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首页> 外文期刊>Translational research: the journal of laboratory and clinical medicine >Proinsulin and heat shock protein 90 as biomarkers of beta-cell stress in the early period after onset of type 1 diabetes
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Proinsulin and heat shock protein 90 as biomarkers of beta-cell stress in the early period after onset of type 1 diabetes

机译：1型糖尿病发作后早期胰岛素原和热休克蛋白90作为β细胞应激的生物标志物

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Rapid evaluation of therapies designed to preserve beta cells in persons with type 1 diabetes (T1D) is hampered by limited availability of sensitive beta-cell health biomarkers. In particular, biomarkers elucidating the presence and degree of beta-cell stress are needed. We characterized p-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), beta-cell function (random C-peptide (C) and proinsulin (PI)), beta-cell stress (PI:C ratio), and the beta-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 similar to 4-fold compared with those in islets isolated from matched CD1 controls, further substantiating HSP90 as a marker of beta-cell stress in T1D. Our data indicate that beta-cell stress can be assessed using PLC and HSP90. This stress persists after T1D diagnosis. Therapeutic approaches to reduce beta-cell stress in new-onset T1D should be considered.
机译：旨在保护1型糖尿病（T1D）患者中β细胞的疗法的快速评估受到敏感β细胞健康生物标志物供应有限的困扰。特别地，需要阐明β细胞应激的存在和程度的生物标记。我们在诊断时确定了29位新发病的T1D受试者（10.6 +/- 3.0岁，男性55％）的p细胞分泌活性和压力，然后在首次临床随访后8.2 +/- 1.2周进行了表征。我们与16个匹配的健康对照组进行了比较。我们评估了血红蛋白A1c（HbA1c），β细胞功能（随机C肽（C）和胰岛素原（PI）），β细胞应激（PI：C比）和β细胞应激标志物热休克蛋白（HSP） 90），并检查了这些参数与诊断时的临床和实验室特征的关系。随访时，平均诊断HbA1c为11.3％（100 mmol / mol）和7.6％（60 mmol / mol）。 C肽在诊断时较低（与对照组相比，P <0.001），在随访时有所增加（P <0.001），与对照组相当。 PI在诊断时与对照组无差异，但在随访时有所增加（P = 0.003），表明PI的释放增加，同时胰岛素分泌改善。在两个时间点，PI：C比和HSP90浓度均升高。年轻的受试者具有较低的C肽和较高的PI，PI：C和HSP90。我们还检查了从糖尿病前非肥胖糖尿病小鼠中分离的胰岛，发现与从匹配的CD1对照中分离的胰岛相比，HSP90的水平增加了约4倍，进一步证实了HSP90作为T1D中β细胞应激的标志物。我们的数据表明可以使用PLC和HSP90评估β细胞的压力。 T1D诊断后这种压力仍然存在。应该考虑减少新发T1D中β细胞应激的治疗方法。

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