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NPFFR2-deficient mice fed a high-fat diet develop strong intolerance to glucose

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F23%3A00573381" target="_blank" >RIV/61388963:_____/23:00573381 - isvavai.cz</a>

  • Alternative codes found

    RIV/67985823:_____/23:00573357 RIV/68378050:_____/23:00573381 RIV/00216208:11110/23:10466015

  • Result on the web

    <a href="https://doi.org/10.1042/CS20220880" target="_blank" >https://doi.org/10.1042/CS20220880</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1042/CS20220880" target="_blank" >10.1042/CS20220880</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    NPFFR2-deficient mice fed a high-fat diet develop strong intolerance to glucose

  • Original language description

    A previous study on neuropeptide FF receptor 2 (NPFFR2)-deficient mice has demonstrated that NPFFR2 is involved in the control of energy balance and thermogenesis. Here, we report on the metabolic impact of NPFFR2 deficiency in male and female mice that were fed either a standard diet (STD) or a high-fat diet (HFD) and each experimental group consisted of ten individuals. Both male and female NPFFR2 knockout (KO) mice exhibited severe glucose intolerance that was exacerbated by a HFD diet. In addition, reduced insulin pathway signaling proteins in NPFFR2 KO mice fed a HFD resulted in the development of hypothalamic insulin resistance. HFD feeding did not cause liver steatosis in NPFFR2 KO mice of either sex, but NPFFR2 KO male mice fed a HFD had lower body weights, white adipose tissues, and liver and lower plasma leptin levels compared with their wild-type (WT) controls. Lower liver weight in NPFFR2 KO male mice compensated for HFD-induced metabolic stress by increased liver PPARα and plasma FGF21 hepatokine, which supported fatty acid β-oxidation in the liver and white adipose tissue. Conversely, NPFFR2 deletion in female mice attenuated the expression of Adra3β and Pparγ, which inhibited lipolysis in adipose tissue.

  • 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

    30105 - Physiology (including cytology)

Result continuities

  • Project

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

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2023

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Clinical science

  • ISSN

    0143-5221

  • e-ISSN

    1470-8736

  • Volume of the periodical

    137

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    16

  • Pages from-to

    847-862

  • UT code for WoS article

    001007424600002

  • EID of the result in the Scopus database

    2-s2.0-85176976671