Enriching Islet Phospholipids With Eicosapentaenoic Acid Reduces Prostaglandin E 2 Signaling and Enhances Diabetic β-Cell Function.

التفاصيل البيبلوغرافية
العنوان:	Enriching Islet Phospholipids With Eicosapentaenoic Acid Reduces Prostaglandin E 2 Signaling and Enhances Diabetic β-Cell Function.
المؤلفون:	Neuman JC; Interdisciplinary Graduate Program in Nutritional Sciences, College of Agriculture and Life Sciences, University of Wisconsin-Madison, Madison, WI.; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI., Schaid MD; Interdisciplinary Graduate Program in Nutritional Sciences, College of Agriculture and Life Sciences, University of Wisconsin-Madison, Madison, WI.; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI., Brill AL; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Fenske RJ; Interdisciplinary Graduate Program in Nutritional Sciences, College of Agriculture and Life Sciences, University of Wisconsin-Madison, Madison, WI.; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI., Kibbe CR; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Fontaine DA; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Sdao SM; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Integrated Program in Biochemistry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Brar HK; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Connors KM; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Wienkes HN; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Eliceiri KW; Department of Biomedical Engineering, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.; Laboratory for Optical and Computational Instrumentation, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Merrins MJ; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.; Integrated Program in Biochemistry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.; Laboratory for Optical and Computational Instrumentation, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.; Department of Biomolecular Chemistry, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI., Davis DB; Interdisciplinary Graduate Program in Nutritional Sciences, College of Agriculture and Life Sciences, University of Wisconsin-Madison, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.; Medical Service, William S. Middleton Memorial Veterans Hospital, Madison, WI., Kimple ME; Interdisciplinary Graduate Program in Nutritional Sciences, College of Agriculture and Life Sciences, University of Wisconsin-Madison, Madison, WI mkimple@medicine.wisc.edu.; Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI.; Department of Medicine, Division of Endocrinology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.; Department of Cell and Regenerative Biology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI.
المصدر:	Diabetes [Diabetes] 2017 Jun; Vol. 66 (6), pp. 1572-1585. Date of Electronic Publication: 2017 Feb 13.
نوع المنشور:	Journal Article
اللغة:	English
بيانات الدورية:	Publisher: American Diabetes Association Country of Publication: United States NLM ID: 0372763 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1939-327X (Electronic) Linking ISSN: 00121797 NLM ISO Abbreviation: Diabetes Subsets: MEDLINE
أسماء مطبوعة:	Publication: Alexandria, VA : American Diabetes Association Original Publication: [New York, American Diabetes Association]
مواضيع طبية MeSH:	Alprostadil/analogs & derivatives , Diabetes Mellitus/metabolism , Dinoprostone/metabolism , Eicosapentaenoic Acid/pharmacology , Glucose/metabolism , Insulin/metabolism , Insulin-Secreting Cells/drug effects , Receptors, Prostaglandin E, EP3 Subtype/drug effects, Alprostadil/metabolism ; Animals ; Arachidonic Acid/metabolism ; Chromatography, Gas ; Gene Expression Profiling ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Interleukin-1beta/pharmacology ; Islets of Langerhans/drug effects ; Islets of Langerhans/metabolism ; Mass Spectrometry ; Mice ; Mice, Inbred NOD ; Mice, Obese ; Optical Imaging ; Phospholipids ; Receptors, Prostaglandin E, EP3 Subtype/metabolism ; Signal Transduction
مستخلص:	Prostaglandin E 2 (PGE 2 ) is derived from arachidonic acid, whereas PGE 3 is derived from eicosapentaenoic acid (EPA) using the same downstream metabolic enzymes. Little is known about the impact of EPA and PGE 3 on β-cell function, particularly in the diabetic state. In this work, we determined that PGE 3 elicits a 10-fold weaker reduction in glucose-stimulated insulin secretion through the EP3 receptor as compared with PGE 2 We tested the hypothesis that enriching pancreatic islet cell membranes with EPA, thereby reducing arachidonic acid abundance, would positively impact β-cell function in the diabetic state. EPA-enriched islets isolated from diabetic BTBR Leptin ^ob/ob mice produced significantly less PGE 2 and more PGE 3 than controls, correlating with improved glucose-stimulated insulin secretion. NAD(P)H fluorescence lifetime imaging showed that EPA acts downstream and independently of mitochondrial function. EPA treatment also reduced islet interleukin-1β expression, a proinflammatory cytokine known to stimulate prostaglandin production and EP3 expression. Finally, EPA feeding improved glucose tolerance and β-cell function in a mouse model of diabetes that incorporates a strong immune phenotype: the NOD mouse. In sum, increasing pancreatic islet EPA abundance improves diabetic β-cell function through both direct and indirect mechanisms that converge on reduced EP3 signaling. (© 2017 by the American Diabetes Association.)
التعليقات:	Comment in: Diabetes. 2017 Jun;66(6):1464-1466. (PMID: 28533298)
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معلومات مُعتمدة:	R01 DK110324 United States DK NIDDK NIH HHS; R01 DK113103 United States DK NIDDK NIH HHS; R21 AG050135 United States AG NIA NIH HHS; K01 DK101683 United States DK NIDDK NIH HHS; T32 AG000213 United States AG NIA NIH HHS; R01 DK102598 United States DK NIDDK NIH HHS; I01 BX001880 United States BX BLRD VA; P50 AG033514 United States AG NIA NIH HHS
المشرفين على المادة:	0 (Insulin) 0 (Interleukin-1beta) 0 (Phospholipids) 0 (Ptger3 protein, mouse) 0 (Receptors, Prostaglandin E, EP3 Subtype) 27YG812J1I (Arachidonic Acid) 802-31-3 (prostaglandin E3) AAN7QOV9EA (Eicosapentaenoic Acid) F5TD010360 (Alprostadil) IY9XDZ35W2 (Glucose) K7Q1JQR04M (Dinoprostone)
تواريخ الأحداث:	Date Created: 20170215 Date Completed: 20170822 Latest Revision: 20210305
رمز التحديث:	20221213
مُعرف محوري في PubMed:	PMC5440023
DOI:	10.2337/db16-1362
PMID:	28193789
قاعدة البيانات:	MEDLINE

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