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Build-ups in the supply chain of the brain: on the neuroenergetic cause of obesity and type 2 diabetes mellitus. 大脑供应链中的堆积物：肥胖和 2 型糖尿病的神经能量原因。

Frontiers in neuroenergetics Pub Date : 2009-04-28 eCollection Date: 2009-01-01 DOI: 10.3389/neuro.14.002.2009

Achim Peters, Dirk Langemann

{"title":"Build-ups in the supply chain of the brain: on the neuroenergetic cause of obesity and type 2 diabetes mellitus.","authors":"Achim Peters, Dirk Langemann","doi":"10.3389/neuro.14.002.2009","DOIUrl":"10.3389/neuro.14.002.2009","url":null,"abstract":"Obesity and type 2 diabetes have become the major health problems in many industrialized countries. A few theoretical frameworks have been set up to derive the possible determinative cause of obesity. One concept views that food availability determines food intake, i.e. that obesity is the result of an external energy \"push\" into the body. Another one views that the energy milieu within the human organism determines food intake, i.e. that obesity is due to an excessive \"pull\" from inside the organism. Here we present the unconventional concept that a healthy organism is maintained by a \"competent brain-pull\" which serves systemic homeostasis, and that the underlying cause of obesity is \"incompetent brain-pull\", i.e. that the brain is unable to properly demand glucose from the body. We describe the energy fluxes from the environment, through the body, towards the brain with a mathematical \"supply chain\" model and test whether its predictions fit medical and experimental data sets from our and other research groups. In this way, we show data-based support of our hypothesis, which states that under conditions of food abundance incompetent brain-pull will lead to build-ups in the supply chain culminating in obesity and type 2 diabetes. In the same way, we demonstrate support of the related hypothesis, which states that under conditions of food deprivation a competent brain-pull mechanism is indispensable for the continuance of the brain s high energy level. In conclusion, we took the viewpoint of integrative physiology and provided evidence for the necessity of brain-pull mechanisms for the benefit of health. Along these lines, our work supports recent molecular findings from the field of neuroenergetics and continues the work on the \"Selfish Brain\" theory dealing with the maintenance of the cerebral and peripheral energy homeostasis.","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2009-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2691548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28366780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential effects of iodoacetamide and iodoacetate on glycolysis and glutathione metabolism of cultured astrocytes. 碘乙酰胺和碘乙酸酯对培养星形胶质细胞糖酵解和谷胱甘肽代谢的差异影响。

Frontiers in neuroenergetics Pub Date : 2009-03-24 eCollection Date: 2009-01-01 DOI: 10.3389/neuro.14.001.2009

Maike M Schmidt, Ralf Dringen

{"title":"Differential effects of iodoacetamide and iodoacetate on glycolysis and glutathione metabolism of cultured astrocytes.","authors":"Maike M Schmidt, Ralf Dringen","doi":"10.3389/neuro.14.001.2009","DOIUrl":"https://doi.org/10.3389/neuro.14.001.2009","url":null,"abstract":"Iodoacetamide (IAA) and iodoacetate (IA) have frequently been used to inhibit glycolysis, since these compounds are known for their ability to irreversibly inhibit the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). However, the consequences of a treatment with such thiol reagents on the glutathione (GSH) metabolism of brain cells have not been explored. Exposure of astroglia-rich primary cultures to IAA or IA in concentrations of up to 1 mM deprived the cells of GSH, inhibited cellular GAPDH activity, lowered cellular lactate production and caused a delayed cell death that was detectable after 90 min of incubation. However, the two thiol reagents differed substantially in their potential to deprive cellular GSH and to inhibit astrocytic glycolysis. IAA depleted the cellular GSH content more efficiently than IA as demonstrated by half-maximal effects for IAA and IA that were observed at concentrations of about 10 and 100 muM, respectively. In contrast, IA was highly efficient in inactivating GAPDH and lactate production with half-maximal effects observed already at a concentration below 100 muM, whereas IAA had to be applied in 10 times higher concentration to inhibit lactate production by 50%. These substantial differences of IAA and IA to affect GSH content and glycolysis of cultured astrocytes suggest that in order to inhibit astrocytic glycolysis without substantially compromising the cellular GSH metabolism, IA - and not IAA - should be used in low concentrations and/or for short incubation periods.","PeriodicalId":88242,"journal":{"name":"Frontiers in neuroenergetics","volume":"1 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2009-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3389/neuro.14.001.2009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28366779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 24

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