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| 2. |
- Berger, Karin, et al.
(författare)
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Mitochondrial ATP synthase--a possible target protein in the regulation of energy metabolism in vitro and in vivo
- 2002
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Ingår i: Nutritional neuroscience. - : Informa UK Limited. - 1028-415X .- 1476-8305. ; 5:3, s. 201-210
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Tidskriftsartikel (refereegranskat)abstract
- The increasing prevalence of obesity in the Western world has stimulated an intense search for mechanisms regulating food intake and energy balance. A number of appetite-regulating peptides have been identified, their receptors cloned and the intracellular events characterized. One possible energy-dissipating mechanism is the mitochondrial uncoupling of ATP-synthesis from respiratory chain oxidation through uncoupling proteins, whereby energy derived from food could be dissipated as heat, instead of stored as ATP. The exact role of the uncoupling proteins in energy balance is, however, uncertain. We show here that mitochondrial F1F0-ATP synthase itself is a target protein for an anorectic peptide, enterostatin, demonstrated both after affinity purification of rat brain membranes and through a direct physical interaction between enterostatin and purified F1-ATP synthase. In insulinoma cells (INS-1) enterostatin was found to target F1F0-ATP synthase, causing an inhibition of ATP production, an increased thermogenesis and increased oxygen consumption. The experiments suggest a role of mitochondrial F1F0-ATP synthase in the suppressed insulin secretion induced by enterostatin. It could be speculated that this targeting mechanism is involved in the decreased energy efficiency following enterostatin treatment in rat.
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| 3. |
- Erlanson-Albertsson, Charlotte
(författare)
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Uncoupling proteins--a new family of proteins with unknown function.
- 2002
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Ingår i: Nutritional Neuroscience. - : Maney Publishing. - 1476-8305 .- 1028-415X. ; 5:1, s. 1-11
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Forskningsöversikt (refereegranskat)abstract
- Uncoupling proteins are inner mitochondrial membrane proteins, which dissipate the proton gradient, releasing the stored energy as heat. Five proteins have been cloned, named UCP1, UCP2, UCP3, UCP4 and UCP5/BMCP1. These proteins are structurally related but differ in tissue expression. UCP1 is expressed uniquely in the brown adipose tissue, while UCP2 is widely distributed, UCP3 is mainly restricted to skeletal muscle and UCP4 and UCP5/BMCP1 expressed in the brain. The properties and regulation of the uncoupling proteins and their exact function has been the focus of an intense research during recent years. This review briefly summarizes the actual knowledge of the properties and function of this new family of proteins. While UCP1 has a clear role in energy homeostasis, the newcomers UCP2-UCP5 may have more delicate physiological importance acting as free radical oxygen scavengers and in the regulation of ATP-dependent processes, such as secretion.
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| 4. |
- Garcia-Serrano, Alba M, et al.
(författare)
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Taurine and N-acetylcysteine treatments prevent memory impairment and metabolite profile alterations in the hippocampus of high-fat diet-fed female mice
- 2023
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Ingår i: Nutritional Neuroscience. - 1476-8305. ; 26:11, s. 1090-1102
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Tidskriftsartikel (refereegranskat)abstract
- Background: Obesity constitutes a risk factor for cognitive impairment. In rodent models, long-term exposure to obesogenic diets leads to hippocampal taurine accumulation. Since taurine has putative cyto-protective effects, hippocampal taurine accumulation in obese and diabetic models might constitute a counteracting response to metabolic stress. Objective: We tested the hypothesis that treatment with taurine or with N-acetylcysteine (NAC), which provides cysteine for the synthesis of taurine and glutathione, prevent high-fat diet (HFD)-associated hippocampal alterations and memory impairment. Methods: Female mice were fed either a regular diet or HFD. Some mice had access to 3%(w/v) taurine or 3%(w/v) NAC in the drinking water. After 2 months, magnetic resonance spectroscopy (MRS) was used to measure metabolite profiles. Memory was assessed in novel object and novel location recognition tests. Results: HFD feeding caused memory impairment in both tests, and reduced concentration of lactate, phosphocreatine-to-creatine ratio, and the neuronal marker N-acetylaspartate in the hippocampus. Taurine and NAC prevented HFD-induced memory impairment and N-acetylaspartate reduction. NAC, but not taurine, prevented the reduction of lactate and phosphocreatine-to-creatine ratio. MRS revealed NAC/taurine-induced increase of hippocampal glutamate and GABA levels. Conclusion: NAC and taurine can prevent memory impairment, while only NAC prevents alterations of metabolite concentrations in HFD-exposed female mice.
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| 5. |
- Håglin, Lena
(författare)
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Using phosphate supplementation to reverse hypophosphatemia and phosphate depletion in neurological disease and disturbance
- 2016
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Ingår i: Nutritional neuroscience. - : Taylor & Francis. - 1028-415X .- 1476-8305. ; 19:5, s. 213-223
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Tidskriftsartikel (refereegranskat)abstract
- Hypophosphatemia (HP) with or without intracellular depletion of inorganic phosphate (Pi) and adenosine triphosphate has been associated with central and peripheral nervous system complications and can be observed in various diseases and conditions related to respiratory alkalosis, alcoholism (alcohol withdrawal), diabetic ketoacidosis, malnutrition, obesity, and parenteral and enteral nutrition. In addition, HP may explain serious muscular, neurological, and haematological disorders and may cause peripheral neuropathy with paresthesias and metabolic encephalopathy, resulting in confusion and seizures. The neuropathy may be improved quickly after proper phosphate replacement. Phosphate depletion has been corrected using potassium-phosphate infusion, a treatment that can restore consciousness. In severe ataxia and tetra paresis, complete recovery can occur after adequate replacement of phosphate. Patients with multiple risk factors, often with a chronic disease and severe HP that contribute to phosphate depletion, are at risk for neurologic alterations. To predict both risk and optimal phosphate replenishment requires assessing the nutritional status and risk for re-feeding hypophosphatemia. The strategy for correcting HP depends on the severity of the underlying disease and the goal for re-establishing a phosphate balance to limit the consequences of phosphate depletion.
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| 6. |
- Köhnke, Rickard, et al.
(författare)
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Fatty acids and glucose in high concentration down-regulates ATP synthase beta-subunit protein expression in INS-1 cells.
- 2007
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Ingår i: Nutritional Neuroscience. - : Informa UK Limited. - 1476-8305 .- 1028-415X. ; 10:5-6, s. 273-278
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Tidskriftsartikel (refereegranskat)abstract
- Chronic hyperglycemia and hyperlipidemia exert deleterious effects on beta-cell function and impair glucose-induced insulin release, referred to as glucotoxicity and lipotoxticity. These abnormalities are associated with decreased glucose-induced ATP production; ATP serves as an important signal for insulin secretion. To investigate the mechanism of the impaired ATP formation, we examined the effects of elevated glucose and fatty acids levels on ATP synthase beta-subunit expression, ATP content and insulin secretion in INS-1 insulinoma beta-cells. ATP synthase beta-subunit expression was measured by western blot, ATP content was monitored by ATP luminescence and insulin secretion detected by radio immunoassay. Our result indicated that chronic exposure to high doses of fatty acids together with high levels glucose produced a marked decrease in ATP synthase beta-subunit protein expression. Reduction of ATP synthase beta-subunit protein expression occurred with a decreased intracellular ATP concentration and insulin secretion at high fatty acid concentrations. These results indicate that high glucose together with fatty acids impair the production of ATP in beta-cells through the suppression of mitochondrial ATP synthesis. We conclude that ATP synthase beta-subunit may have an important role in the glucolipotoxicity of islet cells and suggest that ATP synthase beta-subunit might be a target of lipotoxicity in beta-cells.
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| 7. |
- Li, B. B., et al.
(författare)
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The effect of vitamin D supplementation in treatment of children with autism spectrum disorder: a systematic review and meta-analysis of randomized controlled trials
- 2022
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Ingår i: Nutritional Neuroscience. - : Informa UK Limited. - 1028-415X .- 1476-8305. ; 25:4, s. 835-845
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Tidskriftsartikel (refereegranskat)abstract
- Objective:The effect of vitamin D supplementation on the risk of Autism Spectrum Disorder (ASD) is conflicting. The aim of this study was to estimate the efficacy of vitamin D supplementation on ASD in children. Methods:We conducted a meta-analysis of randomized controlled trials (RCTs) in which vitamin D supplementation was used as a therapy in children with ASD. The PubMed, PsychINFO, Cochrane CENTRAL library, Web of Science, and Cinahl databases were searched from inception to March 20, 2019, for all publications on vitamin D and ASD with no restrictions. Studies involving individuals aged <18 years diagnosed with ASD and with all functional outcomes assessed by measurement scales for ASD were included. Mean differences were pooled, and a meta-analysis was performed using a random-effects model due to differences between the individual RCTs. Results:There were five RCTs with 349 children with ASD in the review, of which three RCTs were included in the meta-analysis. Vitamin D supplementation indicated a small but significant improvement in hyperactivity scores (pooled MD: -3.20; 95% CI: [-6.06, -0.34]) with low heterogeneity (I-2 = 10%,p = 0.33), but there were no other statistically significant differences in ASD symptoms between groups as measured by validated scales. Conclusion:Vitamin D supplementation appears to be beneficial for hyperactivity but not for core symptoms or other co-existing behaviors and conditions of ASD. Future RCTs with large sample sizes examining the effect of vitamin D supplementation on ASD among individuals with low serum vitamin D levels at baseline are needed.
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| 8. |
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| 9. |
- Lindqvist, Andreas, et al.
(författare)
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Decreased UCP2 mRNA expression in rat stomach following vagotomy: novel role for UCP2 as free radical scavenger in the stomach?
- 2004
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Ingår i: Nutritional Neuroscience. - : Informa UK Limited. - 1476-8305 .- 1028-415X. ; 7:4, s. 217-222
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Tidskriftsartikel (refereegranskat)abstract
- Uncoupling protein 2 (UCP2) is a protein, located in the inner mitochondrial membrane, which dissipates the proton gradient of this membrane and uncouples respiration from oxidative phosphorylation. We found, by in situ hybridisation, UCP2 mRNA to be located in the proliferating zone of the mucous neck cells in the fundus part of the rat stomach. We also found that UCP2 expression in fundus was significantly decreased after seven days of vagotomy. Furthermore, we found manganese-containing superoxide dismutase (SOD2), in fundus, to be down-regulated in a way similar to UCP2. The amount of ATP was significantly decreased following vagotomy. It is concluded that UCP2 in the gastro-intestinal tract is regulated through vagal innervation and suggested to act as a free radical scavenger.
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| 10. |
- Lindqvist, Andreas, et al.
(författare)
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Enterostatin up-regulates the expression of the beta-subunit of F(1)F(o)-ATPase in the plasma membrane of INS-1 cells.
- 2008
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Ingår i: Nutritional Neuroscience. - 1476-8305. ; 11:2, s. 55-60
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to high-fat diet easily promotes overeating while at the same time disrupting insulin secretion and islet function. Enterostatin is a peptide which is secreted from the pancreas in response to high-fat feeding and has been shown to inhibit fat intake as well as insulin secretion in experimental animal models. Until recently, there was no known receptor for enterostatin. In 2002, Berger and co-workers found enterostatin to target the beta-subunit of the F(1)-ATPase in rat brain membranes as well as in a clonal beta-cell line (INS-1). In this study, we found the beta-subunit of F(1)-ATPase to be ectopically expressed in the plasma membrane of INS-1 cells using both immunohistochemistry and Western blotting. Incubation with enterostatin for 60 min resulted in a 3.5-fold increase of the protein expression of the beta-subunit of F(1)-ATPase in the plasma membrane. Furthermore, we found ATP to be able to displace the binding of enterostatin to purified bovine F(1)-ATPase. This reported targeting of enterostatin to the beta-subunit of F(1)-ATPase in insulin cells may provide a link between high-fat intake and islet function.
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