Correction: Inflammatory Stress on Autophagy in Peripheral Blood Mononuclear Cells from Patients with Alzheimer's Disease during 24 Months of Follow-Up

Audigier, François; Julian, Adrien; Ragot, Stéphanie; Dugast, Emilie; Blanchard, Ludovic; Brishoual, Sonia; Terro, Faraj; Chassaing, Damien; Page, Guylène; Pocard, Marc

doi:10.1371/journal.pone.0143933

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“…Thus, these cells closely reflect the prevailing physiological milieu at the insulin target sites and β-cells. Furthermore, PBMCs are easily accessible and have been used previously in a couple of studies to demonstrate the alterations in mitochondrial stress indices as well as autophagy ( 18 – 20 ).…”

Section: Introductionmentioning

confidence: 99%

Alterations in Mitochondrial Oxidative Stress and Mitophagy in Subjects with Prediabetes and Type 2 Diabetes Mellitus

Bhansali

Walia

et al. 2017

Front. Endocrinol.

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Background and aimHyperglycemia-mediated oxidative stress impedes cell-reparative process like autophagy, which has been implicated in impairment of β-cell function in type 2 diabetes mellitus (T2DM). However, the role of mitophagy (selective mitochondrial autophagy) in progression of hyperglycemia remains elusive. This study aimed to assess the impact of increasing severity of hyperglycemia on mitochondrial stress and mitophagy.Design and methodsA case–control study included healthy controls, subjects with prediabetes, newly diagnosed T2DM (NDT2DM) and advanced duration of T2DM (ADT2DM) (n = 20 each). Mitochondrial stress indices, transcriptional and translational expression of mitophagy markers (PINK1, PARKIN, MFN2, NIX, LC3-II, and LAMP-2) and transmission electron microscopic (TEM) studies were performed in peripheral blood mononuclear cells.ResultsWith mild hyperglycemia in subjects with prediabetes, to moderate to severe hyperglycemia in NDT2DM and ADT2DM, a progressive rise in mitochondrial oxidative stress was observed. Prediabetic subjects exhibited significantly increased expression of mitophagy-related markers and showed a positive association with HOMA-β, whereas, patients with NDT2DM and ADT2DM demonstrated decreased expression, with a greater decline in ADT2DM subjects. TEM studies revealed significantly reduced number of distorted mitochondria in prediabetics, as compared to the T2DM patients. In addition, receiver operating characteristic analysis showed HbA1C > 7% (53 mmol/mol) was associated with attenuated mitophagy.ConclusionIncreasing hyperglycemia is associated with progressive rise in oxidative stress and altered mitochondrial morphology. Sustenance of mitophagy at HbA1C < 7% (53 mmol/mol) strengthens the rationale of achieving HbA1C below this cutoff for good glycemic control. An “adaptive” increase in mitophagy may delay progression to T2DM by preserving the β-cell function in subjects with prediabetes.

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Section: Introductionmentioning

confidence: 99%