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Naslov:Human beta cell functional adaptation and dysfunction in insulin resistance and its reversibility
Avtorji:ID Skelin, Maša (Avtor)
ID Kopecky, Jan (Avtor)
ID Dolenšek, Jurij (Avtor)
ID Stožer, Andraž (Avtor)
Datoteke:.pdf Klemen-2023-Human_Beta_Cell_Functional_Adaptat.pdf (387,53 KB)
MD5: 27AFDFAC50C4E8BFD7E3DE19A448B7AE
 
URL https://doi.org/10.1159/000534667
 
Jezik:Angleški jezik
Vrsta gradiva:Znanstveno delo
Tipologija:1.03 - Drugi znanstveni članki
Organizacija:MF - Medicinska fakulteta
FNM - Fakulteta za naravoslovje in matematiko
Opis:Background: Beta cells play a key role in the pathophysiology of diabetes since their functional adaptation is able to maintain euglycemia in the face of insulin resistance, and beta cell decompensation or dysfunction is a necessary condition for full-blown type 2 diabetes (T2D). The mechanisms behind compensation and decompensation are incompletely understood, especially for human beta cells, and even less is known about influences of chronic kidney disease (CKD) or immunosupressive therapy after transplantation on these processes and the development of posttransplant diabetes. Summary: During compensation, beta cell sensitivity to glucose becomes left-shifted, i.e., their sensitivity to stimulation increases, and this is accompanied by enhanced signals along the stimulus-secretion coupling cascade from membrane depolarization to intracellular calcium and the most distal insulin secretion dynamics. There is currently no clear evidence regarding changes in intercellular coupling during this stage of disease progression. During decompensation, intracellular stimulus-secretion coupling remains enhanced to some extent at low or basal glucose concentrations but seems to become unable to generate effective signals to stimulate insulin secretion at high or otherwise stimulatory glucose concentrations. Additionally, intercellular coupling becomes disrupted, lowering the number of cells that contribute to secretion. During progression of CKD, beta cells also seem to drift from a compensatory left-shift to failure, and immunosupressants can further impair beta cell function following kidney transplantation. Key Messages: Beta cell stimulus-secretion coupling is enhanced in compensated insulin resistance. With worsening insulin resistance, both intra- and intercellular coupling become disrupted. CKD can progressively disrupt beta cell function, but further studies are needed, especially regarding changes in intercellular coupling.
Ključne besede:human beta cell, functional adaptation, dysfunction, insulin resistance
Status publikacije:Objavljeno
Verzija publikacije:Objavljena publikacija
Poslano v recenzijo:31.03.2023
Datum sprejetja članka:07.10.2023
Datum objave:26.10.2023
Založnik:S. Karger
Leto izida:2023
Št. strani:Str. 78-84
Številčenje:Letn. 148, Št. 2
PID:20.500.12556/DKUM-88311 Novo okno
UDK:612
COBISS.SI-ID:173873411 Novo okno
DOI:10.1159/000534667 Novo okno
ISSN pri članku:2235-3186
Datum objave v DKUM:15.04.2024
Število ogledov:89
Število prenosov:8
Metapodatki:XML RDF-CHPDL DC-XML DC-RDF
Področja:Ostalo
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Skupna ocena:(0 glasov)
Vaša ocena:Ocenjevanje je dovoljeno samo prijavljenim uporabnikom.
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Gradivo je del revije

Naslov:Nephron journals
Skrajšan naslov:Nephron J.
Založnik:S. Karger
ISSN:2235-3186
COBISS.SI-ID:527697945 Novo okno

Licence

Licenca:CC BY-NC 4.0, Creative Commons Priznanje avtorstva-Nekomercialno 4.0 Mednarodna
Povezava:http://creativecommons.org/licenses/by-nc/4.0/deed.sl
Opis:Licenca Creative Commons, ki prepoveduje komercialno uporabo, vendar uporabniki ne rabijo upravljati materialnih avtorskih pravic na izpeljanih delih z enako licenco.
Začetek licenciranja:26.10.2023

Sekundarni jezik

Jezik:Slovenski jezik
Ključne besede:človeške beta celice, funkcionalne prilagoditve, disfunkcija, inzulinska rezistenca


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