Two-dimensional gel electrophoresis of rat kidney lysate; Coomassie blue-stained gels from control (a) and MSG-treated rats (b).

<p>Proteins were resolved on 7 cm pH 3–11 IEF strips (NL) followed by SDS-PAGE (12%). The differentially expressed spots detected by the image Master 2D Platinum 7.0 software are circled. The gels shown are representative of three independent experiments.</p

Proposed model of MSG-induced ROS production in rat kidney.

<p>The higher level of glutamate on chronic MSG intake accelerates TCA cycle. The increased level of α-KGDH may stimulate ROS production hence oxidative stress occurs in the kidney of the MSG-treated rats.</p

List of renal proteins with significantly altered expression after long term chronic MSG treatment.

<p>List of renal proteins with significantly altered expression after long term chronic MSG treatment.</p

Western blot analysis of α-ketoglutarate dehydrogenase (α-KGDH) and glutathione S-transferase P (GSTP) in the kidney tissues of control and MSG treated groups (A), Quantitative analysis indicated that α-KGDH expression was significantly higher in the kidney of the MSG-treated group than that of control (B), whereas, GSTP expression was found significantly lower than that of control (C).

<p>The blots shown are representative of two independent experiments. C1–C5 and T1–T5 indicate animals in the control and MSG-treated groups, respectively.</p

Pancreatic function in control and MSG-treated groups as measured by (A) insulin levels at 1, 3, 6, and 9 months (mean ± SEM) and (B) oral glucose tolerance test (OGTT) at 9 months(mean ± SD).

<p>Pancreatic function in control and MSG-treated groups as measured by (A) insulin levels at 1, 3, 6, and 9 months (mean ± SEM) and (B) oral glucose tolerance test (OGTT) at 9 months(mean ± SD).</p

Representative histology (left) and prevalence (right) of islets hemorrhage/hemosiderin deposits in the control and MSG-treated group at 1, 3, 6, and 9 months (x400).

<p>Representative histology (left) and prevalence (right) of islets hemorrhage/hemosiderin deposits in the control and MSG-treated group at 1, 3, 6, and 9 months (x400).</p

Representative immunohistochemistry (left) and prevalence (right) of 4-HNE staining which was divided into 3 categories (weak, moderate, and strong) based on its intensity in control versus MSG-treated groups at 1 and 6 months (x200).

<p>* <i>P</i> = 0.001.</p

Representative immunohistochemistry (left) and prevalence (right) of insulin staining in control versus MSG-treated groups at 1, 3, 6, and 9 months (x400).

<p>* <i>P</i><0.05.</p

Islet size (um²) distribution in control and MSG-treated groups at 1, 3, 6, and 9 months.

<p>Islet size (um²) distribution in control and MSG-treated groups at 1, 3, 6, and 9 months.</p

Body weight (panel A), food (panel B) and water (panel C) intake in the control and MSG-treated groups at 1, 3, 6, and 9 months of study.

<p>* <i>P</i><0.05.</p