PMID- 35039874
OWN - NLM
STAT- MEDLINE
DCOM- 20220328
LR  - 20240226
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 25
IP  - 3
DP  - 2022 Mar
TI  - Hyperbaric oxygen treatment improves pancreatic beta‑cell function and hepatic 
      gluconeogenesis in STZ‑induced type‑2 diabetes mellitus model mice.
LID - 90 [pii]
LID - 10.3892/mmr.2022.12606 [doi]
AB  - Type‑2 diabetes mellitus (T2DM) causes several complications that affect the 
      quality of life and life span of patients. Hyperbaric oxygen therapy (HBOT) has 
      been used to successfully treat several diseases, including carbon monoxide 
      poisoning, ischemia, infections and diabetic foot ulcer, and increases insulin 
      sensitivity in T2DM. The present study aimed to determine the effect of HBOT on 
      beta‑cell function and hepatic gluconeogenesis in streptozotocin (STZ)‑induced 
      type‑2 diabetic mice. To establish a T2DM model, 7‑week‑old male C57BL/6J mice 
      were fed a high‑fat diet (HFD) and injected once daily with low‑dose STZ for 
      3 days after 1‑week HFD feeding. At the 14th week, HFD+HBOT and T2DM+HBOT groups 
      received 1‑h HBOT (2 ATA; 100% pure O(2)) daily from 5:00 to 6:00 p.m. for 
      7 days. The HFD and T2DM groups were maintained under normobaric oxygen 
      conditions and used as controls. During HBOT, the 12‑h nocturnal food intake and 
      body weight were measured daily. Moreover, blood glucose was measured by using a 
      tail vein prick and a glucometer. After the final HBO treatment, all mice were 
      sacrificed to conduct molecular biology experiments. Fasting insulin levels of 
      blood samples of sacrificed mice were measured by an ultrasensitive ELISA kit. 
      Pancreas and liver tissues were stained with hematoxylin and eosin, while 
      immunohistochemistry was performed to determine the effects of HBOT on insulin 
      resistance. TUNEL was used to determine the effects of HBOT on beta‑cell apoptosis, 
      and immunoblotting was conducted to determine the beta‑cell apoptosis pathway. HBOT 
      notably reduced fasting blood glucose and improved insulin sensitivity in T2DM 
      mice. After HBOT, beta‑cell area and beta‑cell mass in T2DM mice were significantly 
      increased. HBOT significantly decreased the beta‑cell apoptotic rate in T2DM mice 
      via the pancreatic Bcl‑2/caspase‑3/poly(ADP‑ribose) polymerase (PARP) apoptosis 
      pathway. Moreover, HBOT improved the morphology of the liver tissue and increased 
      hepatic glycogen storage in T2DM mice. These findings suggested that HBOT 
      ameliorated the insulin sensitivity of T2DM mice by decreasing the beta‑cell 
      apoptotic rate via the pancreatic Bcl‑2/caspase‑3/PARP apoptosis pathway.
FAU - Zhang, Caishun
AU  - Zhang C
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
FAU - Zhang, Di
AU  - Zhang D
AD  - Shandong Provincial Engineering Laboratory of Novel Pharmaceutical Excipients, 
      Sustained and Controlled Release Preparations, College of Medicine and Nursing, 
      Dezhou University, Dezhou, Shandong 253023, P.R. China.
FAU - Wang, Haidan
AU  - Wang H
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
FAU - Lin, Qian
AU  - Lin Q
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
FAU - Li, Manwen
AU  - Li M
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
FAU - Yuan, Junhua
AU  - Yuan J
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
FAU - Gao, Guangkai
AU  - Gao G
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
FAU - Dong, Jing
AU  - Dong J
AD  - Special Medicine Department, College of Basic Medicine, Qingdao University, 
      Qingdao, Shandong 266071, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20220118
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Blood Glucose)
RN  - 0 (Insulin)
SB  - IM
MH  - Animals
MH  - Apoptosis/physiology
MH  - Blood Glucose/metabolism
MH  - Blotting, Western
MH  - Diabetes Mellitus, Experimental/blood/etiology/*metabolism
MH  - Diabetes Mellitus, Type 2/blood/etiology/*metabolism
MH  - Diet, High-Fat/adverse effects
MH  - Disease Models, Animal
MH  - Fasting/blood
MH  - Gluconeogenesis/*physiology
MH  - Glucose Tolerance Test/methods
MH  - Humans
MH  - Hyperbaric Oxygenation/*methods
MH  - Insulin/blood
MH  - Insulin-Secreting Cells/cytology/*metabolism
MH  - Liver/*metabolism
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Mice
PMC - PMC8809048
OTO - NOTNLM
OT  - Bcl-2/caspase-3/poly(ADP-ribose) polymerase pathway
OT  - hyperbaric oxygen
OT  - type-2 diabetes mellitus
OT  - beta‑cell apoptosis
COIS- The authors declare that they have no competing interests.
EDAT- 2022/01/19 06:00
MHDA- 2022/03/29 06:00
PMCR- 2022/01/17
CRDT- 2022/01/18 06:05
PHST- 2021/07/06 00:00 [received]
PHST- 2021/10/14 00:00 [accepted]
PHST- 2022/01/18 06:05 [entrez]
PHST- 2022/01/19 06:00 [pubmed]
PHST- 2022/03/29 06:00 [medline]
PHST- 2022/01/17 00:00 [pmc-release]
AID - 90 [pii]
AID - MMR-25-03-12606 [pii]
AID - 10.3892/mmr.2022.12606 [doi]
PST - ppublish
SO  - Mol Med Rep. 2022 Mar;25(3):90. doi: 10.3892/mmr.2022.12606. Epub 2022 Jan 18.