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Orphan G-protein co...
Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced β-cell dysfunction
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- Taneera, Jalal (author)
- University of Sharjah
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- Mohammed, Israa (author)
- Lund University,Lunds universitet,Diabetes - öpatofysiologi,Forskargrupper vid Lunds universitet,Diabetes - Islet Patophysiology,Lund University Research Groups
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- Mohammed, Abdul Khader (author)
- University of Sharjah
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- Hachim, Mahmood (author)
- University of Sharjah
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- Dhaiban, Sarah (author)
- University of Sharjah
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- Malek, Abdullah (author)
- University of Sharjah
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- Dunér, Pontus (author)
- Lund University,Lunds universitet,Kardiovaskulär forskning - matrix och inflammation i ateroskleros,Forskargrupper vid Lunds universitet,Cardiovascular Research - Matrix and Inflammation in Atherosclerosis,Lund University Research Groups
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- Elemam, Noha M. (author)
- University of Sharjah
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- Sulaiman, Nabil (author)
- University of Sharjah
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- Hamad, Mawieh (author)
- University of Sharjah
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- Salehi, Albert (author)
- Gothenburg University,Göteborgs universitet,University of Gothenburg,Lund University,Lunds universitet,Diabetes - öpatofysiologi,Forskargrupper vid Lunds universitet,Diabetes - Islet Patophysiology,Lund University Research Groups,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology
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(creator_code:org_t)
- Elsevier BV, 2020
- 2020
- English.
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In: Molecular and Cellular Endocrinology. - : Elsevier BV. - 0303-7207. ; 499
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http://dx.doi.org/10...
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Abstract
Subject headings
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- The expression and functional impact of most expression orphan G-protein coupled receptors (GPCRs) in β-cell is not fully understood. Microarray expression indicated that 36 orphan GPCRs are restricted in human islets, while 55 receptors overlapped between human islets and INS-1 cells. GPR183 showed higher expression in diabetic compared to non-diabetic human islets. GPR183 expression co-localized with β-cells while it was lacking in α-cells in human islets. The GPR183 agonist (7α-25-DHC) potentiated insulin secretion and protected against glucotoxicity-induced β-cell damage in human islets. Silencing of GPR183 in INS-1 cells decreased the expression of proinsulin genes, Pdx1, Mafa and impaired insulin secretion with a concomitant decrease in cAMP generation. Cultured INS-1 cells with 7α-25-DHC were associated with increased proliferation and expression of GPR183, INS2, PDX1, NeuroD, and INSR. In conclusion, the beneficial impact of GPR183 activation on β-cell function makes it a potential therapeutic target to prevent or reverse β-cell dysfunction.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)
Keyword
- 7α-25-DHC
- GPCRs
- GPR183
- Microarray gene expression
- RNA-Sequencing
- Type 2 diabetes
Publication and Content Type
- art (subject category)
- ref (subject category)
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- By the author/editor
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Taneera, Jalal
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Mohammed, Israa
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Mohammed, Abdul ...
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Hachim, Mahmood
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Dhaiban, Sarah
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Malek, Abdullah
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show more...
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Dunér, Pontus
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Elemam, Noha M.
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Sulaiman, Nabil
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Hamad, Mawieh
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Salehi, Albert
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show less...
- About the subject
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- MEDICAL AND HEALTH SCIENCES
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MEDICAL AND HEAL ...
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and Clinical Medicin ...
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and Endocrinology an ...
- Articles in the publication
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Molecular and Ce ...
- By the university
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Lund University
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University of Gothenburg