The risk of plasma vitamin A, C, E and D deficiency in patients with metabolic syndrome: a case-control study

Godala, Małgorzata; Materek-Kuśmierkiewicz, Izabela; Moczulski, Dariusz; Rutkowski, Maciej; Szatko, Franciszek; Gaszyńska, Ewelina; Tokarski, Sławomir; Kowalski, Jan

doi:10.17219/acem/62453

Cited by 55 publications

(43 citation statements)

References 26 publications

(38 reference statements)

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“…Recently, a case-control study conducted by Godala et al revealed that patients with metabolic syndrome had a higher risk of antioxidant vitamins deficiency, particularly deficiencies in vitamin A, C, and E [18,32]. In the present study, we found that a high proportion of patients with oral cancer had β-carotene and ubiquinone deficiency (Fig.…”

Section: Discussionsupporting

confidence: 65%

The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer

et al. 2020

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Background: Cancer development is mediated by oxidative stress and inflammation, which may correlate with metabolic disorders. The aim of this study was to evaluate antioxidant vitamins status and metabolic parameters in patients with oral cancer according to tumor-node-metastasis (TNM) stages. Methods: A total of 194 patients with oral cancer were enrolled in this study. The patients were stratified for four groups according to cancer stages and that the statistics are comparisons across these groups. The levels of antioxidant vitamins (ubiquinone, β-carotene, vitamin A and E), metabolic parameters, oxidative stress, antioxidant enzymes activity, and inflammatory markers were measured.Results: More than half of the subjects had high blood pressure, central obesity, hyperglycemia, and hyperlipidemia regardless of TNM stage. With regard to antioxidant vitamins status, 46 and 94% of patients had β-carotene and ubiquinone deficiency, respectively. Patients in T3 and T4 stages had significantly lower antioxidant enzyme (catalase, p = 0.03) activity and higher inflammatory markers levels (high sensitivity C-reactive protein and interleukin-6, p < 0.01) than patients in the other stages. In addition, the level of β-carotene was negatively associated with waist circumference, and ubiquinone was positively associated with the level of high-density lipoprotein cholesterol (p < 0.05). Higher β-carotene and ubiquinone levels were negatively associated with hypertriglyceridemia and the risk of metabolic syndrome (p < 0.05). Conclusions:A high proportion of patients with oral cancer had ubiquinone or β-carotene deficiency and metabolic disorders. The level of ubiquinone or β-carotene was negatively associated with the risk of central obesity, hypertriglyceridemia, and metabolic syndrome. Since patients with oral cancer suffer from high oxidative stress and inflammation (particularly in the T3 and T4 stages), supplementation with antioxidant vitamins such as ubiquinone or β-carotene could be preferentially applied.

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Section: Discussionsupporting

confidence: 65%

The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer

et al. 2020

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Section: Discussionsupporting

confidence: 65%

The risks of ubiquinone and b-carotene deficiency and metabolic disorders in patients with oral cancer

Chan

Lee

Chang

et al. 2020

Preprint

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Background: Cancer development is mediated by oxidative stress and inflammation, which may correlate with metabolic disorders. The aim of this study was to evaluate antioxidant vitamins status and metabolic parameters in patients with oral cancer according to tumor-node-metastasis (TNM) stages.Methods: A total of 194 patients with oral cancer were enrolled in this study. The patients were stratified for four groups according to cancer stages and that the statistics are comparisons across these groups. The levels of antioxidant vitamins (ubiquinone, b-carotene, vitamin A and E), metabolic parameters, oxidative stress, antioxidant enzymes activity, and inflammatory markers were measured.Results: More than half of the subjects had high blood pressure, central obesity, hyperglycemia, and hyperlipidemia regardless of TNM stage. With regard to antioxidant vitamins status, 46% and 94% of patients had β-carotene and ubiquinone deficiency, respectively. Patients in T3 and T4 stages had significantly lower antioxidant enzyme (catalase, p = 0.03) activity and higher inflammatory markers levels (high sensitivity C-reactive protein and interleukin-6, p < 0.01) than patients in the other stages. In addition, the level of b-carotene was negatively associated with waist circumference, and ubiquinone was positively associated with the level of high-density lipoprotein cholesterol (p < 0.05). Higher b-carotene and ubiquinone levels were negatively associated with hypertriglyceridemia and the risk of metabolic syndrome (p < 0.05).Conclusions: A high proportion of patients with oral cancer had ubiquinone or b-carotene deficiency and metabolic disorders. The level of ubiquinone or b-carotene was negatively associated with the risk of central obesity, hypertriglyceridemia, and metabolic syndrome. Since patients with oral cancer suffer from high oxidative stress and inflammation (particularly in the T3 and T4 stages), supplementation with antioxidant vitamins such as ubiquinone or b-carotene could be preferentially applied.

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“…Numerous studies have reported on vitamin A status in MetS, while reports specifically focusing on NAFLD are limited. Almost all studies documenting vitamin A status in MetS report reductions in serum retinol, retinoic acid, and/or β-carotene that are inversely correlated with MetS features, including obesity, insulin resistance, glucose intolerance, and hypertriglyceridemia [ 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 ]. In line with these observations, inadequate serum retinol levels (<1.05 μmol/L) were found in 11–36% of morbidly obese adults with ultrasonography-proven NAFLD, and a significant association between low retinol levels and insulin resistance (IR) was found [ 25 , 53 ].…”

Section: Vitamin a And Rbp4 In The Clinical Course Of Nafld And Mementioning

confidence: 99%

Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD)

et al. 2017

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Vitamin A is required for important physiological processes, including embryogenesis, vision, cell proliferation and differentiation, immune regulation, and glucose and lipid metabolism. Many of vitamin A’s functions are executed through retinoic acids that activate transcriptional networks controlled by retinoic acid receptors (RARs) and retinoid X receptors (RXRs).The liver plays a central role in vitamin A metabolism: (1) it produces bile supporting efficient intestinal absorption of fat-soluble nutrients like vitamin A; (2) it produces retinol binding protein 4 (RBP4) that distributes vitamin A, as retinol, to peripheral tissues; and (3) it harbors the largest body supply of vitamin A, mostly as retinyl esters, in hepatic stellate cells (HSCs). In times of inadequate dietary intake, the liver maintains stable circulating retinol levels of approximately 2 μmol/L, sufficient to provide the body with this vitamin for months. Liver diseases, in particular those leading to fibrosis and cirrhosis, are associated with impaired vitamin A homeostasis and may lead to vitamin A deficiency. Liver injury triggers HSCs to transdifferentiate to myofibroblasts that produce excessive amounts of extracellular matrix, leading to fibrosis. HSCs lose the retinyl ester stores in this process, ultimately leading to vitamin A deficiency. Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is a spectrum of conditions ranging from benign hepatic steatosis to non-alcoholic steatohepatitis (NASH); it may progress to cirrhosis and liver cancer. NASH is projected to be the main cause of liver failure in the near future. Retinoic acids are key regulators of glucose and lipid metabolism in the liver and adipose tissue, but it is unknown whether impaired vitamin A homeostasis contributes to or suppresses the development of NAFLD. A genetic variant of patatin-like phospholipase domain-containing 3 (PNPLA3-I148M) is the most prominent heritable factor associated with NAFLD. Interestingly, PNPLA3 harbors retinyl ester hydrolase activity and PNPLA3-I148M is associated with low serum retinol level, but enhanced retinyl esters in the liver of NAFLD patients. Low circulating retinol in NAFLD may therefore not reflect true “vitamin A deficiency”, but rather disturbed vitamin A metabolism. Here, we summarize current knowledge about vitamin A metabolism in NAFLD and its putative role in the progression of liver disease, as well as the therapeutic potential of vitamin A metabolites.

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The risk of plasma vitamin A, C, E and D deficiency in patients with metabolic syndrome: a case-control study

Cited by 55 publications

References 26 publications

The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer

The risks of ubiquinone and β-carotene deficiency and metabolic disorders in patients with oral cancer

The risks of ubiquinone and b-carotene deficiency and metabolic disorders in patients with oral cancer

Disturbed Vitamin A Metabolism in Non-Alcoholic Fatty Liver Disease (NAFLD)

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