PMID- 35333936
OWN - NLM
STAT- MEDLINE
DCOM- 20220608
LR  - 20220614
IS  - 1420-908X (Electronic)
IS  - 1023-3830 (Linking)
VI  - 71
IP  - 5-6
DP  - 2022 Jun
TI  - IGF-1 ameliorates streptozotocin-induced pancreatic beta cell dysfunction and 
      apoptosis via activating IRS1/PI3K/Akt/FOXO1 pathway.
PG  - 669-680
LID - 10.1007/s00011-022-01557-3 [doi]
AB  - BACKGROUND AND OBJECTIVE: Type 2 diabetes mellitus (T2DM) is an endocrine 
      disorder with pancreatic beta cell dysfunction and/or reduced insulin sensitivity. 
      IGF-1 is critically involved in pancreatic beta cell growth, differentiation, and 
      insulin secretion. Insulin-mediated IRS1/PI3K/Akt/FOXO1 signaling has been proved 
      to be closely associated with pancreatic beta cell function, hepatic glucose 
      metabolism, and the development of T2DM. This present work was designed to 
      demonstrate the protective role of IGF-1 against pancreatic beta cell dysfunction 
      and to probe into the underlying mechanisms. METHODS: Herein, cell viability, 
      cell apoptosis, insulin secretion, oxidative stress, and glycolysis in 
      STZ-treated INS-1 cells were measured, so as to determine the biological function 
      of IGF-1 against pancreatic beta cell dysfunction in T2DM. Additionally, whether 
      IGF-1 could activate IRS1/PI3K/Akt/FOXO1 signaling pathway to manipulate the 
      progression of T2DM was also investigated. RESULTS: It was discovered that IGF-1 
      treatment enhanced the viability and suppressed the apoptosis of STZ-treated 
      INS-1 cells. Besides, IGF-1 treatment augmented insulin secretion of INS-1 cells 
      in response to STZ. Moreover, IGF-1 exerted protective role against oxidative 
      damage and displayed inhibitory effect on glycolysis in STZ-treated INS-1 cells. 
      Mechanistically, IGF-1 treatment markedly boosted the activation of 
      IRS1/PI3K/Akt/FOXO1 pathway. Furthermore, treatment with AG1024 (an inhibitor of 
      IGF-1R) partially abolished the actions of IGF-1 on cell viability, cell 
      apoptosis, insulin secretion, oxidative stress, and glycolysis in STZ-treated 
      INS-1 cells. CONCLUSION: To conclude, IGF-1 could improve the viability and 
      inhibit the apoptosis of STZ-treated pancreatic beta cells, induce insulin 
      secretion, alleviate oxidative damage, as well as arrest glycolysis by activating 
      IRS1/PI3K/Akt/FOXO1 pathway.
CI  - (c) 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.
FAU - Cui, Fan
AU  - Cui F
AD  - Department of Clinical Laboratory, The First People's Hospital of Wuhu, Wuhu, 
      241000, Anhui Province, China.
FAU - He, Xin
AU  - He X
AUID- ORCID: 0000-0003-0267-0035
AD  - Clinical Laboratory Center, The First Affiliated Hospital of Jinan University, 
      Tianhe District, No. 613 West Huangpu Avenue, Guangzhou, 510630, Guangdong 
      Province, China. hexin12233@163.com.
LA  - eng
GR  - No. B2021329)/Medical Science and Technology Foundation of Guangdong Province/
GR  - No. KJ2020A0341/Key Project of Natural Science Research of Anhui Universities/
PT  - Journal Article
DEP - 20220325
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (FOXO1 protein, human)
RN  - 0 (Forkhead Box Protein O1)
RN  - 0 (IRS1 protein, human)
RN  - 0 (Insulin)
RN  - 0 (Insulin Receptor Substrate Proteins)
RN  - 5W494URQ81 (Streptozocin)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Apoptosis
MH  - *Diabetes Mellitus, Type 2/drug therapy/metabolism/pathology
MH  - Forkhead Box Protein O1/metabolism/pharmacology
MH  - Humans
MH  - Insulin
MH  - Insulin Receptor Substrate Proteins/metabolism
MH  - Insulin-Like Growth Factor I/metabolism/pharmacology
MH  - *Insulin-Secreting Cells/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Streptozocin/toxicity
OTO - NOTNLM
OT  - IGF-1
OT  - IRS-1/PI3K/Akt/FOXO1 pathway
OT  - Pancreatic beta cell
OT  - T2DM
EDAT- 2022/03/26 06:00
MHDA- 2022/06/09 06:00
CRDT- 2022/03/25 17:25
PHST- 2021/08/11 00:00 [received]
PHST- 2022/02/28 00:00 [accepted]
PHST- 2022/02/18 00:00 [revised]
PHST- 2022/03/26 06:00 [pubmed]
PHST- 2022/06/09 06:00 [medline]
PHST- 2022/03/25 17:25 [entrez]
AID - 10.1007/s00011-022-01557-3 [pii]
AID - 10.1007/s00011-022-01557-3 [doi]
PST - ppublish
SO  - Inflamm Res. 2022 Jun;71(5-6):669-680. doi: 10.1007/s00011-022-01557-3. Epub 2022 
      Mar 25.