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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003881naa a2200481 4500
001oai:DiVA.org:uu-483752
003SwePub
008220905s2022 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4837522 URI
024a https://doi.org/10.1080/21623945.2022.21021162 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Ahmed, Foziau Uppsala universitet,Klinisk diabetologi och metabolism4 aut0 (Swepub:uu)fozah903
2451 0a ESR2 expression in subcutaneous adipose tissue is related to body fat distribution in women, and knockdown impairs preadipocyte differentiation
264 c 2022-08-17
264 1b Informa UK Limited,c 2022
338 a electronic2 rdacarrier
520 a Oestrogen receptor 2 (ESR2) expression has been shown to be higher in subcutaneous adipose tissue (SAT) from postmenopausal compared to premenopausal women. The functional significance of altered ESR2 expression is not fully known. This study investigates the role of ESR2 for adipose tissue lipid and glucose metabolism. SAT biopsies were obtained from 44 female subjects with or without T2D. Gene expression of ESR2 and markers of adipose function and metabolism was assessed. ESR2 knockdown was performed using CRISPR/Cas9 in preadipocytes isolated from SAT of females, and differentiation rate, lipid storage, and glucose uptake were measured. ESR2 expression was inversely correlated with measures of central obesity and expression of some fatty acid oxidation markers, and positively correlated with lipid storage and glucose transport markers. Differentiation was reduced in ESR2 knockdown preadipocytes. This corresponded to reduced expression of markers of differentiation and lipogenesis. Glucose uptake was reduced in knockdown adipocytes. Our results indicate that ESR2 deficiency in women is associated with visceral adiposity and impaired subcutaneous adipocyte differentiation as well as glucose and lipid utilization. High ESR2 expression, as seen after menopause, could be a contributing factor to SAT expansion. This may support a possible target to promote a healthy obesity phenotype.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
653 a Adipocytes
653 a adipogenesis
653 a CRISPR
653 a cas9
653 a lipid metabolism
653 a obesity
653 a insulin resistance
653 a type 2 diabetes
700a Hetty, Susanne,c PhD,d 1979-u Uppsala universitet,Klinisk diabetologi och metabolism4 aut0 (Swepub:uu)sustr921
700a Vranic, Milicau Uppsala universitet,Klinisk diabetologi och metabolism4 aut0 (Swepub:uu)milvr380
700a Fanni, Giovanniu Uppsala universitet,Klinisk diabetologi och metabolism4 aut0 (Swepub:uu)giofa361
700a Kullberg, Joel,d 1979-u Uppsala universitet,Radiologi4 aut0 (Swepub:uu)jokul377
700a Pereira, Maria J.,d 1981-u Uppsala universitet,Klinisk diabetologi och metabolism4 aut0 (Swepub:uu)marpe927
700a Eriksson, Janu Uppsala universitet,Klinisk diabetologi och metabolism4 aut0 (Swepub:uu)janer909
710a Uppsala universitetb Klinisk diabetologi och metabolism4 org
773t Adipocyted : Informa UK Limitedg 11:1, s. 434-447q 11:1<434-447x 2162-3945x 2162-397X
856u https://doi.org/10.1080/21623945.2022.2102116y Fulltext
856u https://uu.diva-portal.org/smash/get/diva2:1693032/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-483752
8564 8u https://doi.org/10.1080/21623945.2022.2102116

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