glycogen synthesis Dotaz Zobrazit nápovědu
Previous studies have indicated that polyphenol-rich Chrysanthemum morifolium extract (CME) may inhibit the formation of hyperlipidemic fatty liver in mice. But there has been no report about therapeutic effect on diabetes mellitus. In the present study, we investigated the action of CME and its potential mechanisms. A mouse model with diabetes mellitus was induced by alloxan. The results showed that after treatment of diabetic mice with polyphenol-rich CME 150 and 300 mg/kg for 6 weeks, the levels of fasting blood glucose (FBG) as well as water and food consumption were decreased (P < 0.05 or P < 0.01), the content of hepatic glycogen was increased, especially in the 300 mg/kg group (P < 0.05), but no significant variations in the body-weight gain, fasting serum insulin, and muscular glycogen were observed. Importantly, toxic alloxan treatment might decrease the protein expressions of hepatic peroxisome proliferator-activated receptor (PPAR) α/γ, glycogen synthase (GS), and glucose transporter-2 (Glut-2) (P < 0.05 or P < 0.01), while CME might reverse the changes (P < 0.01). These findings demonstrate that the reduction of PPARα/γ-mediated hepatic glycogen synthesis may involve in the alloxan-induced hyperglycemia, and the hypoglycemic mechanisms of CME may be mainly associated with the increment of hepatic glycogen synthesis via upregulation of PPARα/γ-mediated GS and Glut-2 protein expressions.
- MeSH
- Chrysanthemum chemie MeSH
- experimentální diabetes mellitus * farmakoterapie MeSH
- glykogensynthasa farmakologie metabolismus účinky léků MeSH
- hypoglykemika MeSH
- krevní glukóza účinky léků MeSH
- modely u zvířat MeSH
- myši inbrední NOD MeSH
- polyfenoly farmakologie metabolismus MeSH
- receptory aktivované proliferátory peroxizomů metabolismus účinky léků MeSH
- rostlinné extrakty farmakologie terapeutické užití MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
Low production rates are still one limiting factor for the industrial climate-neutral production of biovaluable compounds in cyanobacteria. Next to optimized cultivation conditions, new production strategies are required. Hence, the use of established molecular tools could lead to increased product yields in the cyanobacterial model organism Synechocystis sp. PCC6803. Its main storage compound glycogen was chosen to be increased by the use of these tools. In this study, the three genes glgC, glgA1 and glgA2, which are part of the glycogen synthesis pathway, were combined with the Pcpc560 promoter and the neutral cloning site NSC1. The complete genome integration, protein formation, biomass production and glycogen accumulation were determined to select the most productive transformants. The overexpression of glgA2 did not increase the biomass or glycogen production in short-term trials compared to the other two genes but caused transformants death in long-term trials. The transformants glgA1_11 and glgC_2 showed significantly increased biomass (1.6-fold - 1.7-fold) and glycogen production (3.5-fold - 4-fold) compared to the wild type after 96 h making them a promising energy source for further applications. Those could include for example a two-stage production process, with first energy production (glycogen) and second increased product formation (e.g. ethanol).
- MeSH
- glykogen MeSH
- Synechocystis * genetika MeSH
- Publikační typ
- časopisecké články MeSH
Glycogen synthase kinase-3β (GSK-3β) is a multifunctional serine/threonine protein kinase that was originally identified as an enzyme involved in the control of glycogen metabolism. It plays a key role in diverse physiological processes including metabolism, the cell cycle, and gene expression by regulating a wide variety of well-known substances like glycogen synthase, tau-protein, and β-catenin. Recent studies have identified GSK-3β as a potential therapeutic target in Alzheimer´s disease, bipolar disorder, stroke, more than 15 types of cancer, and diabetes. GSK-3β is one of the most attractive targets for medicinal chemists in the discovery, design, and synthesis of new selective potent inhibitors. In the current study, twenty-eight Amaryllidaceae alkaloids of various structural types were studied for their potency to inhibit GSK-3β. Promising results have been demonstrated by alkaloids of the homolycorine-{9-O-demethylhomolycorine (IC50 = 30.00 ± 0.71 µM), masonine (IC50 = 27.81 ± 0.01 μM)}, and lycorine-types {caranine (IC50 = 30.75 ± 0.04 μM)}.
- MeSH
- estery metabolismus MeSH
- finanční podpora výzkumu jako téma MeSH
- glykogen metabolismus MeSH
- hypertriglyceridemie krev MeSH
- inhibitory ACE farmakologie MeSH
- kosterní svaly metabolismus účinky léků MeSH
- krysa rodu rattus MeSH
- mastné kyseliny biosyntéza krev MeSH
- tuková tkáň metabolismus účinky léků MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
AIMS/HYPOTHESIS: Fatty acids of marine origin, i.e. docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) act as hypolipidaemics, but they do not improve glycaemic control in obese and diabetic patients. Thiazolidinediones like rosiglitazone are specific activators of peroxisome proliferator-activated receptor gamma, which improve whole-body insulin sensitivity. We hypothesised that a combined treatment with a DHA and EPA concentrate (DHA/EPA) and rosiglitazone would correct, by complementary additive mechanisms, impairments of lipid and glucose homeostasis in obesity. METHODS: Male C57BL/6 mice were fed a corn oil-based high-fat diet. The effects of DHA/EPA (replacing 15% dietary lipids), rosiglitazone (10 mg/kg diet) or a combination of both on body weight, adiposity, metabolic markers and adiponectin in plasma, as well as on liver and muscle gene expression and metabolism were analysed. Euglycaemic-hyperinsulinaemic clamps were used to characterise the changes in insulin sensitivity. The effects of the treatments were also analysed in dietary obese mice with impaired glucose tolerance (IGT). RESULTS: DHA/EPA and rosiglitazone exerted additive effects in prevention of obesity, adipocyte hypertrophy, low-grade adipose tissue inflammation, dyslipidaemia and insulin resistance, while inducing adiponectin, suppressing hepatic lipogenesis and decreasing muscle ceramide concentration. The improvement in glucose tolerance reflected a synergistic stimulatory effect of the combined treatment on muscle glycogen synthesis and its sensitivity to insulin. The combination treatment also reversed dietary obesity, dyslipidaemia and IGT. CONCLUSIONS/INTERPRETATION: DHA/EPA and rosiglitazone can be used as complementary therapies to counteract dyslipidaemia and insulin resistance. The combination treatment may reduce dose requirements and hence the incidence of adverse side effects of thiazolidinedione therapy. PMID:19277604[PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, SubstancesPublication TypesResearch Support, Non-U.S. Gov'tMeSH TermsAnimalsCorn Oil/pharmacologyDietary Fats/pharmacology*Docosahexaenoic Acids/pharmacologyEicosapentaenoic Acid/pharmacologyFatty Acids, Omega-3/pharmacology*Glucose Intolerance/metabolismGlycogen/biosynthesis*Hypoglycemic Agents/pharmacologyInsulin/physiology*MaleMiceMice, Inbred C57BLMuscle, Skeletal/drug effectsMuscle, Skeletal/metabolism*Thiazolidinediones/pharmacology*SubstancesDietary FatsFatty Acids, Omega-3Hypoglycemic AgentsThiazolidinedionesInsulinrosiglitazoneEicosapentaenoic AcidDocosahexaenoic AcidsCorn OilGlycogen LinkOut - more resourcesFull Text SourcesSpringerEBSCOOhioLINK Electronic Journal CenterProQuest Information and LearningSwets Information ServicesMedicalDietary Fats - MedlinePlus Health InformationDiabetes Medicines - MedlinePlus Health Information • Supplemental Content Related citations Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet. [Diabetologia. 2006] Polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet. Flachs P, Mohamed-Ali V, Horakova O, Rossmeisl M, Hosseinzadeh-Attar MJ, Hensler M, Ruzickova J, Kopecky J. Diabetologia. 2006 Feb; 49(2):394-7. Epub 2006 Jan 6.Prominent role of liver in elevated plasma palmitoleate levels in response to rosiglitazone in mice fed high-fat diet. [J Physiol Pharmacol. 2009] Prominent role of liver in elevated plasma palmitoleate levels in response to rosiglitazone in mice fed high-fat diet. Kuda O, Stankova B, Tvrzicka E, Hensler M, Jelenik T, Rossmeisl M, Flachs P, Kopecky J. J Physiol Pharmacol. 2009 Dec; 60(4):135-40. Prevention and reversal of obesity and glucose intolerance in mice by DHA derivatives. [Obesity (Silver Spring). 2009] Prevention and reversal of obesity and glucose intolerance in mice by DHA derivatives. Rossmeisl M, Jelenik T, Jilkova Z, Slamova K, Kus V, Hensler M, Medrikova D, Povysil C, Flachs P, Mohamed-Ali V, et al. Obesity (Silver Spring). 2009 May; 17(5):1023-31. Epub 2009 Jan 15.Review N-3 long chain polyunsaturated fatty acids: a nutritional tool to prevent insulin resistance associated to type 2 diabetes and obesity? [Reprod Nutr Dev. 2004] Review N-3 long chain polyunsaturated fatty acids: a nutritional tool to prevent insulin resistance associated to type 2 diabetes and obesity? Delarue J, LeFoll C, Corporeau C, Lucas D. Reprod Nutr Dev. 2004 May-Jun; 44(3):289-99. Review Central role of the adipocyte in the insulin-sensitising and cardiovascular risk modifying actions of the thiazolidinediones. [Biochimie. 2003] Review Central role of the adipocyte in the insulin-sensitising and cardiovascular risk modifying actions of the thiazolidinediones. Smith SA. Biochimie. 2003 Dec; 85(12):1219-30. See reviews... See all... Cited by 2 PubMed Central articles Different adipose depots: their role in the development of metabolic syndrome and mitochondrial response to hypolipidemic agents. [J Obes. 2011] Different adipose depots: their role in the development of metabolic syndrome and mitochondrial response to hypolipidemic agents. Bjorndal B, Burri L, Staalesen V, Skorve J, Berge RK. J Obes. 2011; 2011:490650. Epub 2011 Feb 15.Can vagus nerve stimulation halt or ameliorate rheumatoid arthritis and lupus? [Lipids Health Dis. 2011] Can vagus nerve stimulation halt or ameliorate rheumatoid arthritis and lupus? Das UN. Lipids Health Dis. 2011 Jan 24; 10:19. Epub 2011 Jan 24.All links from this record Related Citations Calculated set of PubMed citations closely related to the selected article(s) retrieved using a word weight algorithm. Related articles are displayed in ranked order from most to least relevant, with the “linked from” citation displayed first.Compound (MeSH Keyword) PubChem chemical compound records that are classified under the same Medical Subject Headings (MeSH) controlled vocabulary as the current articles.Substance (MeSH Keyword) PubChem chemical substance (submitted) records that are classified under the same Medical Subject Headings (MeSH) controlled vocabulary as the current articles.Cited in PMC Full-text articles in the PubMed Central Database that cite the current articles.
- MeSH
- dietní tuky farmakologie MeSH
- glykogen biosyntéza MeSH
- hypoglykemika farmakologie MeSH
- inzulin fyziologie MeSH
- kosterní svaly metabolismus účinky léků MeSH
- kukuřičný olej farmakologie MeSH
- kyselina eikosapentaenová farmakologie MeSH
- kyseliny dokosahexaenové farmakologie MeSH
- kyseliny mastné omega-3 farmakologie MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- porucha glukózové tolerance metabolismus MeSH
- thiazolidindiony farmakologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
- Klíčová slova
- řezy mozkové kůry,
- MeSH
- experimenty na zvířatech MeSH
- histologické techniky metody využití MeSH
- ionty * chemická syntéza metabolismus MeSH
- lithium fyziologie metabolismus MeSH
- metabolismus sacharidů * fyziologie účinky léků MeSH
- morčata MeSH
- mozková kůra * anatomie a histologie metabolismus MeSH
- nervová tkáň anatomie a histologie metabolismus MeSH
- rubidium fyziologie metabolismus MeSH
- statistika jako téma MeSH
- vápník fyziologie izolace a purifikace metabolismus MeSH
- voda metabolismus MeSH
- zvířata MeSH
- Check Tag
- morčata MeSH
- zvířata MeSH