 (April 1, 2022): 71–78. http://dx.doi.org/10.2478/abm-2022-0009.

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Abstract Background An association between dysregulated glucose levels in patients with diabetes mellitus and detrimental effects on the central nervous system, particularly in Alzheimer disease, has been recognized. Atorvastatin treatment has improved memory and cognition in some patients with diabetes mellitus and Alzheimer disease. Objectives To determine possible neuroprotective effects of atorvastatin on memory and cognition by measuring changes in an adverse stimulus avoidance learning deficit induced by alloxan in a murine model of diabetes mellitus and impaired memory and cognition. Methods We administered 150 mg/kg and 100 mg/kg alloxan in saline (intraperitoneally, i.p.) at a 48 h interval to produce a model of diabetes mellitus in male BALB/c mice. An oral glucose tolerance test (OGTT) was used to assess blood glucose regulation. After demonstrating hyperglycemia in mice (n = 7 per group) we administered vehicle (saline, i.p.), atorvastatin (10 mg/kg, i.p.), or liraglutide (200 μg/kg, i.p.) for 28 d except for those in a negative control group, which were given saline instead of alloxan, and a group administered atorvastatin alone, which were given saline instead of alloxan followed by atorvastatin (10 mg/kg, i.p.) for 28 d. Locomotor activity was measured 24 h after the final drug treatments, and subsequently their learned behavioral response to an adverse electrical stimulus to their plantar paw surface in a dark compartment was measured using a passive avoidance apparatus (Ugo Basile) in a model of impaired memory and cognition associated with Alzheimer disease. To determine any deficit in their learned avoidance of the adverse stimulus, we measured the initial latency or time mice spent in an illuminated white compartment before entering the dark compartment in the learning trial, and on the day after learning to avoid the adverse stimulus, the retention period latency in the light compartment and time spent in the dark compartment. Results Atorvastatin alone produced no significant change in blood glucose levels (F 4,10 = 0.80, P = 0.55) within 2 h. Liraglutide decreased blood glucose levels after 0.5 h (F 4,10 = 11.7, P < 0.001). We found no significant change in locomotor activity in any group. In mice with alloxan-induced diabetes, atorvastatin significantly attenuated the decreased avoidance associated with the diabetes (F 4,30 = 38.0, P = 0.02) and liraglutide also significantly attenuated the decreased avoidance (F 4,30 = 38.0, P < 0.001). Atorvastatin alone had no significant effect on the adversive learned response compared with vehicle treatment (F 4,30 = 38.0, P > 0.05). Atorvastatin significantly decreased the time mice with alloxan-induced diabetes spent in the dark compartment compared with mice in the diabetes group without atorvastatin treatment (F 4,30 = 53.9, P = 0.046). Liraglutide also significantly reduced the time mice with alloxan-induced diabetes spent in the dark compartment compared with vehicle-treated mice with alloxan-induced diabetes (F 4,30 = 53.9, P < 0.001). Atorvastatin treatment alone had no significant effect on the time mice spent in dark compartment compared with the control group (F 4,30 = 53.9, P > 0.05). Conclusion Atorvastatin significantly attenuated the adverse stimulus avoidance learning deficit in the alloxan-induced murine model of diabetes suggesting decreased impairment of memory and cognition.

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Defour, Merel, Guido J. E. J. Hooiveld, Michel van Weeghel, and Sander Kersten. "Probing metabolic memory in the hepatic response to fasting." Physiological Genomics 52, no. 12 (December 1, 2020): 602–17. http://dx.doi.org/10.1152/physiolgenomics.00117.2020.

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Tissues may respond differently to a particular stimulus if they have been previously exposed to that same stimulus. Here, we tested the hypothesis that a strong metabolic stimulus such as fasting may influence the hepatic response to a subsequent fast and thus elicit a memory effect. Overnight fasting in mice significantly increased plasma free fatty acids, glycerol, β-hydroxybutyrate, and liver triglycerides, and decreased plasma glucose, plasma triglycerides, and liver glycogen levels. In addition, fasting dramatically changed the liver transcriptome, upregulating genes involved in gluconeogenesis and in uptake, oxidation, storage, and mobilization of fatty acids, and downregulating genes involved in fatty acid synthesis, fatty acid elongation/desaturation, and cholesterol synthesis. Fasting also markedly impacted the liver metabolome, causing a decrease in the levels of numerous amino acids, glycolytic-intermediates, TCA cycle intermediates, and nucleotides. However, these fasting-induced changes were unaffected by two previous overnight fasts. Also, no significant effect was observed of prior fasting on glucose tolerance. Finally, analysis of the effect of fasting on the transcriptome in hepatocyte humanized mouse livers indicated modest similarity in gene regulation in mouse and human liver cells. In general, genes involved in metabolic pathways were upregulated or downregulated to a lesser extent in human liver cells than in mouse liver cells. In conclusion, we found that previous exposure to fasting in mice did not influence the hepatic response to a subsequent fast, arguing against the concept of metabolic memory in the liver. Our data provide a useful resource for the study of liver metabolism during fasting.

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Sünram-Lea, Sandra I., Jonathan K. Foster, Paula Durlach, and Catalina Perez. "The effect of retrograde and anterograde glucose administration on memory performance in healthy young adults." Behavioural Brain Research 134, no. 1-2 (August 2002): 505–16. http://dx.doi.org/10.1016/s0166-4328(02)00086-4.

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Dash, P. K., S. A. Orsi, and A. N. Moore. "Spatial Memory Formation and Memory-Enhancing Effect of Glucose Involves Activation of the Tuberous Sclerosis Complex-Mammalian Target of Rapamycin Pathway." Journal of Neuroscience 26, no. 31 (August 2, 2006): 8048–56. http://dx.doi.org/10.1523/jneurosci.0671-06.2006.

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Ye, Minsook, Bong Hee Han, Jin Su Kim, Kyungsoo Kim, and Insop Shim. "Neuroprotective Effect of Bean Phosphatidylserine on TMT-Induced Memory Deficits in a Rat Model." International Journal of Molecular Sciences 21, no. 14 (July 11, 2020): 4901. http://dx.doi.org/10.3390/ijms21144901.

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Background: Trimethyltin (TMT) is a potent neurotoxin affecting various regions of the central nervous system, including the neocortex, the cerebellum, and the hippocampus. Phosphatidylserine (PS) is a membrane phospholipid, which is vital to brain cells. We analyzed the neuroprotective effects of soybean-derived phosphatidylserine (Bean-PS) on cognitive function, changes in the central cholinergic systems, and neural activity in TMT-induced memory deficits in a rat model. Methods: The rats were randomly divided into an untreated normal group, a TMT group (injected with TMT + vehicle), and a group injected with TMT + Bean-PS. The rats were treated with 10% hexane (TMT group) or TMT + Bean-PS (50 mg·kg−1, oral administration (p.o.)) daily for 21 days, following a single injection of TMT (8.0 mg/kg, intraperitoneally (i.p.)). The cognitive function of Bean-PS was assessed using the Morris water maze (MWM) test and a passive avoidance task (PAT). The expression of acetylcholine transferase (ChAT) and acetylcholinesterase (AchE) in the hippocampus was assessed via immunohistochemistry. A positron emission tomography (PET) scan was used to measure the glucose uptake in the rat brain. Results: Treatment with Bean-PS enhanced memory function in the Morris water maze (MWM) test. Consistent with the behavioral results, treatment with Bean-PS diminished the damage to cholinergic cells in the hippocampus, in contrast to those of the TMT group. The TMT+Bean-PS group showed elevated glucose uptake in the frontal lobe of the rat brain. Conclusion: These results demonstrate that Bean-PS protects against TMT-induced learning and memory impairment. As such, Bean-PS represents a potential treatment for neurodegenerative disorders, such as Alzheimer’s disease.

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Wang, Pengwen, Caixin Su, Huili Feng, Xiaopei Chen, Yunfang Dong, Yingxue Rao, Ying Ren, et al. "Curcumin regulates insulin pathways and glucose metabolism in the brains of APPswe/PS1dE9 mice." International Journal of Immunopathology and Pharmacology 30, no. 1 (January 26, 2017): 25–43. http://dx.doi.org/10.1177/0394632016688025.

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Recent studies have shown the therapeutic potential of curcumin in Alzheimer’s disease (AD). In 2014, our lab found that curcumin reduced Aβ40, Aβ42 and Aβ-derived diffusible ligands in the mouse hippocampus, and improved learning and memory. However, the mechanisms underlying this biological effect are only partially known. There is considerable evidence in brain metabolism studies indicating that AD might be a brain-specific type of diabetes with progressive impairment of glucose utilisation and insulin signalling. We hypothesised that curcumin might target both the glucose metabolism and insulin signalling pathways. In this study, we monitored brain glucose metabolism in living APPswe/PS1dE9 double transgenic mice using a micro-positron emission tomography (PET) technique. The study showed an improvement in cerebral glucose uptake in AD mice. For a more in-depth study, we used immunohistochemical (IHC) staining and western blot techniques to examine key factors in both glucose metabolism and brain insulin signalling pathways. The results showed that curcumin ameliorated the defective insulin signalling pathway by upregulating insulin-like growth factor (IGF)-1R, IRS-2, PI3K, p-PI3K, Akt and p-Akt protein expression while downregulating IR and IRS-1. Our study found that curcumin improved spatial learning and memory, at least in part, by increasing glucose metabolism and ameliorating the impaired insulin signalling pathways in the brain.

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Manning, C. A., J. L. Hall, and P. E. Gold. "Glucose Effects on Memory and Other Neuropsychological Tests in Elderly Humans." Psychological Science 1, no. 5 (September 1990): 307–11. http://dx.doi.org/10.1111/j.1467-9280.1990.tb00223.x.

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Gamaro, G. D., J. D. Denardin, M. B. Michalowski, D. Catelli, J. B. Correa, M. H. Xavier, and C. Dalmaz. "Epinephrine Effects on Memory Are Not Dependent on Hepatic Glucose Release." Neurobiology of Learning and Memory 68, no. 3 (November 1997): 221–29. http://dx.doi.org/10.1006/nlme.1997.3787.

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Journal articles on the topic 'Memory – Effect of glucose on'

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