• Fat soluble vitamins
• Oil type
• Particle size
• Pickering emulsion
• Protein concentration

• anti-inflammation
• gut microbiota
• inflammatory bowel disease
• intestinal barrier
• oxidative stress
• vitamin E

• No.2022YFF1100200 the Key Project of State Key R & D Program, China
• No.2021JJ31075 the Natural Science Foundation of Hunan Province, China
• 2019TP1029 the Program for Science & Technology Innovation Platform of Hunan Province

• drug delivery
• nanocarriers
• pharmaceutical dosage form
• pharmacokinetics of vitamins
• vitamins

• child care
• fortified food
• micronutrients
• nutritional deficiencies
• vitamin E

• Child
• Humans
• alpha-Tocopherol
• Food, Fortified
• Malnutrition
• Vitamin E Deficiency/complications
• Vitamin E Deficiency/epidemiology
• Nutritional Status

• isolated vitamin E deficiency
• lipid transfer protein
• polyphosphoinositide
• tocopherol

• Ataxia with vitamin E deficiency (AVED)
• Intracellular lipid transport
• Vitamin E
• α-Tocopherol
• α-Tocopherol transfer protein

• Animals
• Carrier Proteins/genetics
• Vitamin E
• Vitamin E Deficiency
• alpha-Tocopherol

• C-T complexes
• absorption
• fluorescence
• lifetimes
• photooxidation
• time-resolved
• tocopherols

• Argon/chemistry
• Dimerization
• Free Radical Scavengers/chemistry
• Hexanes/chemistry
• Oxidation-Reduction
• Photochemical Processes
• Solvents
• Spectrometry, Fluorescence
• Spectrophotometry
• Stereoisomerism
• Tocopherols/chemistry
• Tocopherols/radiation effects
• Ultraviolet Rays

• 010/RID/2018/19 The Minister of Science and Higher Education
• 17.610.011-110 The Minister of Science and Higher Education

Recent advances in the field of nutrigenetics have provided evidence on how genetic variations can impact the individuals' response to dietary intakes. An objective and reliable assessment of dietary exposures should rely on combinations of methodologies including frequency questionnaires, short-term recalls or records, together with biological samples to evaluate markers of intake or status and to identify genetic susceptibilities. In an attempt to present current knowledge on how genetic fingerprints contribute to an individual's nutritional status, we present a review of current literature describing associations between genetic variants and levels of well-established biomarkers of vitamin status in free-living and generally healthy individuals. Based on the outcomes of candidate gene, genome-wide-association studies and meta-analyses thereof, we have identified several single nucleotide polymorphisms (SNPs) involved in the vitamins' metabolic pathways. Polymorphisms in genes encoding proteins involved in vitamin metabolism and transport are reported to have an impact on vitamin D status; while genetic variants of vitamin D receptor were most frequently associated with health outcomes. Genetic variations that can influence vitamin E status include SNPs involved in its uptake and transport, such as in SCAR-B1 gene, and in lipoprotein metabolism. Variants of the genes encoding the sodium-dependent vitamin C transport proteins are greatly associated with the body's status on vitamin C. Regarding the vitamins of the B-complex, special reference is made to the widely studied variant in the MTHFR gene. Methodological attributes of genetic studies that may limit the comparability and interpretability of the findings are also discussed. Our understanding of how genes affect our responses to nutritional triggers will enhance our capacity to evaluate dietary exposure and design personalized nutrition programs to sustain health and prevent disease.

• SNPs
• diet
• genes
• genetic variants
• nutrigenetics
• nutritional status
• vitamins

• Feeding system
• Gene expression
• Sheep
• Vitamin E

Forty-four different animal biles obtained from both invertebrates and vertebrates (including human bile) have been used for centuries for a host of maladies in traditional Chinese medicine (TCM) beginning with dog, ox and common carp biles approximately in the Zhou dynasty (c. 1046-256 BCE). Overall, different animal biles were prescribed principally for the treatment of liver, biliary, skin (including burns), gynecological and heart diseases, as well as diseases of the eyes, ears, nose, mouth and throat. We present an informed opinion of the clinical efficacy of the medicinal uses of the different animal biles based on their presently known principal chemical components which are mostly steroidal detergent-like molecules and the membrane lipids such as unesterified cholesterol and mixed phosphatidylcholines and sometimes sphingomyelin, as well as containing lipopigments derived from heme principally bilirubin glucuronides. All of the available information on the ethnopharmacological uses of biles in TCM were collated from the rich collection of ancient Chinese books on materia medica held in libraries in China and United States and the composition of various animal biles was based on rigorous separatory and advanced chemical identification techniques published since the mid-20^th century collected via library (Harvard’s Countway Library) and electronic searches (PubMed and Google Scholar). Our analysis of ethnomedical data and information on biliary chemistry shows that specific bile salts, as well as the common bile pigment bilirubin and its glucuronides plus the minor components of bile such as vitamins A, D, E, K, as well as melatonin (N-acetyl-5-methoxytryptamine) are salutary in improving liver function, dissolving gallstones, inhibiting bacterial and viral multiplication, promoting cardiac chronotropsim, as well as exhibiting anti-inflammatory, anti-pyretic, anti-oxidant, sedative, anti-convulsive, anti-allergic, anti-congestive, anti-diabetic and anti-spasmodic effects. Pig, wild boar and human biles diluted with alcohol were shown to form an artificial skin for burns and wounds one thousand years ago in the Tang dynasty (618-907 CE). Although various animal biles exhibit several generic effects in common, a number of biles appear to be advantageous for specific therapeutic indications. We attempt to understand these effects based on the pharmacology of individual components of bile as well as attempting to identify a variety of future research needs.

• Bile acids
• Bile pigments
• Bilirubinates
• Liquid crystals
• Materia medica
• Mixed micelles
• Bear bile
• Ox gallstones
• Paleo-pharmacology
• Phospholipids

• Animals
• Bile/chemistry
• China
• Ethnopharmacology/history
• History, 19th Century
• History, 20th Century
• History, 21st Century
• History, Ancient
• Humans
• Materia Medica/history
• Materia Medica/therapeutic use
• Medicine, Chinese Traditional/history
• Medicine, Chinese Traditional/methods
• Organotherapy/history
• Treatment Outcome

• maize
• tocopherols
• qtl mapping

• Biosynthetic Pathways/genetics
• Chromosome Segregation/genetics
• Chromosomes, Plant/genetics
• Genetic Association Studies
• Genetic Linkage
• Genetic Markers
• Haplotypes/genetics
• Humans
• Inheritance Patterns/genetics
• Phenotype
• Physical Chromosome Mapping
• Polymorphism, Single Nucleotide/genetics
• Quantitative Trait Loci/genetics
• Quantitative Trait, Heritable
• Tocopherols/metabolism
• Zea mays/genetics
• Zea mays/metabolism

To further investigate the potential role of α-tocopherol in maintaining immuno-homeostasis in bovine cells (Madin-Darby bovine kidney epithelial cell line), we undertook in vitro experiments using recombinant TNF-α as an immuno-stimulant to simulate inflammation response in cells with or without α-tocopherol pre-treatment. Using microarray global-profiling and IPA (Ingenuity Pathways Analysis, Ingenuity^® Systems, http://www.ingenuity.com) data analysis on TNF-α-induced gene perturbation in those cells, we focused on determining whether α-tocopherol treatment of normal bovine cells in a standard cell culture condition can modify cell’s immune response induced by TNF-α challenge. When three datasets were filtered and compared using IPA, there were a total of 1750 genes in all three datasets for comparison, 97 genes were common in all three sets; 615 genes were common in at least two datasets; there were 261 genes unique in TNF-α challenge, 399 genes were unique in α-tocopherol treatment, and 378 genes were unique in the α-tocopherol plus TNF-α treatment. TNF-α challenge induced significant change in gene expression. Many of those genes induced by TNF-α are related to the cells immune and inflammatory responses. The results of IPA data analysis showed that α-tocopherol-pretreatment of cells modulated cell’s response to TNF-α challenge. In most of the canonical pathways, α-tocopherol pretreatment showed the antagonistic effect against the TNF-α-induced pro-inflammatory responses. We concluded that α-tocopherol pre-treatment has a significant antagonistic effect that modulates the cell’s response to the TNF-α challenge by altering the gene expression activities of some important signaling molecules.

• alpha-tocopherol
• bovine
• inflammatory response
• transcription
• tumor necrosis factor

Using global expression profiling and pathway analysis on α-tocopherol-induced gene perturbation in bovine cells, this study has generated comprehensive information on the physiological functions of α-tocopherol. The data confirmed α-tocopherol is a potent regulator of gene expression and α-tocopherol possesses novel transcriptional activities that affect essential biological processes. The genes identified fall within a broad range of functional categories and provide the molecular basis for its distinctive effects. Enrichment analyses of gene regulatory networks indicate α-tocopherol alter the canonical pathway of lipid metabolism and transcription factors SREBP1 and SREBP2, (Sterol regulatory element binding proteins), which mediate the regulatory functions of lipid metabolism. Transcription factors HNF4-α (Hepatocyte nuclear factor 4), c-Myc, SP1 (Sp1 transcription factor), ESR1 (estrogen receptor 1, nuclear), and androgen receptor, along with several others, were centered as the hubs of transcription regulation networks. The data also provided direct evidence that α-tocopherol is involved in maintaining immuno-homeostasis through targeting the C3 (Complement Component 3) gene.

• ESR1
• bovine cells
• gene regulation
• lipid metabolism
• α-tocopherol

Various factors impact the severity of malaria, including the nutritional status of the host. Vitamin E, an intra and extracellular anti-oxidant, is one such nutrient whose absence was shown previously to negatively affect Plasmodium development. However, mechanisms of this Plasmodium inhibition, in addition to means by which to exploit this finding as a therapeutic strategy, remain unclear.

α-TTP knockout mice were infected with Plasmodium berghei NK65 or Plasmodium yoelii XL-17, parasitaemia, survival rate were monitored. In one part of the experiments mice were fed with a supplemented diet of vitamin E and then infected. In addition, parasite DNA damage was monitored by means of comet assay and 8-OHdG test. Moreover, infected mice were treated with chloroquine and parasitaemia and survival rate were monitored.

Inhibition of α-tocopherol transfer protein (α-TTP), a determinant of vitamin E concentration in circulation, confers resistance to malarial infection as a result of oxidative damage to the parasites. Furthermore, in combination with the anti-malarial drug chloroquine results were even more dramatic.

Considering that these knockout mice lack observable negative impacts typical of vitamin E deficiency, these results suggest that inhibition of α-TTP activity in the liver may be a useful strategy in the prevention and treatment of malaria infection. Moreover, a combined strategy of α-TTP inhibition and chloroquine treatment might be effective against drug resistant parasites.

• Animals
• Antioxidants/metabolism
• Carrier Proteins/antagonists & inhibitors
• Carrier Proteins/genetics
• Disease Models, Animal
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Oxidative Stress
• Reactive Oxygen Species/metabolism
• Trypanosoma congolense/immunology
• Trypanosomiasis, African/genetics
• Trypanosomiasis, African/immunology
• Trypanosomiasis, African/veterinary
• Vitamin E/pharmacology
• Vitamin E Deficiency/genetics
• Vitamin E Deficiency/immunology