ABSTRACT
Flavonoids intake has been linked to risk of type 2 diabetes theoretically, but the findings were conflicting from observational studies. Results from the recent meta-analysis suggested a moderate favorable effect of total dietary flavonoids consumption on type 2 diabetes risk. However, the relationship, if exists, between total dietary flavonoids consumption and type 2 diabetes risk is unclear, especially further in the association between flavonoid subclasses and risk of type 2 diabetes. Thus, the dose-response relationship was assessed by restricted cubic spline model and multivariate random-effect meta-regression. Among flavonoid subclasses, protective effects were obtained for intakes of flavonols, flavan-3-ols, isoflavones and anthocyanidins in high vs. low analysis and dose-response analysis.
Subject(s)
Diabetes Mellitus, Type 2 , Flavonoids , Diet , Humans , Prospective Studies , Risk FactorsABSTRACT
The objectives of this study are to assess T-2 toxin's involvement in low selenium (Se)-induced Kashin-Beck disease (KBD) in rats and unveil the mechanisms underlying this disease. Two hundred thirty rats were randomly divided into two groups after weaning and fed normal or low-Se diets (n = 115), respectively, for a month. After low-Se model confirmation, rats in each group were subdivided into five: two subgroups (n = 20) were fed their current diets (normal or low-Se diets, respectively) for 30 and 90 days, respectively; two other subgroups (n = 25) received their current diets + low T-2 toxin (100 ng/g BW/day) for 30 and 90 days, respectively; and 25 rats were fed their current diets + high T-2 toxin (200 ng/g BW/day) for 30 days. Articular cartilage samples were extracted for hematoxylin and eosin (H&E) staining and immunohistochemistry. Western blot and reverse transcription-polymerase chain reaction (RT-PCR) were used to assess protein and mRNA levels, respectively, of collagen II, matrix metalloproteinase (MMP-1), MMP -3, MMP-13, and tissue inhibitor of metalloproteinase-1 (TIMP-1). Low Se and T-2 toxin synergistically affected animal fitness. Interestingly, low Se + T-2 toxin groups showed KBD characteristics. MMP-1, -3, and -13 mRNA and protein levels generally increased in low-Se groups, while collagen II and TIMP-1 levels showed a downward trend, compared with normal diet fed animals for the same treatment (P < 0.05). T-2 toxin's effect was dose but not time dependent. Low Se and T-2 toxin synergistically alter the expression levels of collagen II as well as its regulatory enzymes MMP-1, MMP-3, MMP-13, and TIMP-1, inducing cartilage damage. Therefore, T-2 toxin may cause KBD in low-Se conditions.
Subject(s)
Collagen Type II/metabolism , Kashin-Beck Disease/metabolism , Matrix Metalloproteinases/metabolism , Selenium/deficiency , T-2 Toxin/toxicity , Tissue Inhibitor of Metalloproteinase-1/metabolism , Animals , Blotting, Western , Cartilage/drug effects , Cartilage/metabolism , Disease Models, Animal , Hindlimb/drug effects , Hindlimb/metabolism , Immunohistochemistry , Kashin-Beck Disease/chemically induced , Kashin-Beck Disease/enzymology , Male , Rats, Sprague-Dawley , Reverse Transcriptase Polymerase Chain Reaction , Selenium/blood , Sternum/drug effects , Sternum/metabolismABSTRACT
Fincoal type fluorosis has only been reported from China, but its pathogenesis is unclear. Many people believe that fluorosis is associated with oxidative stress. Oxidative stress can be reduced at higher selenium (Se) level. Heat shock protein (HSP70) is the most conserved and induced against different stressors. The aim of this study is to detect the expression of HSP70 in fluorosis patients and explore the role of Se in fluorosis protection. The subjects were divided into four groups: "High Se + F group" (n = 50), "High F group" (n = 50), "High Se group" (n = 20) and "Control group" (n = 46). Expression of HSP70 was evaluated by Western blotting and real-time PCR techniques. The concentration of fluoride, content of Se in hair, activity of antioxidant enzymes (GSH-Px, SOD, CAT) and content of malondialdehyde (MDA) were determined. The relative amount of HSP70 gene transcription was significantly higher in "High Se + F group" than the other groups. The same results were found for expression of HSP70 protein to beta-actin ratio. There was a significant difference between "High Se + F group" and "High F group" regarding MDA content and glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activity. These results suggest that oxidative stress plays an important role in the pathogenesis of the Fincoal type fluorosis and it can be reduced at higher Se level.
