Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD38

Ota, Hiroyo; Tamaki, Shinji; Itaya‐Hironaka, Asako; Yamauchi, Akiyo; Sakuramoto‐Tsuchida, Sumiyo; Morioka, Takashi; Takasawa, Shin; Kimura, Hiroshi

doi:10.1016/j.lfs.2011.11.011

Cited by 65 publications

(114 citation statements)

References 44 publications

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“…We then examined the mRNA levels of several genes involved in glucose-induced insulin secretion and found that the mRNA levels of glucose transporter 2, glucokinase, sulfonylurea receptor 1, and the α 1c subunit of voltage-dependent L-type calcium channels were unchanged between IH-treated and normoxia-treated islets [17]. These results suggest that IH has no effect on the gene expression concerning Ca2+ influx from extracellular sources for glucose-induced insulin secretion.…”

Section: Down-regulation Of Cd38 Mrnamentioning

confidence: 97%

“…IH was generated/controlled in an incubator by a controlled gas delivery system that regulated the flow of nitrogen and oxygen. Cells/islets were exposed to sustained hypoxia (1% O2), 64 On the other hand, the levels of insulin mRNAs in HIT-T15 cells (hamster insulin mRNA) and rat islets (rat Ins1 and Ins2 mRNAs) were unchanged by IH treatment, suggesting that IH attenuates glucose-induced insulin secretion without changing insulin gene transcription [17]. Recent reports of β cell dysfunction in vivo IH exposure animal models [20][21][22] also support the concept of pancreatic β cell dysfunction including glucose-induced insulin secretion by IH exposure.…”

Section: Attenuation Of Glucose-induced Insulin Secretion From Ih-trementioning

confidence: 99%

“…We then analyzed genes involved in Ca2+ mobilization from intracellular pools, such as CD38, type 2 ryanodine receptor Ca2+ channel, and FK506-binding protein 12.6 and found that the mRNA level of CD38 was significantly lower in IH-treated islets than in normoxia-treated islets [17]. To investigate whether IH inhibits CD38 transcription, HIT-T15 cells were transiently transfected with the reporter plasmid consisting of a luciferase reporter gene under the control of human CD38 promoter.…”

Section: Down-regulation Of Cd38 Mrnamentioning

confidence: 99%

“…In a mouse model, IH was found to cause β cell replication without hyperglycemia [15,16], suggesting a possible mechanism that IH directly stimulates β cell replication. Here, we focus on the impact of IH on pancreatic β cells, particularly β cell dysfunction and proliferation, using an in vitro IH system [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Intermittent Hypoxia in Pancreatic beta Cells

Ota¹,

Takasawa²,

Yamauchi³

et al. 2015

Pancreat Disord Ther

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Sleep apnea syndrome (SAS) a highly prevalent disorder, and characterized by repetitive episodes of intermittent hypoxia (IH), i.e. recurrent episodes of oxygen desaturation during sleep, the development of daytime sleepiness, and deterioration in the quality of life. Multiple epidemiological studies have provided evidence implicating the presence of SAS as a risk factor for insulin resistance and type 2 diabetes and have reported that type 2 diabetes is associated with SAS independently of age, sex, and body habitus. One of the postulated mechanisms for the metabolic alterations associated with SAS is that IH leads to substantial alterations in both pancreatic β cell function and organ glucose homeostasis. On the other hand, hyperglycemia is known to increase the rate of β cell replication, which can provide an increased source of insulin to combat insulin resistance. Although accumulating evidence suggests associations between SAS and type 2 diabetes, the direct effect of IH on pancreatic β cell has been unknown. In this review, we focus on the impact of IH on pancreatic β cells, particularly β cell dysfunction and cell proliferation.

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Section: Down-regulation Of Cd38 Mrnamentioning

confidence: 97%

Section: Attenuation Of Glucose-induced Insulin Secretion From Ih-trementioning

confidence: 99%

Section: Down-regulation Of Cd38 Mrnamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Intermittent Hypoxia in Pancreatic beta Cells

Ota¹,

Takasawa²,

Yamauchi³

et al. 2015

Pancreat Disord Ther

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“…All the PCR primers were synthesized by NGRL (Sendai, Japan). Real-time PCR was performed using KAPA SYBR ® Fast qPCR Master Mix (Kapa Biosystems, Boston, MA, USA) and the Thermal Cycler Dice Real Time System (Takara, Otsu, Japan), as described previously [35]. PCR was performed with an initial step of 3 min at 95°C followed by 40 …”

Section: Quantitative Real-time Reverse Transcriptase-polymerase Chaimentioning

confidence: 99%

Involvement of autoimmunity to REG, a regeneration factor, in patients with primary Sjögren's syndrome

Yoshimoto

Fujimoto

Itaya‐Hironaka

et al. 2013

Clinical and Experimental Immunology

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SummaryThe regenerating gene (Reg) was isolated originally as a gene specifically over-expressed in regenerating pancreatic islets and constitute a growth factor family. Reg gene product (Reg) is important in the pathophysiology of various human inflammatory diseases. Recently, the possible involvement of human REG in the regeneration of salivary ductal epithelial cells of patients with primary Sjögren's syndrome (SS) was reported. However, the expression of the REG family genes in minor salivary glands (MSG) and the occurrence of anti-REG Iα autoantibodies in SS patients were obscured. In this study, we examined the expression of REG family genes in the MSG of SS and screened anti-REG Iα autoantibodies in SS. The mRNA levels of REG family genes in MSG were quantified using real-time reverse transcriptionpolymerase chain reaction (RT-PCR) and REG Iα expression in the MSG was analysed by immunohistochemistry. The mRNA level of REG Iα in the MSG of SS patients was significantly higher than that of control. REG Iα protein was expressed highly in SS ductal epithelial cells. Anti-REG Iα autoantibodies in the sera were found in 11% of SS. All the MSG in the anti-REG Iα autoantibody-positive group showed REG Iα expression, whereas only 40% showed REG Iα expression in the anti-REG Iα autoantibodynegative group. The anti-REG Iα autoantibody-positive group showed significantly lower saliva secretion and a higher ratio of grade 4 (by RubinHolt) in sialography. These data suggest strongly that autoimmunity to REG Iα might play a role in the degeneration of MSG ductal epithelial cells in primary SS.

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Intermittent hypoxia‐induced epiregulin expression by IL‐6 production in human coronary artery smooth muscle cells

et al. 2018

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Patients with obstructive sleep apnea ( OSA ) experience repetitive episodes of desaturation and resaturation of blood oxygen (known as intermittent hypoxia or IH ), during sleep. We showed previously that IH induced excessive proliferation of rat vascular smooth muscle cells through upregulation of members of the epidermal growth factor family, especially epiregulin ( EREG ), and the erbB2 receptor. In this study, we exposed human coronary artery smooth muscle cells to IH and found that IH significantly increased the expression of EREG . IH increased the production of interleukin‐6 ( IL ‐6) in smooth muscle cells, and the addition of IL ‐6 induced EREG expression. Small interfering RNA for IL ‐6 or IL ‐6 receptor attenuated the IH ‐induced increase in EREG . IL ‐6 may play a pivotal role in EREG upregulation by IH and consequently OSA ‐related atherosclerosis.

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Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD38

Cited by 65 publications

References 44 publications

Intermittent Hypoxia in Pancreatic beta Cells

Intermittent Hypoxia in Pancreatic beta Cells

Involvement of autoimmunity to REG, a regeneration factor, in patients with primary Sjögren's syndrome

Intermittent hypoxia‐induced epiregulin expression by IL‐6 production in human coronary artery smooth muscle cells

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