Activity-expression profiling of glucose-6-phosphate dehydrogenase in tissues of normal and diabetic mice

Seo, Jae-Ah; Jung, Se-Hui; Jeon, Hye‐Yoon; Lee, Yeon-Ju; Lee, Jee-Yeon; Han, Eun‐Taek; Park, Won Sun; Hong, Seok‐Ho; Kim, Young‐Myeong; Ha, Kwon‐Soo

doi:10.1016/j.bbrc.2020.01.165

Cited by 6 publications

(3 citation statements)

References 22 publications

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“…The latter explanation makes sense because we find that diabetic patients show a positive correlation between GSH and G6PD (r = 0.312, p = 0.031). Several patients and animal model studies detected decreased GSH, GRd, and G6PD levels [ 8 , 56 , 57 , 58 ]. As a result, an increased GSSG/GSH ratio had a significant positive correlation with TG, and an almost significant positive correlation with glucose, supporting the idea that this oxidative stress marker is related to poor metabolic conditions.…”

Section: Discussionmentioning

confidence: 99%

Role of c-miR-21, c-miR-126, Redox Status, and Inflammatory Conditions as Potential Predictors of Vascular Damage in T2DM Patients

López-Armas¹,

Yessenbekova

González-Castañeda

et al. 2022

Antioxidants

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The development of type 2 diabetes mellitus (T2DM) vascular complications (VCs) is associated with oxidative stress and chronic inflammation and can result in endothelial dysfunctions. Circulating microRNAs play an important role in epigenetic regulation of the etiology of T2DM. We studied 30 healthy volunteers, 26 T2DM patients with no complications, and 26 T2DM patients with VCs, to look for new biomarkers indicating a risk of developing VCs in T2DM patients. Peripheral blood samples were used to determine redox state, by measuring the endogenous antioxidant defense system (superoxide dismutase, SOD; catalase, CAT; glutathione reductase, GRd; glutathione peroxidase, GPx; and glucose-6-phosphate dehydrogenase, G6DP) and markers of oxidative damage (advanced oxidation protein products, AOPP; lipid peroxidation, LPO). Additionally, inflammatory marker levels (IL-1, IL-6, IL-18, and TNF-α), c-miR-21, and c-miR-126 expression were analyzed. T2DM patients showed the highest oxidative damage with increased GSSG/GSH ratios, LPO, and AOPP levels. In both diabetic groups, we found that diminished SOD activity was accompanied by increased CAT and decreased GRd and G6PD activities. Diabetic patients presented with increased relative expression of c-miR-21 and decreased relative expression of c-miR-126. Overall, c-miR-21, SOD, CAT, and IL-6 had high predictive values for diabetes diagnoses. Finally, our data demonstrated that IL-6 exhibited predictive value for VC development in the studied population. Moreover, c-miR-21 and c-miR-126, along with GPx and AOPP levels, should be considered possible markers for VC development in future studies.

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Section: Discussionmentioning

confidence: 99%

Role of c-miR-21, c-miR-126, Redox Status, and Inflammatory Conditions as Potential Predictors of Vascular Damage in T2DM Patients

López-Armas¹,

Yessenbekova

González-Castañeda

et al. 2022

Antioxidants

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“…Briefly, HRECs were grown to confluence on gelatin-coated inserts of Transwell Permeable Supports (0.4 µm, Costar, Corning, NY, USA) and incubated at 37 °C for 6 days in low-glucose, high-glucose, or HGM conditions. The treated cells were then probed with 1 mg/mL 40-kDa FITC-dextran for 60 min, and the amount of FITC-dextran in the lower chambers of the culture wells was measured by a fluorescence scanner (InnoScan 300, Innopsys, Carbonne, France) using well-type arrays ( n = 4), fabricated by mounting PDMS gaskets onto clean glass slides as previously described [ 29 ].…”

Section: Methodsmentioning

confidence: 99%

Simultaneous attenuation of hyperglycemic memory-induced retinal, pulmonary, and glomerular dysfunctions by proinsulin C-peptide in diabetes

Jeon

Moon

Kim

et al. 2023

BMC Med

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Background Hyperglycemic memory (HGM) is a pivotal phenomenon in the development of diabetic complications. Although coincident diabetic complications are reported, research on their development and treatment is limited. Thus, we investigated whether C-peptide can simultaneously inhibit HGM-induced retinal, pulmonary, and glomerular dysfunctions in diabetic mice supplemented with insulin. Methods Insulin-treated diabetic mice were supplemented with human C-peptide by subcutaneous implantation of K9-C-peptide depots for 4 weeks, and reactive oxygen species (ROS) generation, transglutaminase (TGase) activity, and vascular leakage were examined in the retina, lung, and kidney. Results We found hyperglycemia-induced persistent ROS generation and TGase activation after blood glucose normalization in the retina, lung, and kidney of insulin-supplemented diabetic mice. These pathological events were inhibited by systemic supplementation of human C-peptide via subcutaneous implantation of a thermosensitive biopolymer-conjugated C-peptide depot. ROS generation and TGase activation were in a vicious cycle after glucose normalization, and C-peptide suppressed the vicious cycle and subsequent endothelial permeability in human retinal endothelial cells. Moreover, C-peptide supplementation ameliorated HGM-induced retinal vascular leakage and neurodegeneration, pulmonary vascular leakage and fibrosis, and glomerular adherens junction disruption and vascular leakage. Conclusions Overall, our findings demonstrate that C-peptide supplementation simultaneously attenuates vascular and neuronal dysfunctions in the retina, lung, and glomerulus of insulin-supplemented diabetic mice.

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“…Seo et al, and Fomina have both highlighted significant increases in the expression and activity of G6PD in streptozotocin-induced diabetic mice [ 47 , 48 ]. G6PD, a pivotal enzyme in the pentose phosphate pathway, showed elevated levels in various tissues, suggesting a systemic response to the hyperglycemic state induced by diabetes.…”

Section: Changes In Expression Of Nadph Producing Enzymes In Diabetes...mentioning

confidence: 99%

NADPH Dynamics: Linking Insulin Resistance and β-Cells Ferroptosis in Diabetes Mellitus

Moon

2023

IJMS

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This review offers an in-depth exploration of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) in metabolic health. It delves into how NADPH affects insulin secretion, influences insulin resistance, and plays a role in ferroptosis. NADPH, a critical cofactor in cellular antioxidant systems and lipid synthesis, plays a central role in maintaining metabolic homeostasis. In adipocytes and skeletal muscle, NADPH influences the pathophysiology of insulin resistance, a hallmark of metabolic disorders such as type 2 diabetes and obesity. The review explores the mechanisms by which NADPH contributes to or mitigates insulin resistance, including its role in lipid and reactive oxygen species (ROS) metabolism. Parallelly, the paper investigates the dual nature of NADPH in the context of pancreatic β-cell health, particularly in its relation to ferroptosis, an iron-dependent form of programmed cell death. While NADPH’s antioxidative properties are crucial for preventing oxidative damage in β-cells, its involvement in lipid metabolism can potentiate ferroptotic pathways under certain pathological conditions. This complex relationship underscores the delicate balance of NADPH homeostasis in pancreatic health and diabetes pathogenesis. By integrating findings from recent studies, this review aims to illuminate the nuanced roles of NADPH in different tissues and its potential as a therapeutic target. Understanding these dynamics offers vital insights into the development of more effective strategies for managing insulin resistance and preserving pancreatic β-cell function, thereby advancing the treatment of metabolic diseases.

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Activity-expression profiling of glucose-6-phosphate dehydrogenase in tissues of normal and diabetic mice

Cited by 6 publications

References 22 publications

Role of c-miR-21, c-miR-126, Redox Status, and Inflammatory Conditions as Potential Predictors of Vascular Damage in T2DM Patients

Role of c-miR-21, c-miR-126, Redox Status, and Inflammatory Conditions as Potential Predictors of Vascular Damage in T2DM Patients

Simultaneous attenuation of hyperglycemic memory-induced retinal, pulmonary, and glomerular dysfunctions by proinsulin C-peptide in diabetes

NADPH Dynamics: Linking Insulin Resistance and β-Cells Ferroptosis in Diabetes Mellitus

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