Effect of 1, 25(OH)2 vitamin D3 on glucose homeostasis and DNA damage in type 2 diabetic mice

Meerza, Dilnasheen; Naseem, Imrana; Ahmed, Jamal Uddin

doi:10.1016/j.jdiacomp.2012.05.013

Cited by 30 publications

(19 citation statements)

References 51 publications

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“…We showed that 1 year cholecalciferol treatment improved DPB and fasting glucose without significant changes in terms of BMI. Although in a small group of children, these data are in line with other observations in some pilot studies in animals [35] and in adults [36]. As our patients did not improve their weight, our results seem dependent on VD without an influence of body fat changes.…”

Section: Discussionsupporting

confidence: 93%

Pediatric Obesity and Vitamin D Deficiency: A Proteomic Approach Identifies Multimeric Adiponectin as a Key Link between These Conditions

et al. 2014

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Key circulating molecules that link vitamin D (VD) to pediatric obesity and its co-morbidities remain unclear. Using a proteomic approach, our objective was to identify key molecules in obese children dichotomized according to 25OH-vitamin D (25OHD) levels. A total of 42 obese children (M/F = 18/24) were divided according to their 25OHD3 levels into 25OHD3 deficient (VDD; n = 18; 25OHD<15 ng/ml) or normal subjects (NVD; n = 24; >30 ng/ml). Plasma proteomic analyses by two dimensional (2D)-electrophoresis were performed at baseline in all subjects. VDD subjects underwent a 12mo treatment with 3000 IU vitamin D3 once a week to confirm the proteomic analyses. The proteomic analyses identified 53 “spots” that differed between VDD and NVD (p<0.05), amongst which adiponectin was identified. Adiponectin was selected for confirmational studies due to its tight association with obesity and diabetes mellitus. Western Immunoblot (WIB) analyses of 2D-gels demonstrated a downregulation of adiponectin in VDD subjects, which was confirmed in the plasma from VDD with respect to NVD subjects (p<0.035) and increased following 12mo vitamin D3 supplementation in VDD subjects (p<0.02). High molecular weight (HMW) adiponectin, a surrogate indicator of insulin sensitivity, was significantly lower in VDD subjects (p<0.02) and improved with vitamin D3 supplementation (p<0.042). A direct effect in vitro of 1α,25-(OH)2D3 on adipocyte adiponectin synthesis was demonstrated, with adiponectin and its multimeric forms upregulated, even at low pharmacological doses (10−9 M) of 1α,25-(OH)2D3. This upregulation was paralleled by the adiponectin interactive protein, DsbA-L, suggesting that the VD regulation of adiponectin involves post-transciptional events. Using a proteomic approach, multimeric adiponectin has been identified as a key plasma protein that links VDD to pediatric obesity.

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Section: Discussionsupporting

confidence: 93%

Pediatric Obesity and Vitamin D Deficiency: A Proteomic Approach Identifies Multimeric Adiponectin as a Key Link between These Conditions

et al. 2014

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“…Our studies are further supported by those of Koren et al [36] who have shown that calcitriol is a proxidant only in malignant cells. Studies from our laboratory have shown that calcitriol is not a proxidant in non malignant tissue [37], possibly because the prooxidant nature of calcitriol is dependent on its ability to interact with copper, which is only elevated in malignancies.…”

Section: Discussionmentioning

confidence: 94%

Calcitriol–copper interaction leads to non enzymatic, reactive oxygen species mediated DNA breakage and modulation of cellular redox scavengers in hepatocellular carcinoma

et al. 2016

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Calcitriol is the metabolically active form of Vitamin D and is known to kill cancer cells. Using the rat model of DEN induced hepatocellular carcinoma we show that there is a marked increase in cellular levels of copper in hepatocellular carcinoma and that calcitriol-copper interaction leads to reactive oxygen species mediated DNA breakage selectively in hepatocellular carcinoma cells. In vivo studies show that calcitriol selectively induces severe fluctuations in cellular enzymatic and non enzymatic scavengers of reactive oxygen species in the malignant tissue. Lipid peroxidation, a well established marker of oxidative stress, was found to increase, and substantial cellular DNA breakage was observed. We propose that calcitriol is a proxidant in the cellular milieu of hepatocellular carcinoma cells, and this copper mediated prooxidant action of calcitriol causes selective DNA breakage in malignant cells, while sparing normal (non malignant) cells.

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“…Briefly, images were opened in CometScore software and the individual cells were scored using the scoring tool which automatically measures the % tail DNA and olive tail moment for that particular cell. Approximately, 100 cells per gel were analysed [28,44,48].…”

Section: Alkaline Comet Assaymentioning

confidence: 99%

Differential molecular and cellular responses of GLP-1 secreting L-cells and pancreatic alpha cells to glucotoxicity and lipotoxicity

Vasu

Moffett

McClenaghan

et al. 2015

Experimental Cell Research

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Effect of 1, 25(OH)2 vitamin D3 on glucose homeostasis and DNA damage in type 2 diabetic mice

Cited by 30 publications

References 51 publications

Pediatric Obesity and Vitamin D Deficiency: A Proteomic Approach Identifies Multimeric Adiponectin as a Key Link between These Conditions

Pediatric Obesity and Vitamin D Deficiency: A Proteomic Approach Identifies Multimeric Adiponectin as a Key Link between These Conditions

Calcitriol–copper interaction leads to non enzymatic, reactive oxygen species mediated DNA breakage and modulation of cellular redox scavengers in hepatocellular carcinoma

Differential molecular and cellular responses of GLP-1 secreting L-cells and pancreatic alpha cells to glucotoxicity and lipotoxicity

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