Vitamin B6 Prevents Endothelial Dysfunction, Insulin Resistance, and Hepatic Lipid Accumulation in<i>Apoe</i><sup>−/−</sup>Mice Fed with High-Fat Diet

Zhan, Lijun; Li, Peng; Zhao, Zhihong; Zhang, Yu; Ma, Zufu; Wang, Shuangxi

doi:10.1155/2016/1748065

Cited by 62 publications

(53 citation statements)

References 31 publications

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“…Traditionally, VitB6 may treat depression, stroke, anaemia, nausea during pregnancy, clogged arteries, eye diseases, diabetes and inflammation associated with rheumatoid arthritis . Recently, we have identified that VitB6 improves insulin resistance in Apoe −/− mice fed with high‐fat diet and prevents isocarbophos‐induced vascular dementia in rats . Here, we further demonstrated that VitB6 suppresses pulmonary inflammation by inhibiting macrophage activation, as reduced productions of TNF‐α and IL‐1β in vivo, consistent with other reports in patients with rheumatoid arthritis .…”

Section: Discussionsupporting

confidence: 89%

“…Traditionally, VitB6 may treat depression, stroke, anaemia, nausea during pregnancy, clogged arteries, eye diseases, diabetes and inflammation associated with rheumatoid arthritis. [28][29][30][31] Recently, we have identified that VitB6 improves insulin resistance in Apoe −/− mice fed with high-fat diet 32 and prevents isocarbophos-induced vascular dementia in rats. 33 Here, we further demonstrated that Mechanistically, we uncovered that the AMPK-DOK3 pathway contributes to the anti-inflammatory effects of VitB6 by inhibiting macrophage activation.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

Shan

Zhou

et al. 2020

J Cellular Molecular Medi

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Macrophage activation participates in the pathogenesis of pulmonary inflammation. As a coenzyme, vitamin B6 (VitB6) is mainly involved in the metabolism of amino acids, nucleic acids, glycogen and lipids. We have previously reported that activation of AMP‐activated protein kinase (AMPK) produces anti‐inflammatory effects both in vitro and in vivo. Whether VitB6 via AMPK activation prevents pulmonary inflammation remains unknown. The model of acute pneumonia was induced by injecting mice with lipopolysaccharide (LPS). The inflammation was determined by measuring the levels of interleukin‐1 beta (IL‐1β), IL‐6 and tumour necrosis factor alpha (TNF‐α) using real time PCR, ELISA and immunohistochemistry. Exposure of cultured primary macrophages to VitB6 increased AMP‐activated protein kinase (AMPK) Thr172 phosphorylation in a time/dose‐dependent manner, which was inhibited by compound C. VitB6 downregulated the inflammatory gene expressions including IL‐1β, IL‐6 and TNF‐α in macrophages challenged with LPS. These effects of VitB6 were mirrored by AMPK activator 5‐aminoimidazole‐4‐carboxamide ribonucleoside (AICAR). However, VitB6 was unable to inhibit LPS‐induced macrophage activation if AMPK was in deficient through siRNA‐mediated approaches. Further, the anti‐inflammatory effects produced by VitB6 or AICAR in LPS‐treated macrophages were abolished in DOK3 gene knockout (DOK3−/−) macrophages, but were enhanced in macrophages if DOK3 was overexpressed. In vivo studies indicated that administration of VitB6 remarkably inhibited LPS‐induced both systemic inflammation and acute pneumonia in wild‐type mice, but not in DOK3−/− mice. VitB6 prevents LPS‐induced acute pulmonary inflammation in mice via the inhibition of macrophage activation.

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Section: Discussionsupporting

confidence: 89%

“…Traditionally, VitB6 may treat depression, stroke, anaemia, nausea during pregnancy, clogged arteries, eye diseases, diabetes and inflammation associated with rheumatoid arthritis. [28][29][30][31] Recently, we have identified that VitB6 improves insulin resistance in Apoe −/− mice fed with high-fat diet 32 and prevents isocarbophos-induced vascular dementia in rats. 33 Here, we further demonstrated that Mechanistically, we uncovered that the AMPK-DOK3 pathway contributes to the anti-inflammatory effects of VitB6 by inhibiting macrophage activation.…”

Section: Discussionmentioning

confidence: 99%

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

Shan

Zhou

et al. 2020

J Cellular Molecular Medi

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“…In vivo or ex vivo organ chamber study was performed as we described previously3233. Rats were sacrificed under anesthesia by intravenous injection with pentobarbital sodium (30 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

Glycation of paraoxonase 1 by high glucose instigates endoplasmic reticulum stress to induce endothelial dysfunction in vivo

Liu

Feng

et al. 2017

Sci Rep

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High-density lipoprotein (HDL) modulates low-density lipoprotein and cell membrane oxidation through the action of paraoxonase-1 (PON1). Endoplasmic reticulum (ER) stress has been linked to a wide range of human pathologies including diabetes, obesity, and atherosclerosis. Previous studies have reported that PON1 is glycated in diabetes. The aim of this study is to investigate whether and how PON1 glycation contributes to endothelial dysfunction in diabetes. ER stress markers were monitored by western blot. Endothelial function was determined by organ bath. Incubation of recombinant PON1 proteins with high glucose increased PON1 glycation and reduced PON1 activity. Exposure of HUVECs to glycated PON1 induced prolonged ER stress and reduced SERCA activity, which were abolished by tempol, apocynin, BAPTA, and p67 and p22 siRNAs. Chronic administration of amino guanidine or 4-PBA prevented endothelial dysfunction in STZ-injected rats. Importantly, injection of glycated PON1 but not native PON1 induced aberrant ER stress and endothelial dysfunction in rats, which were attenuated by tempol, BAPTA, and 4-PBA. In conclusion, glycation of PON1 by hyperglycemia induces endothelial dysfunction through ER stress. In perspectives, PON1 glycation is a novel risk factor of hyperglycemia-induced endothelial dysfunction. Therefore, inhibition of oxidative stress, chelating intracellular Ca2+, and ER chaperone would be considered to reduce vascular complications in diabetes.

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“…In fact, it has been suggested that vitamin B6 can affect insulin resistance by regulating adipogenesis-associated genes [87]. However, it has also been proposed that reduced levels of vitamin B6 may induce insulin resistance by increasing homocysteine levels in consequence of the disrupted activity of cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CGL), enzymes requiring vitamin B6 as coenzyme [88].…”

Section: Physical Exercise and Changes In Gut Microbiota In Obese Indmentioning

confidence: 99%

Molecular and Lifestyle Factors Modulating Obesity Disease

et al. 2020

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Obesity adversely affects bone health by means of multiple mechanisms, e.g., alterations in bone-regulating hormones, inflammation, and oxidative stress. Substantial evidence supports the relationship between adiposity and bone disorders in overweight/obese individuals. It is well known that the balance between mutually exclusive differentiation of progenitor cells into osteoblasts or adipocytes is controlled by different agents, including growth factors, hormones, genetic and epigenetic factors. Furthermore, an association between vitamin D deficiency and obesity has been reported. On the other hand, regular physical activity plays a key role in weight control, in the reduction of obesity-associated risks and promotes osteogenesis. The aim of this review is to highlight relevant cellular and molecular aspects for over-weight containment. In this context, the modulation of progenitor cells during differentiation as well as the role of epigenetics and microbiota in obesity disease will be discussed. Furthermore, lifestyle changes including an optimized diet as well as targeted physical activity will be suggested as strategies for the treatment of obesity disease.

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Vitamin B6 Prevents Endothelial Dysfunction, Insulin Resistance, and Hepatic Lipid Accumulation inApoe^−/−Mice Fed with High-Fat Diet

Cited by 62 publications

References 31 publications

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

Glycation of paraoxonase 1 by high glucose instigates endoplasmic reticulum stress to induce endothelial dysfunction in vivo

Molecular and Lifestyle Factors Modulating Obesity Disease

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Vitamin B6 Prevents Endothelial Dysfunction, Insulin Resistance, and Hepatic Lipid Accumulation inApoe−/−Mice Fed with High-Fat Diet

Cited by 62 publications

References 31 publications

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

Glycation of paraoxonase 1 by high glucose instigates endoplasmic reticulum stress to induce endothelial dysfunction in vivo

Molecular and Lifestyle Factors Modulating Obesity Disease

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Vitamin B6 Prevents Endothelial Dysfunction, Insulin Resistance, and Hepatic Lipid Accumulation inApoe^−/−Mice Fed with High-Fat Diet