کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6155889 | 1597942 | 2016 | 29 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Proinsulin and heat shock protein 90 as biomarkers of beta-cell stress in the early period after onset of type 1 diabetes
ترجمه فارسی عنوان
پروینسولین و پروتئین شوک حرارتی 90 به عنوان بیومارکرهای استرس بتا-سلولی در دوره اولیه پس از شروع دیابت نوع 1
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کلمات کلیدی
glutamic acid decarboxylase 65mIAAIA-2LLDHbA1cGAD65UPRNODHspBiP - BIPc-Peptide - c پپتیدهInsulin autoantibody - آنتی بادی انسولینCHOP - تکه کردنType 1 diabetes - دیابت نوع۱Nonobese diabetic - دیابتی NonobeseTID - زمانbody mass index - شاخص توده بدنBMI - شاخص توده بدنیendoplasmic reticulum - شبکه آندوپلاسمی lower limit of detection - محدودیت پایین تشخیصHemoglobin A1c - هموگلوبین A1cUnfolded protein response - پاسخ پروتئین آشکارHeat shock protein - پروتئین شوک حرارتCCAAT/enhancer-binding protein homologous protein - پروتئین هموسیستون پروتئین پروتئین CCAAT / پروتئین تقویت کنندهProinsulin - پروینسولین
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
چکیده انگلیسی
Rapid evaluation of therapies designed to preserve β cells in persons with type 1 diabetes (T1D) is hampered by limited availability of sensitive β-cell health biomarkers. In particular, biomarkers elucidating the presence and degree of β-cell stress are needed. We characterized β-cell secretory activity and stress in 29 new-onset T1D subjects (10.6 ± 3.0 years, 55% male) at diagnosis and then 8.2 ± 1.2 weeks later at first clinic follow-up. We did comparisons with 16 matched healthy controls. We evaluated hemoglobin A1c (HbA1c), β-cell function (random C-peptide [C] and proinsulin [PI]), β-cell stress (PI:C ratio), and the β-cell stress marker heat shock protein (HSP)90 and examined these parameters' relationships with clinical and laboratory characteristics at diagnosis. Mean diagnosis HbA1c was 11.3% (100 mmol/mol) and 7.6% (60 mmol/mol) at follow-up. C-peptide was low at diagnosis (P < 0.001 vs controls) and increased at follow-up (P < 0.001) to comparable with controls. PI did not differ from controls at diagnosis but increased at follow-up (P = 0.003) signifying increased release of PI alongside improved insulin secretion. PI:C ratios and HSP90 concentrations were elevated at both time points. Younger subjects had lower C-peptide and greater PI, PI:C, and HSP90. We also examined islets isolated from prediabetic nonobese diabetic mice and found that HSP90 levels were increased â¼4-fold compared with those in islets isolated from matched CD1 controls, further substantiating HSP90 as a marker of β-cell stress in T1D. Our data indicate that β-cell stress can be assessed using PI:C and HSP90. This stress persists after T1D diagnosis. Therapeutic approaches to reduce β-cell stress in new-onset T1D should be considered.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 168, February 2016, Pages 96-106.e1
Journal: Translational Research - Volume 168, February 2016, Pages 96-106.e1
نویسندگان
Renecia A. Watkins, Carmella Evans-Molina, Jennifer K. Terrell, Kathleen H. Day, Lynette Guindon, Ivan A. Restrepo, Raghavendra G. Mirmira, Janice S. Blum, Linda A. DiMeglio,