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Futwan A. Al-mohanna - One of the best experts on this subject based on the ideXlab platform.
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Effect of developmental NMDAR antagonism with CGP 39551 on Aspartame-induced hypothalamic and adrenal gene expression
2018Co-Authors: Kate S. Collison, Angela Inglis, Sherin Shibin, Soad Saleh, Bernard Andres, Rosario Ubungen, Jennifer Thiam, Princess Mata, Futwan A. Al-mohannaAbstract:RationaleAspartame (L-aspartyl phenylalanine methyl ester) is a non-nutritive sweetener (NNS) approved for use in more than 6000 dietary products and pharmaceuticals consumed by the general public including adults and children, pregnant and nursing mothers. However a recent prospective study reported a doubling of the risk of being overweight amongst 1-year old children whose mothers consumed NNS-sweetened beverages daily during pregnancy. We have previously shown that chronic Aspartame (ASP) exposure commencing in utero may detrimentally affect adulthood adiposity status, glucose metabolism and aspects of behavior and spatial cognition, and that this can be modulated by developmental N-methyl-D-aspartate receptor (NMDAR) blockade with the competitive antagonist CGP 39551 (CGP). Since glucose homeostasis and certain aspects of behavior and locomotion are regulated in part by the NMDAR-rich hypothalamus, which is part of the hypothalamic-pituitary-adrenal- (HPA) axis, we have elected to examine changes in hypothalamic and adrenal gene expression in response to ASP exposure in the presence or absence of developmental NMDAR antagonism with CGP, using Affymetrix microarray analysis.ResultsUsing 2-factor ANOVA we identified 189 ASP-responsive differentially expressed genes (DEGs) in the adult male hypothalamus and 2188 in the adrenals, and a further 23 hypothalamic and 232 adrenal genes significantly regulated by developmental treatment with CGP alone. ASP exposure robustly elevated the expression of a network of genes involved in hypothalamic neurosteroidogenesis, together with cell stress and inflammatory genes, consistent with previous reports of Aspartame-induced CNS stress and oxidative damage. These genes were not differentially expressed in ASP mice with CGP antagonism. In the adrenal glands of ASP-exposed mice, GABA and Glutamate receptor subunit genes were amongst those most highly upregulated. Developmental NMDAR antagonism alone had less effect on adulthood gene expression and affected mainly hypothalamic neurogenesis and adrenal steroid metabolism. Combined ASP + CGP treatment mainly upregulated genes involved in adrenal drug and cholesterol metabolism.ConclusionASP exposure increased the expression of functional networks of genes involved in hypothalamic neurosteroidogenesis and adrenal catecholamine synthesis, patterns of expression which were not present in ASP-exposed mice with developmental NMDAR antagonism.
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Effect of developmental NMDAR antagonism with CGP 39551 on Aspartame-induced hypothalamic and adrenal gene expression.
'Public Library of Science (PLoS)', 2018Co-Authors: Kate S. Collison, Angela Inglis, Sherin Shibin, Soad Saleh, Bernard Andres, Rosario Ubungen, Jennifer Thiam, Princess Mata, Futwan A. Al-mohannaAbstract:Aspartame (L-aspartyl phenylalanine methyl ester) is a non-nutritive sweetener (NNS) approved for use in more than 6000 dietary products and pharmaceuticals consumed by the general public including adults and children, pregnant and nursing mothers. However a recent prospective study reported a doubling of the risk of being overweight amongst 1-year old children whose mothers consumed NNS-sweetened beverages daily during pregnancy. We have previously shown that chronic Aspartame (ASP) exposure commencing in utero may detrimentally affect adulthood adiposity status, glucose metabolism and aspects of behavior and spatial cognition, and that this can be modulated by developmental N-methyl-D-aspartate receptor (NMDAR) blockade with the competitive antagonist CGP 39551 (CGP). Since glucose homeostasis and certain aspects of behavior and locomotion are regulated in part by the NMDAR-rich hypothalamus, which is part of the hypothalamic-pituitary-adrenal- (HPA) axis, we have elected to examine changes in hypothalamic and adrenal gene expression in response to ASP exposure in the presence or absence of developmental NMDAR antagonism with CGP, using Affymetrix microarray analysis.Using 2-factor ANOVA we identified 189 ASP-responsive differentially expressed genes (DEGs) in the adult male hypothalamus and 2188 in the adrenals, and a further 23 hypothalamic and 232 adrenal genes significantly regulated by developmental treatment with CGP alone. ASP exposure robustly elevated the expression of a network of genes involved in hypothalamic neurosteroidogenesis, together with cell stress and inflammatory genes, consistent with previous reports of Aspartame-induced CNS stress and oxidative damage. These genes were not differentially expressed in ASP mice with CGP antagonism. In the adrenal glands of ASP-exposed mice, GABA and Glutamate receptor subunit genes were amongst those most highly upregulated. Developmental NMDAR antagonism alone had less effect on adulthood gene expression and affected mainly hypothalamic neurogenesis and adrenal steroid metabolism. Combined ASP + CGP treatment mainly upregulated genes involved in adrenal drug and cholesterol metabolism.ASP exposure increased the expression of functional networks of genes involved in hypothalamic neurosteroidogenesis and adrenal catecholamine synthesis, patterns of expression which were not present in ASP-exposed mice with developmental NMDAR antagonism
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Gender Dimorphism in Aspartame-Induced Impairment of Spatial Cognition and Insulin Sensitivity
2012Co-Authors: Kate S. Collison, Angela Inglis, Bernard Andres, Nadine J. Makhoul, Marya Z. Zaidi, Soad M. Saleh, Rana Al-rabiah, Futwan A. Al-mohannaAbstract:Previous studies have linked Aspartame consumption to impaired retention of learned behavior in rodents. Prenatal exposure to Aspartame has also been shown to impair odor-associative learning in guinea pigs; and recently, Aspartame-fed hyperlipidemic zebrafish exhibited weight gain, hyperglycemia and acute swimming defects. We therefore investigated the effects of chronic lifetime exposure to Aspartame, commencing in utero, on changes in blood glucose parameters, spatial learning and memory in C57BL/6J mice. Morris Water Maze (MWM) testing was used to assess learning and memory, and a random-fed insulin tolerance test was performed to assess glucose homeostasis. Pearson correlation analysis was used to investigate the associations between body characteristics and MWM performance outcome variables. At 17 weeks of age, male Aspartame-fed mice exhibited weight gain, elevated fasting glucose levels and decreased insulin sensitivity compared to controls (P
Vivek Sharma - One of the best experts on this subject based on the ideXlab platform.
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stability of Aspartame and neotame in pasteurized and in bottle sterilized flavoured milk
Food Chemistry, 2016Co-Authors: Anuradha Kumari, Sonika Choudhary, Sumit Arora, Vivek SharmaAbstract:Abstract Analytical high performance liquid chromatography (HPLC) conditions were standardized along with the isolation procedure for separation of Aspartame and neotame in flavoured milk (pasteurized and in-bottle sterilized flavoured milk). The recovery of the method was approximately 98% for both Aspartame and neotame. The proposed HPLC method can be successfully used for the routine determination of Aspartame and neotame in flavoured milk. Pasteurization (90 °C/20 min) resulted in approximately 40% loss of Aspartame and only 8% of neotame was degraded. On storage (4–7 °C/7 days) Aspartame and neotame content decreased significantly ( P P
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stability of Aspartame and neotame in pasteurized and in bottle sterilized flavoured milk
Food Chemistry, 2016Co-Authors: Anuradha Kumari, Sonika Choudhary, Sumit Arora, Vivek SharmaAbstract:Analytical high performance liquid chromatography (HPLC) conditions were standardized along with the isolation procedure for separation of Aspartame and neotame in flavoured milk (pasteurized and in-bottle sterilized flavoured milk). The recovery of the method was approximately 98% for both Aspartame and neotame. The proposed HPLC method can be successfully used for the routine determination of Aspartame and neotame in flavoured milk. Pasteurization (90 °C/20 min) resulted in approximately 40% loss of Aspartame and only 8% of neotame was degraded. On storage (4-7°C/7 days) Aspartame and neotame content decreased significantly (P<0.05) from 59.70% to 44.61% and 91.78% to 87.18%, respectively. Sterilization (121 °C/15 min) resulted in complete degradation of Aspartame; however, 50.50% of neotame remained intact. During storage (30 °C/60 days) neotame content decreased significantly (P<0.05) from 50.36% to 8.67%. Results indicated that neotame exhibited better stability than Aspartame in both pasteurized and in-bottle sterilized flavoured milk.
Kate S. Collison - One of the best experts on this subject based on the ideXlab platform.
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Effect of developmental NMDAR antagonism with CGP 39551 on Aspartame-induced hypothalamic and adrenal gene expression
2018Co-Authors: Kate S. Collison, Angela Inglis, Sherin Shibin, Soad Saleh, Bernard Andres, Rosario Ubungen, Jennifer Thiam, Princess Mata, Futwan A. Al-mohannaAbstract:RationaleAspartame (L-aspartyl phenylalanine methyl ester) is a non-nutritive sweetener (NNS) approved for use in more than 6000 dietary products and pharmaceuticals consumed by the general public including adults and children, pregnant and nursing mothers. However a recent prospective study reported a doubling of the risk of being overweight amongst 1-year old children whose mothers consumed NNS-sweetened beverages daily during pregnancy. We have previously shown that chronic Aspartame (ASP) exposure commencing in utero may detrimentally affect adulthood adiposity status, glucose metabolism and aspects of behavior and spatial cognition, and that this can be modulated by developmental N-methyl-D-aspartate receptor (NMDAR) blockade with the competitive antagonist CGP 39551 (CGP). Since glucose homeostasis and certain aspects of behavior and locomotion are regulated in part by the NMDAR-rich hypothalamus, which is part of the hypothalamic-pituitary-adrenal- (HPA) axis, we have elected to examine changes in hypothalamic and adrenal gene expression in response to ASP exposure in the presence or absence of developmental NMDAR antagonism with CGP, using Affymetrix microarray analysis.ResultsUsing 2-factor ANOVA we identified 189 ASP-responsive differentially expressed genes (DEGs) in the adult male hypothalamus and 2188 in the adrenals, and a further 23 hypothalamic and 232 adrenal genes significantly regulated by developmental treatment with CGP alone. ASP exposure robustly elevated the expression of a network of genes involved in hypothalamic neurosteroidogenesis, together with cell stress and inflammatory genes, consistent with previous reports of Aspartame-induced CNS stress and oxidative damage. These genes were not differentially expressed in ASP mice with CGP antagonism. In the adrenal glands of ASP-exposed mice, GABA and Glutamate receptor subunit genes were amongst those most highly upregulated. Developmental NMDAR antagonism alone had less effect on adulthood gene expression and affected mainly hypothalamic neurogenesis and adrenal steroid metabolism. Combined ASP + CGP treatment mainly upregulated genes involved in adrenal drug and cholesterol metabolism.ConclusionASP exposure increased the expression of functional networks of genes involved in hypothalamic neurosteroidogenesis and adrenal catecholamine synthesis, patterns of expression which were not present in ASP-exposed mice with developmental NMDAR antagonism.
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Effect of developmental NMDAR antagonism with CGP 39551 on Aspartame-induced hypothalamic and adrenal gene expression.
'Public Library of Science (PLoS)', 2018Co-Authors: Kate S. Collison, Angela Inglis, Sherin Shibin, Soad Saleh, Bernard Andres, Rosario Ubungen, Jennifer Thiam, Princess Mata, Futwan A. Al-mohannaAbstract:Aspartame (L-aspartyl phenylalanine methyl ester) is a non-nutritive sweetener (NNS) approved for use in more than 6000 dietary products and pharmaceuticals consumed by the general public including adults and children, pregnant and nursing mothers. However a recent prospective study reported a doubling of the risk of being overweight amongst 1-year old children whose mothers consumed NNS-sweetened beverages daily during pregnancy. We have previously shown that chronic Aspartame (ASP) exposure commencing in utero may detrimentally affect adulthood adiposity status, glucose metabolism and aspects of behavior and spatial cognition, and that this can be modulated by developmental N-methyl-D-aspartate receptor (NMDAR) blockade with the competitive antagonist CGP 39551 (CGP). Since glucose homeostasis and certain aspects of behavior and locomotion are regulated in part by the NMDAR-rich hypothalamus, which is part of the hypothalamic-pituitary-adrenal- (HPA) axis, we have elected to examine changes in hypothalamic and adrenal gene expression in response to ASP exposure in the presence or absence of developmental NMDAR antagonism with CGP, using Affymetrix microarray analysis.Using 2-factor ANOVA we identified 189 ASP-responsive differentially expressed genes (DEGs) in the adult male hypothalamus and 2188 in the adrenals, and a further 23 hypothalamic and 232 adrenal genes significantly regulated by developmental treatment with CGP alone. ASP exposure robustly elevated the expression of a network of genes involved in hypothalamic neurosteroidogenesis, together with cell stress and inflammatory genes, consistent with previous reports of Aspartame-induced CNS stress and oxidative damage. These genes were not differentially expressed in ASP mice with CGP antagonism. In the adrenal glands of ASP-exposed mice, GABA and Glutamate receptor subunit genes were amongst those most highly upregulated. Developmental NMDAR antagonism alone had less effect on adulthood gene expression and affected mainly hypothalamic neurogenesis and adrenal steroid metabolism. Combined ASP + CGP treatment mainly upregulated genes involved in adrenal drug and cholesterol metabolism.ASP exposure increased the expression of functional networks of genes involved in hypothalamic neurosteroidogenesis and adrenal catecholamine synthesis, patterns of expression which were not present in ASP-exposed mice with developmental NMDAR antagonism
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Gender Dimorphism in Aspartame-Induced Impairment of Spatial Cognition and Insulin Sensitivity
2012Co-Authors: Kate S. Collison, Angela Inglis, Bernard Andres, Nadine J. Makhoul, Marya Z. Zaidi, Soad M. Saleh, Rana Al-rabiah, Futwan A. Al-mohannaAbstract:Previous studies have linked Aspartame consumption to impaired retention of learned behavior in rodents. Prenatal exposure to Aspartame has also been shown to impair odor-associative learning in guinea pigs; and recently, Aspartame-fed hyperlipidemic zebrafish exhibited weight gain, hyperglycemia and acute swimming defects. We therefore investigated the effects of chronic lifetime exposure to Aspartame, commencing in utero, on changes in blood glucose parameters, spatial learning and memory in C57BL/6J mice. Morris Water Maze (MWM) testing was used to assess learning and memory, and a random-fed insulin tolerance test was performed to assess glucose homeostasis. Pearson correlation analysis was used to investigate the associations between body characteristics and MWM performance outcome variables. At 17 weeks of age, male Aspartame-fed mice exhibited weight gain, elevated fasting glucose levels and decreased insulin sensitivity compared to controls (P
Kyunghyun Cho - One of the best experts on this subject based on the ideXlab platform.
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Aspartame fed zebrafish exhibit acute deaths with swimming defects and saccharin fed zebrafish have elevation of cholesteryl ester transfer protein activity in hypercholesterolemia
Food and Chemical Toxicology, 2011Co-Authors: Jaeyong Kim, Juyi Seo, Kyunghyun ChoAbstract:Although many artificial sweeteners (AS) have safety issues, the AS have been widely used in industry. To determine the physiologic effect of AS in the presence of hyperlipidemia, zebrafish were fed Aspartame or saccharin with a high-cholesterol diet (HCD). After 12 days, 30% of zebrafish, which consumed Aspartame and HCD, died with exhibiting swimming defects. The Aspartame group had 65% survivability, while the control and saccharin groups had 100% survivability. Under HCD, the saccharin-fed groups had the highest increase in the serum cholesterol level (599 mg/dL). Aspartame-fed group showed a remarkable increase in serum glucose (up to 125 mg/dL), which was 58% greater than the increase in the HCD alone group. The saccharin and HCD groups had the highest cholesteryl ester transfer protein (CETP) activity (52% CE-transfer), while the HCD alone group had 42% CE-transfer. Histologic analysis revealed that the Aspartame and HCD groups showed more infiltration of inflammatory cells in the brain and liver sections. Conclusively, under presence of hyperlipidemia, Aspartame-fed zebrafish exhibited acute swimming defects with an increase in brain inflammation. Saccharin-fed zebrafish had an increased atherogenic serum lipid profile with elevation of CETP activity.
Gary M Williams - One of the best experts on this subject based on the ideXlab platform.
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Aspartame a safety evaluation based on current use levels regulations and toxicological and epidemiological studies
Critical Reviews in Toxicology, 2007Co-Authors: B A Magnuson, G A Burdock, John Doull, Rob Kroes, Gary M Marsh, M W Pariza, Peter S Spencer, William J Waddell, R Walker, Gary M WilliamsAbstract:Aspartame is a methyl ester of a dipeptide used as a synthetic nonnutritive sweetener in over 90 countries worldwide in over 6000 products. The purpose of this investigation was to review the scientific literature on the absorption and metabolism, the current consumption levels worldwide, the toxicology, and recent epidemiological studies on Aspartame. Current use levels of Aspartame, even by high users in special subgroups, remains well below the U.S. Food and Drug Administration and European Food Safety Authority established acceptable daily intake levels of 50 and 40 mg/kg bw/day, respectively. Consumption of large doses of Aspartame in a single bolus dose will have an effect on some biochemical parameters, including plasma amino acid levels and brain neurotransmitter levels. The rise in plasma levels of phenylalanine and aspartic acid following administration of Aspartame at doses less than or equal to 50 mg/kg bw do not exceed those observed postprandially. Acute, subacute and chronic toxicity studies with Aspartame, and its decomposition products, conducted in mice, rats, hamsters and dogs have consistently found no adverse effect of Aspartame with doses up to at least 4000 mg/kg bw/day. Critical review of all carcinogenicity studies conducted on Aspartame found no credible evidence that Aspartame is carcinogenic. The data from the extensive investigations into the possibility of neurotoxic effects of Aspartame, in general, do not support the hypothesis that Aspartame in the human diet will affect nervous system function, learning or behavior. Epidemiological studies on Aspartame include several case-control studies and one well-conducted prospective epidemiological study with a large cohort, in which the consumption of Aspartame was measured. The studies provide no evidence to support an association between Aspartame and cancer in any tissue. The weight of existing evidence is that Aspartame is safe at current levels of consumption as a nonnutritive sweetener.
