Abstract
To investigate the effect of intermittent high glucose (IHG) and sustained high glucose (SHG) on inducing β-cell apoptosis and the potential involved mechanisms, INS-1 beta cells were incubated for 72 h in the medium containing different glucose concentrations: control (5.5 mmol/L), SHG (33.3 mmol/L), and IHG (5.5 mmol/L and 33.3 mmol/L glucose alternating every 12 h). Cell viability, apoptosis rate, and oxidative-stress markers were determined. The results showed that the apoptosis induced by IHG was more obvious than that by SHG. Simultaneously, the intracellular level of oxidative stress was more significantly increased in INS-1 cells exposed to IHG. These findings suggest that intermittent high glucose could be more deleterious to β-cell than a constant high concentration of glucose, this may be due to the aggravation of oxidative stress triggered by intermittent high glucose.
Highlights
Apoptosis, an active process of cell suicide morphologically and biochemically different from necrosis and actively regulated, plays an important role in the development of diabetes
RPMI1640 medium and fetal bovine serum were purchased from GIBCO. 2, 7 -dichlorofluorescein diacetate (DCFH-DA), dimethyl sulphoxide (DMSO), 3-(4, 5-dimethylthialzal-z-yl)-2,5-diphenylterazolium bromide (MTT), and Hoechst 33258 dye were purchased from Sigma, Annexin V: FITC apoptosis detection kit was form BD
After being cultured overnight in glucose-free RPMI 1640 with 5.5 mmol/L glucose, INS-1 cells were divided into three groups: (1) control group (CG) exposed to normal concentration of glucose (5.5 mmol/L), (2) stable high glucose (SHG) group exposed to 33.3 mmol/L glucose, and (3) intermittent high glucose (IHG) group exposed to fluctuating concentrations of glucose, and were incubated for 72 h
Summary
An active process of cell suicide morphologically and biochemically different from necrosis and actively regulated, plays an important role in the development of diabetes. Several lines of evidence from autopsy suggested that β-cell mass in diabetic patients is significantly reduced and its reduction is associated with increased apoptosis [1,2,3]. Both animal and human studies have found that increase of β-cell apoptosis is an important reason of insulin deficiency in patients with T2DM [1, 4]. Numerous evidences have suggested that chronic persistent hyperglycemia results in β-cells dysfunction and apoptosis, called βcell glucose toxicity [5]. A few published reports demonstrated the effects of intermittent high glucose on the development of diabetic complications [7, 8], but the effect of intermittent high glucose on β-cell and the potential mechanisms involved remain unknown
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