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348 results on '"Kazdová L"'

1. Fumaric acid esters can block pro-inflammatory actions of human CRP and ameliorate metabolic disturbances in transgenic spontaneously hypertensive rats.

Author

Kurtz, Theodore, Šilhavý, J, Zídek, V, Mlejnek, P, Landa, V, Šimáková, M, Strnad, H, Oliyarnyk, O, Škop, V, and Kazdová, L

Abstract

Inflammation and oxidative stress have been implicated in the pathogenesis of metabolic disturbances. Esters of fumaric acid, mainly dimethyl fumarate, exhibit immunomodulatory, anti-inflammatory, and anti-oxidative effects. In the current study, we tested

Published
2014

3. Conplastic strains for identification of retrograde effects of mitochondrial dna variation on cardiometabolic traits in the spontaneously hypertensive rat

Author

Pravenec, M, primary, Šilhavý, J, additional, Mlejnek, P, additional, Šimáková, M, additional, Mráček, T, additional, Pecinová, A, additional, Tauchmannová, K, additional, Hütl, M, additional, Malínská, H, additional, Kazdová, L, additional, Neckář, J, additional, Kolář, F, additional, Žurmanová, J, additional, Novotný, J, additional, and Houštěk, J, additional

Published
2021
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13. Dissecting the Role of Folr1 and Folh1 Genes in the Pathogenesis of Metabolic Syndrome in Spontaneously Hypertensive Rats

Author

ŠILHAVÝ, J., primary, KRIJT, J., additional, SOKOLOVÁ, J., additional, ZÍDEK, V., additional, MLEJNEK, P., additional, ŠIMÁKOVÁ, M., additional, ŠKOP, V., additional, TRNOVSKÁ, J., additional, OLIYARNYK, O., additional, MARKOVÁ, I., additional, HÜTTL, M., additional, MALÍNSKÁ, H., additional, KAZDOVÁ, L., additional, LIŠKA, F., additional, KOŽICH, V., additional, and PRAVENEC, M., additional

Published
2018
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14. Mutant Wars2 Gene in Spontaneously Hypertensive Rats Impairs Brown Adipose Tissue Function and Predisposes to Visceral Obesity

Author

PRAVENEC, M., primary, ZÍDEK, V., additional, LANDA, V., additional, MLEJNEK, P., additional, ŠILHAVÝ, J., additional, ŠIMÁKOVÁ, M., additional, TRNOVSKÁ, J., additional, ŠKOP, V., additional, MARKOVÁ, I., additional, MALÍNSKÁ, H., additional, HÜTTL, M., additional, KAZDOVÁ, L., additional, BARDOVÁ, K., additional, TAUCHMANNOVÁ, K., additional, VRBACKÝ, M., additional, NŮSKOVÁ, H., additional, MRÁČEK, T., additional, KOPECKÝ, J., additional, and HOUŠTĚK, J., additional

Published
2017
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28. Gender-Related Effects on Substrate Utilization and Metabolic Adaptation in Hairless Spontaneously Hypertensive Rat

Author

TRNOVSKÁ, J., primary, ŠILHAVÝ, J., additional, ZÍDEK, V., additional, ŠIMÁKOVÁ, M., additional, MLEJNEK, P., additional, LANDA, V., additional, EIGNER, S., additional, EIGNER HENKE, K., additional, ŠKOP, V., additional, OLIYARNYK, O., additional, KAZDOVÁ, L., additional, MRÁČEK, T., additional, HOUŠTĚK, J., additional, and PRAVENEC, M., additional

Published
2015
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35. Transgenic expression of CD36 in the spontaneously hypertensive rat is associated with amelioration of metabolic disturbances but has no effect on hypertension

Author

Michal Pravenec, Landa V, Zídek V, Musilová A, Kazdová L, Qi N, Wang J, St Lezin E, and Tw, Kurtz

Subjects
CD36 Antigens, Male, Time Factors, Diaphragm, Gene Expression, Blood Pressure, Hyperlipidemias, Fructose, Fatty Acids, Nonesterified, Kidney, Animals, Genetically Modified, Peptide Elongation Factor 1, Rats, Inbred SHR, Animals, Insulin, Rats, Wistar, Epididymis, Reverse Transcriptase Polymerase Chain Reaction, Muscles, Myocardium, Glucose Tolerance Test, Lipid Metabolism, Rats, Glucose, Adipose Tissue, Liver, Area Under Curve, Hypertension, Insulin Resistance
Abstract

Spontaneously hypertensive rats (SHR/NIH strain) harbor a deletion variant in the Cd36 fatty acid transporter and display defective fatty acid metabolism, insulin resistance and hypertension. Transgenic rescue of Cd36 in SHR ameliorates insulin resistance and improves dyslipidemia. However, the role of Cd36 in blood pressure regulation remains controversial due to inconsistent blood pressure effects that were observed with transgenic expression of Cd36 on the SHR background. In the current studies, we developed two new SHR transgenic lines, which express wild type Cd36 under the control of the universal Ef-1 alpha promoter, and examined the effects of transgenic expression of wild type Cd36 on selected metabolic and cardiovascular phenotypes. Transgenic expression of Cd36 in the new lines was associated with significantly decreased serum fatty acids, amelioration of insulin resistance and glucose intolerance but failed to induce any consistent changes in blood pressure as measured by radiotelemetry. The current findings confirm the genetic association of defective Cd36 with disordered insulin action and fatty acid metabolism in the SHR/NIH strain and suggest that Cd36 is linked to other gene(s) on rat chromosome 4 that regulate blood pressure.

Published
2003

36. Genetic analysis of cardiovascular risk factor clustering in spontaneous hypertension

Author

Michal Pravenec, Zídek V, Landa V, Kostka V, Musilová A, Kazdová L, Fucíková A, Krenová D, Bíla V, and Kren V

Subjects
CD36 Antigens, DNA, Complementary, Genetic Linkage, Lipolysis, Blood Pressure, Hyperlipidemias, Kidney, Translocation, Genetic, Animals, Genetically Modified, Mice, Quantitative Trait, Heritable, Animals, Congenic, Risk Factors, Rats, Inbred SHR, Dietary Carbohydrates, Animals, Humans, Oligonucleotide Array Sequence Analysis, Sequence Deletion, Mice, Knockout, Fatty Acids, Genetic Complementation Test, Chromosome Mapping, Dietary Fats, Rats, Disease Models, Animal, Hypertension, Mutation, Insulin Resistance, Gene Deletion
Abstract

The SHR is the most widely studied animal model of hypertension. In this strain, as in many humans with essential hypertension, increased blood pressure has been reported to cluster with other risk factors for cardiovascular disease, including insulin resistance and dyslipidemia. However, the genetic mechanisms that mediate this clustering of risk factors for cardiovascular disease or the hypertension "metabolic syndrome" remain poorly understood. In the current studies, we have demonstrated (1) that a gene or genes responsible for a whole spectrum of cardiovascular risk factors mapped to a limited segment of the centromeric region of rat chromosome 4, (2) that a spontaneous deletion in the gene for Cd36 that encodes a fatty acid transporter and is located directly at the peak of QTL linkages on chromosome 4 has been indirectly linked to the transmission of insulin resistance, defective fatty acid metabolism, and increased blood pressure, and (3) based on complementation analysis in two transgenic lines expressing wild-type Cd36 on the genetic background of the SHR strain harboring the deletion variant of Cd36, we have established that defective Cd36 can be a determinant of disordered fatty acid metabolism, glucose intolerance, and insulin resistance in spontaneous hypertension.

Published
2001

45. The effect of combination therapy with cyclosporine A and hydrocortisone on glucose metabolism in diabetic rats following pancreatic islet transplantation

Author

Frantisek Saudek, Kazdová L, Nozicková M, Vrána A, Cíhalová E, and Ruzbarský V

Subjects
Blood Glucose, Hydrocortisone, Portal Vein, Anti-Inflammatory Agents, Islets of Langerhans Transplantation, Fasting, Glucose Tolerance Test, Kidney, Lipid Metabolism, Diabetes Mellitus, Experimental, Rats, Disease Models, Animal, Glucose, Liver, Creatinine, Insulin Secretion, Cyclosporine, Animals, Insulin, Drug Therapy, Combination, Carbon Radioisotopes, Rats, Wistar, Immunosuppressive Agents
Abstract

Glucose tolerance, insulin secretion and in vitro insulin action were examined in streptozotocin-induced diabetic rats following pancreatic islet allotransplantation treated with combination of oral cyclosporine A (10 mg/kg) and hydrocortisone (1.5 mg/kg) intramuscularly. 1400 pure islets from multiple donors were implanted either into the portal vein (n = 10) or under the renal capsule (n = 11). Ten sham-operated non-diabetic animals receiving the same immunosuppressive therapy, 8 healthy animals without any treatment and 10 diabetic animals without immunosuppression following islet transplantation were used as controls. In all transplanted animals blood glucose was normalized by day 3 after transplantation with lower levels in those transplanted intraportally (p0.05). Non-immunosuppressed animals rejected the graft after 6.5 +/- 1.2 days after transplantation, immunosuppressed animals in both groups remained normoglycaemic till the end of the experiment on day 28. Oral glucose tolerance tests and insulin levels on days 10 and 28 improved dramatically. No differences in glucose and insulin levels between intraportal and subcapsular groups were found. Post-load glucose levels in immunosuppressed non-transplanted animals were higher on day 28 than before treatment and were also higher than in the healthy non-treated group (p0.05). In vitro insulin action determined by the incorporation of labelled glucose into adipose tissue was impaired only in animals in which islets were transplanted into the liver (p0.05 vs other groups). In conclusion, therapy with cyclosporine A and hydrocortisone prevents allogeneic islet rejection in rats during a short-term experiment. Although glucose tolerance is not completely normalized following transplantation, slight impairment is also demonstrable in healthy animals on the same drug therapy.

Published
1995

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