Physicochemical, textural and viscoelastic properties of palm diacylglycerol bakery shortening during storage

BACKGROUND: Diacylglycerol (DAG), which has health-enhancing properties, is sometimes added to bakery shortening to produce baked products with enhanced physical functionality. Nevertheless, the quantity present is often too little to exert any positive healthful effects. This research aimed to produce bakery shortenings containing significant amounts of palm diacyglycerol (PDG). Physicochemical, textural and viscoelastic properties of the PDG bakery shortenings during 3 months storage were evaluated and compared with those of commercial bakery shortening (CS). RESULTS: PDG bakery shortenings (DS55, DS64 and DS73) had less significant increments in slip melting point (SMP), solid fat content (SFC) and hardness during storage as compared to CS. Unlike CS, melting behaviour and viscoelastic properties of PDG bakery shortenings remained unchanged during storage. As for polymorphic transformation, CS contained only β crystals after 8 weeks of storage. PDG bakery shortenings managed to retard polymorphic transformation for up to 10 weeks of storage in DS55 and 12 weeks of storage in DS64 and DS73. CONCLUSION: PDG bakery shortenings had similar if not better storage stability as compared to CS. This is mainly due to the ability of DAG to retard polymorphic transformation from β′ to β crystals. Thus, incorporation of DAG improved physical functionality of bakery shortening

EFFECTS OF VITAMIN C SUPPLEMENTATION ON THE CHRONIC PHASE OF CHAGAS DISEASE

Introduction: In order to examine the effectiveness of vitamin C (ascorbic acid) in combating the oxidative insult caused by Trypanosoma cruzi during the development of the chronic phase of Chagas disease, Swiss mice were infected intraperitoneally with 5.0 × 104 trypomastigotes of T. cruzi QM1strain. Methods: Mice were given supplements of two different doses of vitamin C for 180 days. Levels of lipid oxidation (as indicated by thiobarbituric acid reactive substances-TBARS), total peroxide, vitamin C, and reduced glutathione were measured in the plasma, TBARS, total peroxide and vitamin C were measured in the myocardium and histopathologic analysis was undertaken in heart, colon and skeletal muscle. Results: Animals that received a dose equivalent to 500 mg of vitamin C daily showed increased production of ROS in plasma and myocardium and a greater degree of inflammation and necrosis in skeletal muscles than those that received a lower dose or no vitamin C whatsoever. Conclusion: Although some research has shown the antioxidant effect of vitamin C, the results showed that animals subject to a 500 mg dose of vitamin C showed greater tissue damage in the chronic phase of Chagas disease, probably due to the paradoxical actions of the substance, which in this pathology, will have acted as a pro-oxidant or pro-inflammatory

Novel loci affecting iron homeostasis and their effects in individuals at risk for hemochromatosis

Variation in body iron is associated with or causes diseases, including anaemia and iron overload. Here, we analyse genetic association data on biochemical markers of iron status from 11 European-population studies, with replication in eight additional cohorts (total up to 48,972 subjects). We find 11 genome-wide-significant (P<5 × 10(-8)) loci, some including known iron-related genes (HFE, SLC40A1, TF, TFR2, TFRC, TMPRSS6) and others novel (ABO, ARNTL, FADS2, NAT2, TEX14). SNPs at ARNTL, TF, and TFR2 affect iron markers in HFE C282Y homozygotes at risk for hemochromatosis. There is substantial overlap between our iron loci and loci affecting erythrocyte and lipid phenotypes. These results will facilitate investigation of the roles of iron in disease

Impact of common genetic determinants of Hemoglobin A1c on type 2 diabetes risk and diagnosis in ancestrally diverse populations : A transethnic genome-wide meta-analysis

Background Glycated hemoglobin (HbA1c) is used to diagnose type 2 diabetes (T2D) and assess glycemic control in patients with diabetes. Previous genome-wide association studies (GWAS) have identified 18 HbA1c-associated genetic variants. These variants proved to be classifiable by their likely biological action as erythrocytic (also associated with erythrocyte traits) or glycemic (associated with other glucose-related traits). In this study, we tested the hypotheses that, in a very large scale GWAS, we would identify more genetic variants associated with HbA1c and that HbA1c variants implicated in erythrocytic biology would affect the diagnostic accuracy of HbA1c. We therefore expanded the number of HbA1c-associated loci and tested the effect of genetic risk-scores comprised of erythrocytic or glycemic variants on incident diabetes prediction and on prevalent diabetes screening performance. Throughout this multiancestry study, we kept a focus on interancestry differences in HbA1c genetics performance that might influence race-ancestry differences in health outcomes. Methods & findings Using genome-wide association meta-analyses in up to 159,940 individuals from 82 cohorts of European, African, East Asian, and South Asian ancestry, we identified 60 common genetic variants associated with HbA1c. We classified variants as implicated in glycemic, erythrocytic, or unclassified biology and tested whether additive genetic scores of erythrocytic variants (GS-E) or glycemic variants (GS-G) were associated with higher T2D incidence in multiethnic longitudinal cohorts (N = 33,241). Nineteen glycemic and 22 erythrocytic variants were associated with HbA1c at genome-wide significance. GS-G was associated with higher T2D risk (incidence OR = 1.05, 95% CI 1.04-1.06, per HbA1c-raising allele, p = 3 x 10-29); whereas GS-E was not (OR = 1.00, 95% CI 0.99-1.01, p = 0.60). In Europeans and Asians, erythrocytic variants in aggregate had only modest effects on the diagnostic accuracy of HbA1c. Yet, in African Americans, the X-linked G6PD G202A variant (T-allele frequency 11%) was associated with an absolute decrease in HbA1c of 0.81%-units (95% CI 0.66-0.96) per allele in hemizygous men, and 0.68%-units (95% CI 0.38-0.97) in homozygous women. The G6PD variant may cause approximately 2% (N = 0.65 million, 95% CI0.55-0.74) of African American adults with T2Dto remain undiagnosed when screened with HbA1c. Limitations include the smaller sample sizes for non-European ancestries and the inability to classify approximately one-third of the variants. Further studies in large multiethnic cohorts with HbA1c, glycemic, and erythrocytic traits are required to better determine the biological action of the unclassified variants. Conclusions As G6PD deficiency can be clinically silent until illness strikes, we recommend investigation of the possible benefits of screening for the G6PD genotype along with using HbA1c to diagnose T2D in populations of African ancestry or groups where G6PD deficiency is common. Screening with direct glucose measurements, or genetically-informed HbA1c diagnostic thresholds in people with G6PD deficiency, may be required to avoid missed or delayed diagnoses.Peer reviewe

Measurement of 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl by high performance liquid chromatography-electrospray ionisation mass spectrometry

Reverse phase high performance liquid chromatography coupled to electrospray ionisation mass spectrometry and tandem mass spectrometry has allowed quantitative measurement of a stable nitroxide, 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl (4-hydroxy-tempo), the latter with high sensitivity

Biochemical changes and cytotoxicity associated with methionine depletion in paediatric central nervous system tumour cell lines

The aim of this study was to investigate the importance of the extent and duration of methionine depletion as a cause of cytotoxicity for CNS tumour cell lines, and also to investigate the associated in vitro cellular biochemical responses. MATERIALS AND METHODS: Cell growth inhibition was assayed by the SRB assay. Intracellular methionine levels were measured by GC/MS following dervatization with MTBSTFA. After methionine depletion, methionine synthase and MGMT activities were also determined. Glutathione levels were assayed by HPLC after derivatization with OPA. RESULTS: Medulloblastoma (Daoy) and glioma (D54) cells were found to be methionine dependent and effects on proliferation, apoptosis and clonogenic survival were dependent on time and degree of methionine depletion. Methionine depletion also caused a demonstrable decrease in L-methionine levels and an increase in glutathione levels for both cell lines, with a decrease in MGMT activity for Daoy cells. CONCLUSION: Daoy and D54 cells are methionine dependent; the degree and duration of methionine depletion is related to cell death. The associated biochemical changes in MGMT and glutathione may be expected to modulate chemosensitivity and this will be investigated in future studies

Methionine restriction reduces the chemosensitivity of central nervous system tumour cell lines

The aim of this study was to investigate the effects of methionine depletion with cytotoxic agents that are potentially influenced by depletion of methionine, and are known to have a role in CNS tumour treatments for children. MATERIALS AND METHODS: Cytotoxicity studies and synergistic interactions were assayed by SRB assay. Glutathione levels were assayed by HPLC after derivatization with OPA. MGMT activity was determined by a restriction endonuclease inhibition assay. RESULTS: Methionine depletion causes a demonstrable increase in glutathione levels for medulloblastoma (Daoy) and glioma (D54) cells, with a decrease in MGMT activity for Daoy cells. For both cell lines, methionine depletion reduces their sensitivity to a range of chemotherapy agents that interface at the level of methionine metabolism, namely temozolomide, cisplatin and methotrexate. CONCLUSION: The results show that methionine depletion increases the resistance of tumour cells to the chemotherapeutic agents tested. However, in methionine-replete conditions, we have demonstrated synergistic activity for various combinations of chemotherapeutic agents that are hitherto unreported and may have clinical utility for the treatment of children with CNS tumours