Molecular Nutrition and Food Research

Diet plays an important role in the development and prevention of cardiovascular disease (CVD), but the molecular mechanisms are not fully understood. DNA methylation has been implicated as an underlying molecular mechanism that may account for the effect of dietary factors on the development and prevention of CVD. DNA methylation is an epigenetic process that provides “marks” in the genome by which genes are set to be transcriptionally activated or silenced. Epigenomic marks are heritable but are also responsive to environmental shifts, such as changes in nutritional status, and are especially vulnerable during development. S‐adenosylmethionine is the methyl group donor for DNA methylation and several nutrients are required for the production of S‐adenosylmethionine. These methyl nutrients include vitamins (folate, riboflavin, vitamin B12, vitamin B6, choline) and amino acids (methionine, cysteine, serine, glycine). As such, imbalances in the metabolism of these nutrients have the potential to affect DNA methylation. The focus of this review is to provide an overview on the current understanding of the relationship between methyl nutrient status and DNA methylation patterns and the potential role of this interaction in CVD pathology.

Scope: Thymol is a component of several plants with antimicrobial activity. Little is known about the effects of thymol on immune cells of the host. This study addressed the effects of thymol on dendritic cells (DCs), regulators of innate and adaptive immunity.

Methods and results: Immunohistochemistry, Western blotting and fluorescence‐activated cell sorting analysis were performed in bone marrow‐derived DCs either from wild‐type mice or from mice lacking acid sphingomyelinase (ASM^−/−) treated and untreated for 24 h with thymol (2–100 μg/mL). Thymol treatment resulted in activation of ASM, stimulation of ceramide formation, downregulation of anti‐apoptotic Bcl‐2 and Bcl‐xL proteins, activation of caspase 3 and caspase 8, DNA fragmentation as well as cell membrane scrambling. The effects were dependent on the presence of ASM and were lacking in ASM^−/− mice or in wild‐type DCs treated with sphingomyelinase inhibitor amitriptyline.

Conclusion: Thymol triggers suicidal DC death, an effect mediated by and requiring activation of ASM.

Both insulin resistance and dyslipidaemia are determined by genetic and environmental factors. Depending on their expression and their function, gene variants may influence either insulin action or other metabolic traits. Nutrition also plays an important role in the development and progression of these conditions. Genetic background may interact with habitual dietary fat composition, affecting predisposition to insulin resistance syndrome and individual responsiveness to changes in dietary fat intake. In this context, nutrigenetics has emerged as a multidisciplinary field focusing on studying the interactions between nutritional and genetic factors and health outcomes. Due to the complex nature of gene–environment interactions, however, dietary therapy may require a “personalized” nutrition approach in the future. Although the results have not always been consistent, gene variants that affect primary insulin action, and particularly their interaction with the environment, are important modulators of glucose metabolism. The purpose of this review is to present some evidence of studies that have already demonstrated the significance of gene–nutrient interactions (adiponectin gene, Calpain‐10, glucokinase regulatory protein, transcription factor 7‐like 2, leptin receptor, scavenger receptor class B type I etc.) that influence insulin resistance in subjects with metabolic syndrome.

Male C57BL/6 mice received diets with either 10% of kcal from fat, or a high fat diet [45% (HF45) or 60% (HF60) kcal from fat]. Diets were prepared with or without freeze‐dried powders (10%) from whole blueberries (BB), strawberries (SB), Concord grape or black raspberry. In the 2nd study, purified anthocyanins (ACNs) from SB or BB were added to the drinking water of the treatments fed the HF60 diet. In Study 1, serum triglycerides were increased by feeding the HF45 diet but were elevated further when black raspberry or BB was included in the HF45 diet. Liver total lipids and triglycerides were increased in mice fed HF45 diet and inclusion of any of the berry powders in the HF45 diet did not alter concentrations compared to HF45 controls. In the 2nd study, mice fed the HF60 diet plus purified ACNs from BB in the water had lower body weight gains and body fat than the HF60 fed. Serum cholesterol and triglyceride levels were elevated with the HF60 diet and decreased to control levels when ACNs from either SB or BB were included in the drinking water. Serum leptin levels were consistently decreased to control low fat levels in those ACN treatments in which measures of body fat were decreased. Administering purified ACNs from BB and strawberry via drinking water prevented the development of dyslipidemia and obesity in mice, but feeding diets containing whole berries or purple corn (PC) ACNs did not alter the development of obesity.

This study explored the dose‐dependent effect of oat cereal β‐glucan on improving metabolic indexes of obesity mice. C57‐Bl mice were randomized to chow diet (N) group and high fat diet group and other three doses of oat β‐glucan groups (low β‐glucan, medium β‐glucan, and high β‐glucan). Energy intake, glucose, lipids, and appetite related hormones were tested. Dose‐dependent relation was observed on oat β‐glucan doses and body weight change, average energy intake, total cholesterol, HDL cholesterol, plasma neural peptide Y, arcuate neural peptide Y mRNA, and arcuate neural peptide Y receptor 2 mRNA level. Oat β‐glucan helped to increase plasma peptide Y‐Y and intestine peptide Y‐Y expression in obesity mice.

The seeds of buckwheat (Fagopyrum esculentum Moench L.) were dehulled and then, following milling, extruded on a counter rotating, twin‐screw extruder with the different barrel temperature profiles: 120, 160, and 200°C. After extrusion cooking process, the following compounds were analyzed: free and conjugated phenolic acids, total polyphenols (TPC), tocopherols (T) and tocotrienols (T3), inositol phosphates (IP), reduced glutathione (GSH), and melatonin (MLT). The antioxidant capacity and superoxide dismutase‐like activity (SOD‐like activity) were determined in the groats and extrudates. Extrusion caused a significant decrease in all the compounds tested, except for phenolic acids. The content of IP decreased by 13%, that of GSH by 42%, and that of T + T3 by 62%. A three‐fold lower level of MLT and TPC was noted whereas the SOD‐like activity disappeared when compared to the nonextruded material. A two‐fold higher content of phenolic acids (free and released from ester bonds) was observed. In spite of the clear decrease in the investigated antioxidants, the extruded dehulled buckwheat seeds contained still significant content of bioactive compounds, which resulted in as little as an average 10% decrease of the antioxidant capacity.

A “prebiotic” is a nondigestible food ingredient whose beneficial effects on the host result from the selective stimulation of growth and/or activity of members of the bacterial community that inhabits the human bowel (the gut microbiota). Although much of the prebiotic literature focuses on nondigestible oligosaccharides, such as oligofructose, most dietary fibres that are fermentable carbohydrates could be considered as prebiotics. Early studies suggested that colonic bacteria were risk factors for colon cancer. However, altering the composition or metabolic activity of the bowel microbiota through the use of dietary fibre might be important in reducing the prevalence of colorectal cancer. Mechanisms for beneficial effects of prebiotics might include changing the activity of exogenous carcinogens through modulating metabolic activation and/or detoxification, or stimulating the production of the short‐chain fatty acid, butyrate. However, modern analytical techniques suggest that an important consequence of a modified bacterial community could be a change in the expression not only of a range of different bacterial genes in bowel contents, but also in the bowel mucosa of the host. Analogous with observations with probiotics, the stimulation of cytokines and modification of immune responses could be important in producing beneficial effects. Compared with transitory effects of probiotics, the prebiotic action of fermentable carbohydrates potentially provide the opportunity for sustainable modulation of activity of the gut microbiota. However, their mechanisms of action in humans are speculative, and research aimed at providing an integrated view of the gut microbiota and dietary fibre nutrition of humans needs to be developed.

Vi khuẩn lam được tìm thấy trong hồ, ao, sông và vùng nước lợ trên toàn thế giới. Trong trường hợp phát triển quá mức như hình thành tảo nở, những vi khuẩn này có thể sản xuất độc tố tự nhiên với số lượng gây độc cho động vật có vú, bao gồm cả con người. Các cyanotoxin này bao gồm peptide vòng và alcaloid. Trong số các peptide vòng có microcystins và nodularins. Các alcaloid bao gồm anatoxin-a, anatoxin-a(S), cylindrospermopsin, saxitoxin (STXs), aplysiatoxins và lyngbyatoxin. Cả phương pháp sinh học và hóa học đều được sử dụng để xác định cyanotoxin. Các thử nghiệm sinh học và thử nghiệm hóa sinh là không đặc hiệu, do đó chỉ có thể được sử dụng như là phương pháp sàng lọc. HPLC có một số triển vọng tốt. Để phát hiện những độc tố này, có thể sử dụng các thiết bị phát hiện khác nhau, từ quang phổ UV đơn giản tới phát hiện huỳnh quang và nhiều loại MS khác nhau. Vấn đề lớn nhất trong việc xác định độc tố vi khuẩn lam là sự thiếu hụt tài liệu tham khảo cho tất cả các độc tố liên quan. Nói chung, dữ liệu độc tính về cyanotoxin khá hiếm. Phần lớn dữ liệu độc tính được biết đến là của microcystin-LR. Đối với nodularins, dữ liệu từ một vài nghiên cứu trên động vật có sẵn. Đối với các alcaloid, dữ liệu độc tính giới hạn tồn tại cho anatoxin-a, cylindrospermopsin và STX. Đánh giá rủi ro cho việc tiếp xúc cấp tính có thể liên quan đến một số loại tiếp xúc. Tuy nhiên, chưa có liều tham khảo cấp tính nào được phát deriv chính thức cho đến nay. Đối với STX(s), nhiều quốc gia đã thiết lập các mức độ tolérance trong động vật hai mảnh vỏ, nhưng các giới hạn này được đặt ra với quan điểm STX(s) như là biotoxins, tích lũy trong hải sản. Các quy định chính thức cho các cyanotoxin khác chưa được thiết lập, mặc dù một số giá trị hướng dẫn (tạm thời) đã được đưa ra cho microcystins trong nước uống bởi WHO và một số quốc gia.