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Thesis (PhD)--University of South Australia, 1995

Thesis (M.Ph.)--Georgia State University, 2008. / Title from file title page. Ike Okosun, committee chair; Richard Rothenberg, Rodney Lyn, committee members. Electronic text (73 p.) : digital, PDF file. Description based on contents viewed November 25, 2008. Includes bibliographical references (p. 69-73).

As the obesity epidemic continues to grow, attention has been turned towards the abundance of processed foods and beverages in the Western diet. Controversy has particularly surrounded high fructose corn syrup (HFCS), which is a commonly used sweetener in these products. Our study is designed to not only investigate the metabolic effects resulting from prolonged exposure to a highly sweetened diet, but also to determine the effects of this maternal diet on the offspring. For the study, three specially made, pelleted diets and a control were administered to weight matched groups of female Long Evans rats: Control "Chow" AIN-G93, Group (2) AIN-G93 + 10% HFCS, Group (3) AIN-G93 + 20% HFCS, and Group (4) 20% sucrose. All of the diets were isocaloric and differed only in the amount of added sweetener. At the end of the initial study, a strong phenotypic difference was not determined among the dams; however, postnatal body weights were increased in the pups born to dams raised on sweetened diets groups compared to the Chow-fed dams. Even further, following exposure to a LF or HF diet, the progeny showed altered sensitivity to the obesogenic effects of the diet as was seen in body weights and caloric intake. Glucose homeostasis, plasma triglyceride levels, and liver weights also appeared to be influenced by the maternal and post-weaning diets. To further examine this maternal diet effect, the study was repeated, and experiments were performed while the pups were in utero and also during lactation. Metabolic parameters measured during pregnancy showed a trend towards higher triglycerides in the HFCS dams compared to Chow. Tests during lactation aimed to determine whether the pups were hyperphagic, but showed no significance. Overall, these studies suggest that sweetener components such as sucrose or HFCS used in beverages and processed foods may potentially contribute to the development to the obesity and the metabolic syndrome in offspring. Additionally, HFCS may amplify this effect even further.

Class of 2014 Abstract / Specific Aims: The purpose of this study is to assess whether baseline rates of metabolic monitoring of scheduled atypical antipsychotics are sustained as a result of a pharmacist intervention. Methods: This study was a retrospective chart review assessing rates of metabolic monitoring two months after a pharmacist intervention that utilized a pharmacist-physician metabolic monitoring recommendation form was discontinued. Patients ages 18 years or older with orders for a scheduled atypical antipsychotic were included. Patients with orders for first-generation antipsychotics or who have orders for as needed atypical antipsychotics were excluded. Main Results: Data from the two month post intervention period was compared to those obtained during the pharmacist intervention. For the monitoring of hemoglobin A1c and fasting lipid panels, which improved during the pharmacist intervention, there was a non-statistically significant trend towards decreased monitoring. For hemoglobin A1c, the rates of monitoring decreased from 21.59% to 12.32% (p = 0.09). For fasting lipid panels, monitoring decreased from 39.77% to 28.99% (p = 0.125). Conclusion: A pharmacist intervention utilizing a recommendation form was effective in sustaining the improvement of baseline metabolic monitoring of personal history of diabetes and cardiovascular disease and monitoring of hemoglobin A1c and lipid panels. However, a trend towards decreased monitoring was observed in both the percentage of hemoglobin A1c and lipid panels ordered. Thus, continuing pharmacist intervention may be necessary in order to ensure that baseline metabolic monitoring for atypical antipsychotics occurs.

No description available.

The central nature of nicotinamide in metabolic processes as a part of the NAD and NADP coenzyme systems prompted the synthesis of a series of N-nicotinyl- and N-isonicotinyl-N'- (substituted)ureas as potential metabolite antagonists of the vitamin. The compounds which were synthesized may be represented by the following general structure, where R = hydrogen, methyl, ethyl, n-propyl, isopropyl, n-butyl, t-butyl, n-hexyl, cyclohexyl, phenyl and a-naphthyl. The observed toxicity of the N-nicotinyl-N'-(substituted)urea analogs may be attributed to the formation of a non-functional N-nicotinyl-N'-(substituted)urea-NAD analog through an exchange reaction catalyzed by NAD-ases in the cell. Support for this view was obtained by an in vitro enzymic synthesis of Nnicotinyl- N'-ethylurea-NAD analog employing N-nicotinyl-7- 1 4CN'- ethylurea. The labeled derivative was characterized through spectral, chromatographic, and chemical reaction studies.

PhD (Chemical Pathology),Faculty of Health Sciences, University of the Witwatersrand, 2009 / Introduction: The data published by the Medical Research Council of South Africa demonstrated that cardiovascular disease and diabetes mellitus are the second and tenth leading causes of death in South Africa, respectively (Bradshaw et al.,2003). The prevalence of obesity is higher in the African than Indian population (Puoane et al., 2002), whereas cardiovascular diseases (CVD) and diabetes are more common in the latter population (Omar et al., 1994, Joffe et al., 1994). Diabetes and hypertension has been related with abdominal obesity in a number of studies conducted in the African and mixed-ancestry communities of the Western Cape (Steyn et al., 1996, Levitt et al., 1993). The reason for the high prevalence of obesity in the African population is not known however it is known that the aetiology of obesity involves both environmental and genetic factors (Grundy, 2004). Objective: The main aim of this project was to ascertain the role of metabolic, hormonal, anthropometric and environmental factors in the pathogenesis of obesity-related disorders in two South African ethnic groups namely Indian and African women. These populations were chosen because of the wide differences in risk factors for the development of CVD and diabetes reported in these groups. Subjects and methods: Plasma and serum samples were taken during a 5-hour OGTT from 20 lean, 20 obese, 20 obese type 2 diabetic patients, and 10 overweight women of African and Indian origin, i.e. 140 subjects in total. All participants were recruited from an urban population of women residing in the Greater Johannesburg area. Serum insulin, C-peptide, proinsulin and adipokines were measured using ELISA kits. Fasting plasma glucose, serum cholesterol, HDL-cholesterol and triglycerides levels were measured on the ROCHE MODULAR System. Insulin resistance was calculated using HOMA. Visceral and subcutaneous fat areas were measured using a 5-level CT-scan. Nutrient intake was assessed using a validated quantified food frequency questionnaire. Socio-economic status was estimated from the level of education and the number of selected household amenities. The data collected from the project was analysed by using SAS System for Windows Release 8.02 SAS Institute Inc., Cary, NC, USA 1999-2001. V Results: Results from the study presented in the table below indicate that Indian females were more insulin resistant and had a worse atherogenic lipid profile than African females (statistically higher LDL and triglycerides levels). The greater visceral fat mass in the Indian subjects appears to be associated with triglycerides and correlated with insulin resistance (r=0.554, p<0.05). This effect was not observed in Africans. African females had a higher proportion of their energy intake as carbohydrates than Indians (49.3% and. 45.2%, respectively, p<0.05), whereas Indians had a higher proportion of their total energy intake as fat than Africans (34.0% and 29.9%, respectively, p<0.05). The level of educational attainment and possession of household amenities was lower in the African than Indian group, but this did not significantly influence any of the anthropometric variables. Conclusions: Visceral fat accumulation was greater in diabetic and lean Indian subjects than in diabetic and lean African groups, which may explain their higher risk for obesity-related disorders at lower BMI. Significantly higher HOMA levels in obese Indians and significantly lower proinsulin/insulin ratio in lean and obese Indian women compared to lean and obese African women suggests that lean and obese Indians have better beta-cell proinsulinprocessing efficiency than Africans, probably due to the higher secretory load imposed on beta cells by the higher level of insulin resistance in the Indian subjects. Triglycerides, one of the major components in the diagnostic criteria of metabolic syndrome, were significantly different in the obese group (higher in Indians) and this may lead to the higher prevalence of CVD in the Indian population. Interethnic differences for leptin levels were observed in the lean group of women with higher levels in the Indian subjects. When all non-diabetic subjects were combined serum leptin levels were significantly higher in Indian than African subjects. This is an intriguing result, since obesity is more common in the African than Indian populations of South Africa. Caloric intake was higher in lean African than Indian females. However, the hypothesis that lower leptin levels in lean African females may lead to higher dietary intake and thus an increased prevalence of obesity in this group must be evaluated in a longitudinal study of leptin levels and weight gain. The impact of lower socio-economic status in African than Indian population is not clear; however data from the literature does demonstrate a negative correlation of obesity prevalence with education and income

Childhood obesity and subsequent poor health implications continue to be a critical health concern and recent literature suggests academics may also be under greater strain among these individuals. This study examined the relationship between metabolic health and academic achievement in students “at risk” for drop. Fifteen adolescences participated in an educational camp aimed at developing knowledge of core curriculum by developing design projects. Metabolic health was assessed via biochemical measurements of blood lipid and glucose, resting blood pressure, and anthropometric measurements of height, weight, and waist circumference. Variables were examined individually and as a combined risk score. Academic achievement measurements were results were obtained from district testing. Little association was found between academic achievement and metabolic health. BMI was greater than the 85th percentile for sample. Participants partook in 32.4 minutes/day of moderate-vigorous physical activity during camp. Slight variation between Pre-and Post- measures of academics suggests presence of confounding variables.

The current epidemic of obesity is driven, at least in part, by excessive caloric intake and fat intake has been implicated as a major contributing factor. The mammalian taste system displays marked plasticity, and it has been shown that the detection of fatty acids, the prototypical fat taste stimulus, leads to reduced sensitivity upon prolonged exposure to a high-fat diet. Increased obesity and metabolic disorders in postmenopausal females indicate that the female steroid hormone, estrogen, may contribute to metabolic homeostasis. Sex differences in the taste system were explored using a multidisciplinary approach to examine the ways in which estrogen influences the detection and recognition of fatty acids in the taste system. The findings suggest that estrogen in females is an essential factor in mediating sex differences in fat taste. Moreover, the stimulatory effect of fatty acid taste cell activation is further enhanced by estradiol (E2), suggesting a specific role of E2 in modulating peripheral fat detection. Genes and protein function important for the transduction pathway of fatty acids vary between males and females and these differences exist across the various taste papillae. In vivo support for the effect of estrogens in taste cells was provided by comparing the fatty acid responsiveness in males, intact females, and ovariectomized (OVX) female mice with and without hormone replacement. In general, females detected fatty acids at lower concentrations and the presence of circulating estrogens increased this apparent fat taste sensitivity. To study the long-term effects of fat intake in males and females, a diet-induced obesity model was used. Estrogen loss in females lead to increases in food intake, body weight, adiposity, and fat mass, and ultimately reduced taste cell activity. These metabolic effects were reversed by estrogen replacement in females. Taken together, these data indicate that increased circulating estrogens in the taste system may play a significant role in physiology and chemosensory cellular activation and, in turn, may alter taste driven behavior and overall nutrient intake.