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Heterozygous Nme7 Mutation Affects Glucose Tolerance in Male Rats

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023761%3A_____%2F21%3AN0000002" target="_blank" >RIV/00023761:_____/21:N0000002 - isvavai.cz</a>

  • Alternative codes found

    RIV/68378050:_____/21:00555570 RIV/00216208:11110/21:10429720 RIV/00064165:_____/21:10429720

  • Result on the web

    <a href="https://www.mdpi.com/2073-4425/12/7/1087/pdf" target="_blank" >https://www.mdpi.com/2073-4425/12/7/1087/pdf</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/genes12071087" target="_blank" >10.3390/genes12071087</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Heterozygous Nme7 Mutation Affects Glucose Tolerance in Male Rats

  • Original language description

    Complex metabolic conditions such as type 2 diabetes and obesity result from the interaction of numerous genetic and environmental factors. While the family of Nme proteins has been connected so far mostly to development, proliferation, or ciliary functions, several lines of evidence from human and experimental studies point to the potential involvement of one of its members, NME7 (non-metastatic cells 7, nucleoside diphosphate kinase 7) in carbohydrate and lipid metabolism. As a complete lack of Nme7 is semilethal in rats, we compared morphometric, metabolic, and transcriptomic profiles of standard diet-fed heterozygous Nme7+/- on male rats vs. their wild-type Nme7+/+ controls. Nme7+/- animals showed increased body weight, adiposity, higher insulin levels together with decreased glucose tolerance. Moreover, they displayed pancreatic islet fibrosis and kidney tubular damage. Despite no signs of overt liver steatosis or dyslipidemia, we found significant changes in the hepatic transcriptome of Nme7+/- male rats with a concerted increase of expression of lipogenic enzymes including Scd1, Fads1, Dhcr7 and a decrease of Cyp7b1 and Nme7. Network analyses suggested possible links between Nme7 and the activation of Srebf1 and Srebf2 upstream regulators. These results further support the implication of NME7 in the pathogenesis of glucose intolerance and adiposity.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10603 - Genetics and heredity (medical genetics to be 3)

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2021

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    GENES

  • ISSN

    2073-4425

  • e-ISSN

  • Volume of the periodical

    12

  • Issue of the periodical within the volume

    7

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    13

  • Pages from-to

    nestrankovano

  • UT code for WoS article

    000677189200001

  • EID of the result in the Scopus database

    2-s2.0-85111363867