No description available.

The determination of total thiamin, free thiamin, thiamin di phosphate (TDP) plus thiamin triphosphate (TTP), and total α- hydroxyethylthiamin (HET) levels in rat brain in control, deficient, oxythiamin- (OTH) and pyrithiamin- (PTH) treated rats was accomplished. It was found that the TDP + TTP/thiamin ratio observed in the thiamin-deficient, OTH- and PTH-treated rats was constant and did not differ from the ratio observed in the control rat brains. The brain levels of TDP + TTP decreased to 39% and 12% of the control thiamin levels in deficient and PTH-treated rats respectively. The brain HET and TDP + TTP levels of the OTH-treated rats were not significantly different from the controls. The HET levels in the PTH rats decreased significantly ( α = 0.005) by treatment day 4 and decreased to one-seventh of the control values in the terminal stages. A significant drop in the HET levels from the control levels was interpreted to mean that the pyruvate utilization was significantly impaired in the brain.

No description available.

published_or_final_version / Biochemistry / Doctoral / Doctor of Philosophy

Call number: LD2668 .T4 1950 W3 / Master of Science

Acute respiratory infections (ARI) are a major global cause of morbidity and mortality. Vitamin D deficiency has been reported to associate with susceptibility to ARI and with greater severity and poorer control of asthma and chronic obstructive pulmonary disease (COPD). Clinical trials of vitamin D for the prevention of ARI have yielded heterogeneous results, with some showing protection and others not. This may reflect variation in the frequency of genetic variants influencing response to vitamin D supplementation in different populations. The impact that genetic variation in the vitamin D pathway has on vitamin D status, disease phenotype and response to vitamin D supplementation in prevention of ARI has not been comprehensively investigated. Methods: I conducted: 1. A systematic review and meta-analysis of clinical studies which have investigated vitamin D as a potential therapy for ARI; 2. Three cross-sectional studies (in n=297 adult asthma patients, n=278 COPD patients, and n=272 older adults) to investigate potential environmental determinants (lifestyle and anthropometric) and genetic determinants (35 single nucleotide polymorphisms [SNP] in 11 vitamin D related genes) of serum 25-hydroxyvitamin D concentration (25[OH]D) and clinical phenotype; 3. Three prospective studies investigating the influence of genetic variation in the vitamin D pathway on a) susceptibility to ARI (main effects analysis) and b) efficacy of vitamin D supplementation for the prevention of ARI (interaction analysis). Results: My systematic review identified consistent reports of an inverse association between vitamin D status and risk of ARI in observational studies, and heterogeneous reports from clinical trials. My cross-sectional studies identified a range of classical environmental factors which predict vitamin D status in the three study populations, but did not identify any genetic variants in the vitamin D pathway that associate with vitamin D status. I identified an association between vitamin D deficiency and decreased lung function in COPD patients, but no associations between vitamin D deficiency and asthma phenotype. Finally, my analysis identified a haplotype of 5 single nucleotide polymorphisms in the vitamin D receptor (VDR) gene which significantly modify the effect of vitamin D supplementation on risk of upper respiratory infection in COPD patients. Conclusions: I identified environmental determinants that predict 25(OH)D concentrations in all three study populations, but only found an association between vitamin D deficiency and disease severity in COPD patients. Furthermore, I identified a haplotype in VDR which modifies the effect of vitamin D supplementation in COPD patients to result in a significantly reduced risk of ARI.

Papua New Guinea has been classified by the World Health Organisation as an area where clinical vitamin A deficiency (VAD) exists. This is at variance with the experience of the local physicians who do not encounter classical VAD in clinical practice. This pilot study was carried out to resolve this contradiction, since many suggestions have been made to fortify foods with Vitamin A. If done in the absence of concrete data to back up this classification, it could take the focus away from the real problem as well as potentially create problems of Vitamin A toxicity. Therefore, answers from this study could have far reaching implications in a country such as PNG, which has high childhood mortality and limited financial and manpower resources. The objective of this study was to determine the vitamin A status and identify risk factors of VAD in children aged 6 months to 6 years in a rural area of Papua New Guinea. The survey was carried out in the Ramu region of Madang province. Households and children were randomly selected and standard questionnaires were used to collect information about diet, previous illnesses and night blindness. The weight and height of all children was recorded and an ocular and physical examination carried out by trained personnel. In addition, haemoglobin estimation and examination of blood films for malaria parasites was carried out in all the children. In a randomly selected number of children, estimations of serum retinol and other micronutrient levels were carried out. Results: A total of 609 children were enrolled in the study. Biochemical parameters were studied in 106 of them .The mean age of the children was 35 months. Possible night blindness was reported in 4 children. No xerophthalmia was seen. The prevalence of serum retinol levels ( 0.7 (mol/L (WHO suggested cut off values for subclinical VAD) was 10.3%. Anthropometric indicators indicated a high proportion of the children had stunting and wasting or both. Analysis of dietary patterns, maternal literacy, food availability and other surrogate indicators indicated that the population is at mild-moderate risk of developing VAD. In conclusion, no evidence of clinical vitamin A deficiency was found. Subclinical vitamin A deficiency seemed to occur in this population at a level of mild-moderate public health importance. Further studies need to be carried out to assess the situation in different areas in PNG before policy decisions can be made with regards to mass vitamin A supplementation.

This thesis describes an investigation of the effects of vitamin A deficiency on gut function, The central hypothesis to be tested was that acute vitamin A deficiency affects glucose uptake from the small intestine- The hypothesis was tested using a system involving perfusion of isolated segments of the small intestine in the anaesthetized rat. The system was used to study effects on glucose uptake under steady-state conditions. In the initial part of the study, experiments were diverted towards setting up the system for measuring steady-state uptake, and determining the relative contributions of active uptake and diffusion. Phenol red was found to be a reliable non-absorbable marker for determining net water movement. Phlorizin, generally at 1 mmol/L, was used as a competitive (reversible) inhibitor of active uptake. It is difficult however to confirm complete inhibition of active uptake by phlorizin because of the limited solubility of the inhibitor. The kinetics of glucose uptake f ram intra-luminal maltose were found to be, in general, not significantly different from those applying to the uptake of glucose from an equivalent glucose solution. Maltase activity in the perfused gut segment was found to be sufficient to hydrolyse most of the maltose (80 per cent or more) in the solution being perfused, a much greater proportion than was absorbed. Glucose absorptive capacity, measured on an intestinal dry weight basis, was greatest in the duodenum and progressively less in the jejunum and ileum. The rate of water uptake f ran the gut was increased by the presence of glucose in the lumen, and was linked to glucose uptake as shown by the inhibition of water uptake by phlorizin. Uptake of glucose by solvent drag was demonstrated by showing an increased rate of glucose uptake when the rate of water uptake was increased by perfusing a solution of reduced osmotic pressure. In the experiment a low intra-luminal glucose concentration was used to preclude net uptake by diffusion and active uptake was blocked with phlorizin. This process was further investigated using streptozotocin-diabetic rats in which the diabetes establishes a hyperosomotic blood with hyperglycaemia. Uptake by solvent drag was more obvious in diabetic animals. A back-diffusion (exsorption) of glucose from the tissues to the lumen was also shown; the rate being proportional to plasma glucose concentration. Vitamin A deficiency was established in weanling rats after 6-7 weeks feeding on a diet based on wheat starch, coconut oil, and casein washed with hot ethanol, together with vitamins and minerals. The vitamin A deficiency led to classic eye signs and was reversed by the addition to the diet of retinoic acid (5 g/g diet). Vitamin A deficiency decreased intestinal mucus production (dry weight) but had no detectable effect on the histology of the villous epithelium as shown under the light microscope. Using perfusion experiments it was shown that vitamin A deficiency had no significant effect on the rate of active uptake of glucose, but that deficiency increased the rate of passive uptake.

Thesis (Ph. D.)--University of Hong Kong, 1984.

Objective：Low vitamin D has been implicated in the development of type 2 diabetes. However, whether vitamin D continues to have a clinically significant effect in existing diabetes is unclear. The objective of this study was to examine the association of serum vitamin D with glycemic control in established type 2 diabetes. Methods: This was a retrospective analysis of medical records. Characteristics of 487 patients with type 2 diabetes were stratified by vitamin D status and serum glycosylated hemoglobin (HbA1c). Vitamin D deficiency among the subjects was studied. The relationship between vitamin D and glycemic control was explored by multiple linear regression, multivariate analysis of variance (MANOVA) and chi-square test. Patients were stratified into overweight and non-overweight group based on body mass index (BMI), and the association of serum vitamin D concentration with glycemic control was evaluated in each group. Insulin resistance and C-peptide as mediators between vitamin D and HbA1c was tested. The impact of vitamin D on cholesterol metabolism was also assessed. Results: (1) Vitamin D deficiency was highly prevalent, accounting for 88.3% of the study sample. (2) Serum vitamin D levels were significantly inversely associated with serum HbA1c. This correlation was stronger in overweight group than in non-overweight group. There was no significant relationship between serum vitamin D levels and fasting plasma glucose (FPG). HbA1c was significantly lower in vitamin D insufficiency group than in vitamin D severe deficiency group. (3) Insulin resistance partially mediated the association between vitamin D and HbA1c. (4) No significant association of Vitamin D with low density lipoprotein (LDL) or high density lipoprotein (HDL) was found in this study. Conclusions: There was an inverse association between serum vitamin D levels and HbA1c. The inverse correlation of serum vitamin D level and HbA1c was stronger in overweight group than in non-overweight group, which indicates patients with obesity might benefit more from vitamin D supplementation. / published_or_final_version / Public Health / Master / Master of Public Health