• MeSH
• diabetes mellitus MeSH
• finanční podpora výzkumu jako téma MeSH
• hormony farmakologie   fyziologie   krev   MeSH
• inzulinová rezistence MeSH
• lidé MeSH
• modely u zvířat MeSH
• molekulární struktura MeSH
• myši MeSH
• obezita etiologie   MeSH
• tuková tkáň fyziologie   sekrece   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• přehledy MeSH
• srovnávací studie MeSH

We studied the effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-alpha agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-alpha activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.

• MeSH
• adiponektin genetika   krev   MeSH
• dieta MeSH
• dietní sacharidy aplikace a dávkování   MeSH
• exprese genu účinky léků   MeSH
• fenofibrát aplikace a dávkování   MeSH
• financování organizované MeSH
• glykemický clamp MeSH
• hmotnostní úbytek účinky léků   MeSH
• inzulin farmakologie   krev   MeSH
• inzulinová rezistence MeSH
• játra chemie   účinky léků   MeSH
• kosterní svaly chemie   MeSH
• krevní glukóza analýza   MeSH
• kyseliny mastné neesterifikované analýza   MeSH
• lipidy biosyntéza   MeSH
• messenger RNA analýza   MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• obezita etiologie   krev   patofyziologie   MeSH
• PPAR alfa agonisté   fyziologie   MeSH
• receptory adiponektinu MeSH
• receptory buněčného povrchu genetika   MeSH
• resistin genetika   krev   MeSH
• triglyceridy krev   MeSH
• tuková tkáň chemie   patologie   MeSH
• velikost orgánu účinky léků   MeSH
• ztučnělá játra etiologie   farmakoterapie   krev   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH

Bradykinin can enhance skeletal muscle glucose uptake (GU), and exercise increases both bradykinin production and muscle insulin sensitivity, but bradykinin's relationship with post-exercise insulin action is uncertain. Our primary aim was to determine if the B2 receptor of bradykinin (B2R) is essential for the post-exercise increase in GU by insulin-stimulated mouse soleus muscles. Wildtype (WT) and B2R knockout (B2RKO) mice were sedentary or performed 60 minutes of treadmill exercise. Isolated soleus muscles were incubated with [(3)H]-2-deoxyglucose +/-insulin (60 or 100 microU/ml). GU tended to be greater for WT vs. B2RKO soleus with 60 microU/ml insulin (P=0.166) and was significantly greater for muscles with 100 microU/ml insulin (P<0.05). Both genotypes had significant exercise-induced reductions (P<0.05) in glycemia and insulinemia, and the decrements for glucose (~14 %) and insulin (~55 %) were similar between genotypes. GU tended to be greater for exercised vs. sedentary soleus with 60 microU/ml insulin (P=0.063) and was significantly greater for muscles with 100 microU/ml insulin (P<0.05). There were no significant interactions between genotype and exercise for blood glucose, plasma insulin or GU. These results indicate that the B2R is not essential for the exercise-induced decrements in blood glucose or plasma insulin or for the post-exercise increase in GU by insulin-stimulated mouse soleus muscle.

• MeSH
• adiponektin sekrece   MeSH
• adrenalin farmakologie   metabolismus   MeSH
• antagonisté adenosinového receptoru A1 farmakologie   MeSH
• dibutyryl cyklický AMP farmakologie   metabolismus   MeSH
• inzulin metabolismus   MeSH
• krysa rodu rattus MeSH
• palmitany farmakologie   metabolismus   MeSH
• potkani Wistar MeSH
• techniky in vitro MeSH
• tukové buňky sekrece   účinky léků   MeSH
• xanthiny farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH

BACKGROUND: The angiotensin receptor blocker telmisartan has unique chemical properties that enable it to partially activate the peroxisome proliferator activated receptor gamma (PPARG) as well as block angiotensin II type 1 receptors. METHODS: To directly test whether some of the metabolic effects of telmisartan require the presence of PPARG, we studied mice in which the gene (Pparg) for PPARG had been deleted in fat or in muscle. RESULTS: We found that knockout of Pparg in fat tissue greatly impaired the ability of telmisartan to increase adiponectin levels and to enhance sensitivity to insulin-stimulated glucose incorporation into adipose tissue lipids. In contrast, muscle-specific Pparg knockout had relatively little or no impact on the ability of telmisartan to increase adiponectin levels or affect glucose metabolism either in fat or muscle. These findings provide compelling evidence that the ability of telmisartan to increase adiponectin levels and stimulate glucose use in adipose tissue may depend on the presence of PPARG in fat. CONCLUSIONS: We conclude that PPARG in adipose tissue is required for at least several of the metabolic actions of telmisartan.

• MeSH
• benzimidazoly farmakokinetika   MeSH
• benzoáty farmakokinetika   MeSH
• blokátory receptorů AT1 pro angiotensin II farmakokinetika   MeSH
• hypertenze farmakoterapie   metabolismus   MeSH
• inzulinová rezistence MeSH
• krevní glukóza metabolismus   MeSH
• modely nemocí na zvířatech MeSH
• myši knockoutované MeSH
• myši MeSH
• PPAR gama biosyntéza   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH

OBJECTIVE: GDF11 is a member of the TGF-β superfamily that was recently implicated as potential "rejuvenating" factor, which can ameliorate metabolic disorders. The main objective of the presented study was to closely characterize the role of GDF11 signaling in the glucose homeostasis and in the differentiation of white adipose tissue. METHODS: We performed microscopy imaging, biochemical and transcriptomic analyses of adipose tissues of 9 weeks old ob/ob mice and murine and human pre-adipocyte cell lines. RESULTS: Our in vivo experiments employing GDF11 treatment in ob/ob mice showed improved glucose/insulin homeostasis, decreased weight gain and white adipocyte size. Furthermore, GDF11 treatment inhibited adipogenesis in pre-adipocytes by ALK5-SMAD2/3 activation in cooperation with the WNT/β-catenin pathway, whose inhibition resulted in adipogenic differentiation. Lastly, we observed significantly elevated levels of the adipokine hormone adiponectin and increased glucose uptake by mature adipocytes upon GDF11 exposure. CONCLUSION: We show evidence that link GDF11 to adipogenic differentiation, glucose, and insulin homeostasis, which are pointing towards potential beneficial effects of GDF11-based "anti-obesity" therapy.

• MeSH
• adipogeneze * MeSH
• adiponektin metabolismus   MeSH
• beta-katenin * metabolismus   MeSH
• buněčná diferenciace fyziologie   MeSH
• glukosa metabolismus   MeSH
• inzulin metabolismus   MeSH
• kostní morfogenetické proteiny metabolismus   MeSH
• lidé MeSH
• myši MeSH
• protein Smad2 MeSH
• protein Smad3 MeSH
• receptory regulované proteiny Smad MeSH
• růstové diferenciační faktory metabolismus   MeSH
• signální dráha Wnt MeSH
• TGF-beta receptor I. typu MeSH
• transformující růstový faktor beta metabolismus   MeSH
• tukové buňky metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Obesity with related complications represents a widespread health problem. The etiopathogenesis of obesity is often studied using numerous rodent models. The mouse model of monosodium glutamate (MSG)-induced obesity was exploited as a model of obesity combined with insulin resistance. The aim of this work was to characterize the metabolic status of MSG mice by NMR-based metabolomics in combination with relevant biochemical and hormonal parameters. NMR analysis of urine at 2, 6, and 9 months revealed altered metabolism of nicotinamide and polyamines, attenuated excretion of major urinary proteins, increased levels of phenylacetylglycine and allantoin, and decreased concentrations of methylamine in urine of MSG-treated mice. Altered levels of creatine, citrate, succinate, and acetate were observed at 2 months of age and approached the values of control mice with aging. The development of obesity and insulin resistance in 6-month-old MSG mice was also accompanied by decreased mRNA expressions of adiponectin, lipogenetic and lipolytic enzymes and peroxisome proliferator-activated receptor-gamma in fat while mRNA expressions of lipogenetic enzymes in the liver were enhanced. At the age of 9 months, biochemical parameters of MSG mice were normalized to the values of the controls. This fact pointed to a limited predictive value of biochemical data up to age of 6 months as NMR metabolomics confirmed altered urine metabolic composition even at 9 months.

• MeSH
• glutamát sodný škodlivé účinky   MeSH
• inzulin metabolismus   MeSH
• játra metabolismus   MeSH
• krevní glukóza metabolismus   MeSH
• lidé MeSH
• metabolismus lipidů MeSH
• metabolomika * MeSH
• moč chemie   MeSH
• myši MeSH
• obezita etiologie   genetika   metabolismus   moč   MeSH
• receptory aktivované proliferátory peroxizomů genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Adipose tissue has a key role in the development of metabolic syndrome (MS), which includes obesity, type 2 diabetes, dyslipidaemia, hypertension and other disorders. Systemic insulin resistance represents a major factor contributing to the development of MS in obesity. The resistance is precipitated by impaired adipose tissue glucose and lipid metabolism, linked to a low-grade inflammation of adipose tissue and secretion of pro-inflammatory adipokines. Development of MS could be delayed by lifestyle modifications, while both dietary and pharmacological interventions are required for the successful therapy of MS. The n-3 long-chain (LC) PUFA, EPA and DHA, which are abundant in marine fish, act as hypolipidaemic factors, reduce cardiac events and decrease the progression of atherosclerosis. Thus, n-3 LC PUFA represent healthy constituents of diets for patients with MS. In rodents n-3 LC PUFA prevent the development of obesity and impaired glucose tolerance. The effects of n-3 LC PUFA are mediated transcriptionally by AMP-activated protein kinase and by other mechanisms. n-3 LC PUFA activate a metabolic switch toward lipid catabolism and suppression of lipogenesis, i.e. in the liver, adipose tissue and small intestine. This metabolic switch improves dyslipidaemia and reduces ectopic deposition of lipids, resulting in improved insulin signalling. Despite a relatively low accumulation of n-3 LC PUFA in adipose tissue lipids, adipose tissue is specifically linked to the beneficial effects of n-3 LC PUFA, as indicated by (1) the prevention of adipose tissue hyperplasia and hypertrophy, (2) the induction of mitochondrial biogenesis in adipocytes, (3) the induction of adiponectin and (4) the amelioration of adipose tissue inflammation by n-3 LC PUFA.

• MeSH
• adiponektin metabolismus   MeSH
• dietní tuky farmakologie   terapeutické užití   MeSH
• inzulinová rezistence MeSH
• krysa rodu rattus MeSH
• lidé MeSH
• metabolický syndrom metabolismus   prevence a kontrola   MeSH
• metabolismus lipidů MeSH
• mitochondrie metabolismus   MeSH
• myši MeSH
• omega-3 mastné kyseliny farmakologie   terapeutické užití   MeSH
• signální transdukce MeSH
• tuková tkáň metabolismus   MeSH
• zánět dietoterapie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• lidé MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• práce podpořená grantem MeSH
• přehledy MeSH

Cíl: Proveřit možnost monitorace efektu anti TNFα terapie u pacientů léčených pro revmatoidní artritidu pomocí multiplexového stanovení sérových hladin vybraných biomarkerů odrážejících základní patofyziologické mechanizmy a aktivitu onemocnění. Metody: Byla hodnocena skupina 23 pacientů s aktivní revmatoidní artritidou, z toho 20 žen, 3 muži, průměrný věk 48,6 ± 10,3 let, průměrná hmotnost 68,5 ± 13 kg před léčbou a po 14–16 týdnech léčby s inhibitorem TNFα adalimumabem 40 mg subkutánně podávaným jednou za dva týdny (N = 21) nebo etanerceptem 25 mg podávaným podkožně dvakrát týdně (N= 2). Z 23 pacientů, 16 (70 %) užívalo současně s glukokortikoidy (GC) a 19 subjektů (84 %) methotrexát. Krev byla odebrána ze žíly pomocí odběrové zkumavky Vacuette (Greiner Bio One, Rakousko). Krevní vzorky byly odstřeďeny při 640 g po dobu 10 min. Sérum bylo rozděleno na alikvoty a zamraženo do provedení analýzy při teplotě -75 °C. Sérové hladiny IL 1β, IL10, IL6, VEGF, MMP9 a adiponektinu byly stanoveny multiplexovou analýzou pomocí technologie XMAP komerčním kitem Human Cardiovascular 1, Lineo Research (USA) podle návodu výrobce k použití. Analýza byla provedena na přístroji Luminex 100 a analýza dat pomocí Luminex 100 IS software verze 2.3. Tyto parametry byly korelovány s krevními hladinami CRP, PCT, TK (stanoveno radioenzymaticky), hmotností pacienta a DAS-28. Pro všechny parametry byl vypočten průměr, medián, směrodatná odchylka, minimální a maximální hodnoty z výsledků před a po terapii. Data byla analyzována Wilcoxonovým párovým testem a koeficientem pořadové korelace. Výsledky: Potvrdili jsme statisticky signifikantní snížení hladiny CRP (p = 0,001), VEGF (p = 0,05) a adiponektinu (p = 0,05), aktivity onemocnění hodnocené pomocí DAS-28 (p = 0,001) a významné zvýšení hmotnosti po léčbě (p = 0,01). Pokles hodnot všech tří prozánětlivých interleukinů nebyl významný. Závěry: Naše pilotní studie prokázala potencionální využitelnost i limity multiplexové analýzy cytokinů a některých dalších biomarkerů v monitorování léčby revmatoidní artritidy. Ke stanovení doporučení pro rutinní klinickou praxi je nezbytné zvolit vhodnější panel a rozšířit skupinu pacientů.

Methods: A group of 23 patients with active rheumatoid arthritis, 20 female, 3 male, average age 48.6 years ± 10.3, average weight 68,5 ± 13 kg was evaluated prior therapy and after 14–16 weeks of therapy with TNFα blocking agent adalimumab 40 mg subcutaneously every two weeks (No = 21) and etanercept 25 mg subcutaneously twice weekly (No = 2). Of 23 patients, 16 (70 %) of subject were treated concomitantly with glucocorticoids (GC), and 19 subject ( 84 %) with methotrexate. The blood was collected by venipuncture using Vacuette collection tubes (Greiner Bio-One, Austria). The blood samples were centrifuged at 640 g for 10 min, serum was aliquoted and stored until analysed in freezer at -75 °C. Serum levels of six parameters: IL 1β, IL10, IL6, VEGF, MMP9 and adiponectin were assessed by multiplex immunoanalysis using xMAP technology with commercially available multiplex kits Human Cardiovascular 1 panel and Human Cytokines-Chemokines panel, both from Linco Research (USA) according to manufacturer‘s instructions for use. The analysis was performed on Luminex 100 instrument and data analysis on Luminex 100 IS software version 2.3. These parameters were correlated with blood levels of CRP, PCT, TK (assessed by traditional immunoassays), patient weight and DAS-2828. For all parameters there was counted average, median, standard deviation, minimal and maximal values from results prior and after therapy. Furthermore, data were analysed by Wilcoxon pair test and Rank-order correlation. Results: We confirmed significantly decreased CRP levels (p = 0,001), VEGF(p = 0,05) and adiponectin (p = 0,05), disease activity score DAS-28 (p = 0,001) and significant increase of weight after therapy (p = 0,01). Decrease of all of three proinflammatory interleukins were not significant. Conclusions: Our pilot study showed the usefulness and limitations of multiplex measurements of cytokines and some other biomarkers in monitoring of rheumatoid arthritis therapy. But to establish guidelines for the routine clinical practice it is necessary to select preferable panel and to enlarge a group of the patients.

• MeSH
• adalimumab terapeutické užití   MeSH
• adiponektin krev   MeSH
• biologické markery * krev   MeSH
• C-reaktivní protein analýza   MeSH
• dospělí MeSH
• etanercept terapeutické užití   MeSH
• interleukin-10 krev   MeSH
• interleukin-1beta krev   MeSH
• interleukin-6 krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• matrixová metaloproteinasa 9 krev   MeSH
• neparametrická statistika MeSH
• pilotní projekty MeSH
• revmatoidní artritida * farmakoterapie   krev   MeSH
• TNF-alfa antagonisté a inhibitory   MeSH
• vaskulární endoteliální růstové faktory krev   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH

OBJECTIVE: Resolution of low-grade inflammation of white adipose tissue (WAT) is one of the keys for amelioration of obesity-associated metabolic dysfunctions. We focused on the identification of adipokines, which could be involved at the early stages of resolution of WAT inflammation. METHODS AND PROCEDURE: Male C57BL/6J mice with obesity induced in response to a 22-week feeding corn oil-based high-fat (cHF) diet were divided into four groups and were fed with, for 2 weeks, control cHF diet or cHF-based diets supplemented with: (i) concentrate of n-3 long-chain polyunsaturated fatty acids, mainly eicosapentaenoic and docosahexaenoic acids (cHF+F); (ii) thiazolidinedione drug rosiglitazone (cHF+TZD); and (iii) both compounds (cHF+F+TZD). RESULTS: The short-term combined intervention exerted additive effect in the amelioration of WAT inflammation in obese mice, namely in the epididymal fat, even in the absence of any changes in either adipocyte volume or fat mass. The combined intervention elicited hypolipidaemic effect and induced adiponectin, whereas the responses to single interventions (cHF+F, cHF+TZD) were less pronounced. In addition, analysis in WAT lysates using protein arrays revealed that the levels of a small set of adipose tissue-related proteins, namely macrophage inflammatory protein 1γ, endoglin, vascular cell adhesion molecule 1 and interleukin 1 receptor antagonist, changed in response to the anti-inflammatory interventions and were strongly reduced in the cHF+F+TZD mice. These results were verified using both the analysis of gene expression and enzyme-linked immunosorbent analysis in WAT lysates. In contrast with adiponectin, which showed changing plasma levels in response to dietary interventions, the levels of the above proteins were affected only in WAT. CONCLUSIONS: We identified several adipose tissue-related proteins, which are locally involved in resolution of low-grade inflammation and remodelling of WAT.

• MeSH
• adipokiny metabolismus   MeSH
• bílá tuková tkáň metabolismus   patologie   MeSH
• dieta s vysokým obsahem tuků MeSH
• dietní tuky MeSH
• ELISA MeSH
• energetický metabolismus MeSH
• imunohistochemie MeSH
• kvantitativní polymerázová řetězová reakce MeSH
• kyseliny dokosahexaenové farmakologie   MeSH
• myši inbrední C57BL MeSH
• myši obézní MeSH
• myši MeSH
• obezita imunologie   patologie   MeSH
• omega-3 mastné kyseliny farmakologie   MeSH
• thiazolidindiony farmakologie   MeSH
• tukové buňky metabolismus   MeSH
• zánět patologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem 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
• myši inbrední C57BL MeSH
• myši MeSH
• omega-3 mastné kyseliny farmakologie   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