World Congress on
Advanced Nutraceuticals and Functional Foods

I completed my undergraduate degree at Dublin City University (DCU) in B.Sc. (Hons) ‘Genetics and Cell Biology’ in 2013. I obtained my master’s degree from Trinity College Dublin in ‘Translational Oncology’ in 2015. I am in the final year of my PhD, completing a Teagasc Walsh Fellowship in Trinity College Dublin. I have 3 publications to date in the journals: Lung Cancer; Journal of Agriculture and Food Chemistry and The Irish Journal of Agricultural and Food Chemistry.

Rapeseed meal is a low-economic value by-product of rapeseed oil production, which is commonly used as animal feed. However, rapeseed (Brassica napus L.) contains more phenolic compounds than any other oilseed plant. Sinapinic (SA) has been identified as a major insoluble phenolic in rapeseed hulls, and constitutes 70-90% of soluble esterified phenolic acids in rapeseed meal. Phenolic acids, including SA, have known bioactive properties, including ant-inflammatory activity. As part of this project, two phenolic extracts containing SA were generated from Irish rapeseed meal supplied by Donegal Rapeseed Oil Company, Donegal. The anti-inflammatory activity of the extracts and commercial SA were determined. Quantitative polymerase chain reaction (QPCR) and enzyme-linked immunosorbent assays (ELISA) were performed using THP-1 cells, human primary monocytes and human derived peripheral blood mononuclear cells (PBMCs). The anti-inflammatory activities of SA containing extracts I and II were determined using two key inflammatory mediators: TNF-alpha and CXCL8. Extract I significantly increased CXCL8 expression but did not affect TNF-alpha expression. Extract II significantly reduced TNF-alpha expression when assayed at concentrations of 1 and 0.5 mg/mL. Extract II at 1 mg/mL also significantly reduced CXCL8 expression, while significantly increasing CXCL8 gene expression. The anti-inflammatory activity of extract II was also assessed using human monocytes over a period of 3 hours, with 1 mg/mL found to significantly reduce CXCL8, and also reduce TNF-alpha expression. This is also the first study to demonstrate the anti-inflammatory activity of SA in human PBMCs. Extracts containing SA from Irish rapeseed meal could be potentially valuable as an ant-inflammatory agent.

Dr Kao, PhD (1997) in Zoology at North Dakota State University in US, Postdoc Research Associate (1997-2000) at University of Chicago, and a distinguished professor of the National Central University in Taiwan, has his expertise in functional green tea catechin in improving the health. His used animal and cell systems based on responsive body weight changes, fat cell function, and prostate cancer activity discover signaling pathways of epigallocatechin gallate for improving obesity and prostate cancer. He has discovered the results after years of experience in research, evaluation, teaching and administration both in research and education institutions. The foundation is based on body weight loss, adipose tissue evaluation, and endocrine system modulation (Kao, Hiipakka & Liao, 2000) which reflect the catechin-selective effect of green tea on body weight and adipose activity. It allows for further demonstrations for direct effects of tea catechins on fat cell growth, autophagy, adipogeic differentiation, metabolism, and endocrine activity. This approach is responsive to all food and nutraceutical scientists and has a different way of focusing.

Statement of the Problem: Green tea catechins, particularly (-)-epigallocatechin gallate (EGCG), have been reported to regulate obesity and white fat cell activity. This study investigated the effects of EGCG on the expression of autophagy pathway proteins in 3T3-L1 white preadipocytes. Methodology & Theoretical Orientation: 3T3-L1 preadipocytes were treated with EGCG and then cell number and autophagy pathway proteins were measured by the dye exclusion method and Western blot analysis, respectively. Findings: EGCG was found to inhibit preadipocyte growth in a dose- and time-dependent manner, as indicated by decreased cell number. Pretreatment with the respectively early-staged and late-staged autophagy inhibitors, such as 3-methyladenine (3-MA) and chloroquine (CQ), suppressed preadipocyte growth and enhanced further EGCG-decreased cell number. This suggests that a functional process of autophagy is necessary for preadipocytes to grow and that EGCG may act differently from 3- MA and CQ in regulating levels of autophagy pathway proteins. Indeed, EGCG was found to time- and dose-dependently reduce the expression of autophagy pathway proteins, such as Beclin-1, ATG3, ATG5, ATG7, ATG16L1, and ERK proteins, while it increased the level of late-staged autophagy proteins, p62 and LC3β-II. Interestingly, 3-MA tended to increase levels of Beclin-1, ATG3, ATG5, ATG7, ATG16L1, p62, LC3β-II, and ERK proteins, while CQ significantly increased levels of Beclin-1, ATG3, ATG16L1, p62, LC3β-II, and ERK proteins, decreased ATG5, and unaltered ATG7. Pretreatment with 3-MA generally reversed EGCG-induced changes in levels of autophagy proteins. Moreover, pretreatment with CQ enhanced the EGCG-increased levels of p62 and LC3β-II proteins.Conclusion & Significance: These data suggest that EGCG exerts its anti-growth action on preadipocytes via regulation of multiple autophagy proteins and its effects may act differently from autophagy inhibitors 3-MA and CQ. Results of this study possibly support that EGCG can be a therapeutic agent to regulate obesity by autophagy mechanism.

Tamara Al Abdi has completed her postgraduate studies in 2006 from Leeds Metropolitan University in the U.K and is a qualified state registered dietitian with the Academy of nutrition and dietetics and the British Dietetic Association. She has been the lecturer and clinical coordinator of the supervised practice program at the human nutrition department in college of health sciences at Qatar University since 2010. Her research interest is in clinical dietetics and practice in the Middle East as well as promoting the role of dietitians in Qatar.

We aimed to examine the association between soft drink consumption and asthma and lung function among Qatari adults. In the cross-sectional study, we used data from 986 Qatari participants aged 20 years and above attending the Qatar Biobank Study. Usual consumption of soft drink was assessed using a food frequency questionnaire. Lung function was measured by spirometry and asthma was based on self-report. The associations between soft drink consumption and asthma and lung function were assessed using multivariable logistic and linear regression, respectively. In total, 65 participants out of 986 (6.6%) reported having asthma. A clear dose-response relationship between soft drink consumption and asthma was found. High soft drink consumers (≥7 times/week) were 2.60 (95% CI 1.20–5.63) times more likely to have asthma as compared to non-consumers. The association was partly mediated by BMI and inflammation. Diet soft drink consumption was positively associated with asthma (OR 1.12 (95% CI 1.02–1.23)) but not with lung function. Regular soft drink consumption was inversely associated with FEV1, but not with FVC. In conclusion, soft drink consumption is positively associated with asthma in Qatari adults. The association is partly mediated by obesity and inflammation. Limiting soft drink consumption should be taken into consideration for asthma prevention