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Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD38.
Life Sci 2012; 90(5-6):206-11LS

Abstract

AIMS

Sleep apnea syndrome (SAS) is characterized by recurrent episodes of oxygen desaturation during sleep, the development of daytime sleepiness, and deterioration in the quality of life. Accumulating evidence suggests the association of intermittent hypoxia (IH), a hallmark of SAS, and type 2 diabetes independently on body mass index and waist circumference. In addition to insulin resistance, the progression to type 2 diabetes is dependent on the impairment of glucose-induced insulin secretion (GIS) from pancreatic β-cells. However, the direct effects of IH on GIS are elusive.

MAIN METHODS

HIT-T15 hamster β-cells and isolated rat islets were exposed to 64 cycles/24 h of IH (5 min hypoxia/10 min normoxia) or normoxia for 24 h. Changes of GIS and gene expression in IH-treated β-cells were analyzed by ELISA and real-time RT-PCR, respectively.

KEY FINDINGS

After IH treatment, GIS both from IH-treated HIT-T15 cells and isolated rat islets were significantly attenuated. The level of insulin mRNA was unchanged by IH. The mRNA levels of glucose transporter 2 (Glut2), glucokinase (GK), sulfonylurea receptor1 (SUR1), and L-type Ca2+channel1.2 (Cav1.2) in IH-treated-islets were similar to those in normoxia-treated islets. In contrast, the mRNA level of CD38 in IH-treated islets was significantly lower than that in normoxia-treated islets. The reporter gene assay revealed that the transcription of CD38 was attenuated by IH, and the transfection of CD38 expression vector recovered the attenuation of GIS by IH.

SIGNIFICANCE

These results indicate that IH stress directly attenuates GIS from β-cells via the down-regulation of CD38.

Authors+Show Affiliations

Second Department of Internal Medicine, Nara Medical University, Kashihara 634-8521, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22154909

Citation

Ota, Hiroyo, et al. "Attenuation of Glucose-induced Insulin Secretion By Intermittent Hypoxia Via Down-regulation of CD38." Life Sciences, vol. 90, no. 5-6, 2012, pp. 206-11.
Ota H, Tamaki S, Itaya-Hironaka A, et al. Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD38. Life Sci. 2012;90(5-6):206-11.
Ota, H., Tamaki, S., Itaya-Hironaka, A., Yamauchi, A., Sakuramoto-Tsuchida, S., Morioka, T., ... Kimura, H. (2012). Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD38. Life Sciences, 90(5-6), pp. 206-11. doi:10.1016/j.lfs.2011.11.011.
Ota H, et al. Attenuation of Glucose-induced Insulin Secretion By Intermittent Hypoxia Via Down-regulation of CD38. Life Sci. 2012 Jan 30;90(5-6):206-11. PubMed PMID: 22154909.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Attenuation of glucose-induced insulin secretion by intermittent hypoxia via down-regulation of CD38. AU - Ota,Hiroyo, AU - Tamaki,Shinji, AU - Itaya-Hironaka,Asako, AU - Yamauchi,Akiyo, AU - Sakuramoto-Tsuchida,Sumiyo, AU - Morioka,Takashi, AU - Takasawa,Shin, AU - Kimura,Hiroshi, Y1 - 2011/12/01/ PY - 2011/08/22/received PY - 2011/10/29/revised PY - 2011/11/09/accepted PY - 2011/12/14/entrez PY - 2011/12/14/pubmed PY - 2012/4/5/medline SP - 206 EP - 11 JF - Life sciences JO - Life Sci. VL - 90 IS - 5-6 N2 - AIMS: Sleep apnea syndrome (SAS) is characterized by recurrent episodes of oxygen desaturation during sleep, the development of daytime sleepiness, and deterioration in the quality of life. Accumulating evidence suggests the association of intermittent hypoxia (IH), a hallmark of SAS, and type 2 diabetes independently on body mass index and waist circumference. In addition to insulin resistance, the progression to type 2 diabetes is dependent on the impairment of glucose-induced insulin secretion (GIS) from pancreatic β-cells. However, the direct effects of IH on GIS are elusive. MAIN METHODS: HIT-T15 hamster β-cells and isolated rat islets were exposed to 64 cycles/24 h of IH (5 min hypoxia/10 min normoxia) or normoxia for 24 h. Changes of GIS and gene expression in IH-treated β-cells were analyzed by ELISA and real-time RT-PCR, respectively. KEY FINDINGS: After IH treatment, GIS both from IH-treated HIT-T15 cells and isolated rat islets were significantly attenuated. The level of insulin mRNA was unchanged by IH. The mRNA levels of glucose transporter 2 (Glut2), glucokinase (GK), sulfonylurea receptor1 (SUR1), and L-type Ca2+channel1.2 (Cav1.2) in IH-treated-islets were similar to those in normoxia-treated islets. In contrast, the mRNA level of CD38 in IH-treated islets was significantly lower than that in normoxia-treated islets. The reporter gene assay revealed that the transcription of CD38 was attenuated by IH, and the transfection of CD38 expression vector recovered the attenuation of GIS by IH. SIGNIFICANCE: These results indicate that IH stress directly attenuates GIS from β-cells via the down-regulation of CD38. SN - 1879-0631 UR - https://www.unboundmedicine.com/medline/citation/22154909/Attenuation_of_glucose_induced_insulin_secretion_by_intermittent_hypoxia_via_down_regulation_of_CD38_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024-3205(11)00573-X DB - PRIME DP - Unbound Medicine ER -