PhD candidate , University of Nottingham Malaysia Campus
To study how FTO gene variants can modulate the effect of diet on body weight and metabolic health
Obesity is caused by a state of positive energy balance, when energy consumption exceeds energy expenditure and results in storage of excess body fat (Spiegelman & Flier, 2001). It has now reached epidemic proportions globally and become a major public health problem. According to the recent research from British medical journal, The Lancet, almost 49% of women and 44% of men in Malaysia were found to be overweight and obese (Ng et al., 2014). Obesity, especially abdominal obesity, is the main cause of metabolic syndrome which includes hypertension, hyperglycemia, hyperinsulinemia, insulin resistance and dyslipidemia (Monteiro & Azevedo 2010). These complications often increase the risk of developing other non-communicable diseases (NCDs) such as cardiovascular disease, stroke, dyslipidemia and type II diabetes. National Health and Morbidity Survey Malaysia 2015 reported that, about 17.5% and 47.7% of Malaysian adults above 18 were suffering from type 2 diabetes mellitus and hypercholesterolemia respectively (Health, 2011). Although the obesity epidemic and excess fat related non-communicable diseases have been certainly driven by lifestyle and environmental factors, it is also suggested that there is an individual variation in response to these factors, suggesting a strong genetic predisposition(Marti, Moreno-Aliaga, Hebebrand, & Martínez, 2004). To combat obesity, lifestyle modification with combination of behavioural changes, reduction in energy intake and increase in physical activity is the most commonly used strategy to reduce weight and prevent weight regain (Jakicic et al., 2001). These strategies might show successfulness in losing weight and improving metabolic risk factors in obese individuals. However, each individual has shown huge variability in weight loss rate in response to these interventions (Bray, 2008). Several interventions have been carried out to identify the potential physiologic and behavioural factors that lead to this variability in weight loss and there are evidences suggest that the differences in such responses are due to genetic factors (Loos & Rankinen, 2005). These findings have suggested that gene variants not only contribute to the development of risk for obesity, but modulate the effect of weight loss intervention. Thus, it is important to study the interaction between gene variants, diet and physical activity and its modulation on body weight and metabolic health.
Abstract: It is well known that omega-3 long-chain polyunsaturated fatty acids (LC-PUFAs) control some key molecular cell mechanisms, resulting in a beneficial role in inflammatory diseases. Such mechanisms are complex and reflect the diversity of their functions, mainly as modulators of the dynamic properties of membranes, regulators of gene expression and as precursors of active mediators. In the present review we aim to summarize the state of the art of the effects and mechanisms by which omega-3 LC-PUFAs such as eicosapentaenoic acid (EPA, C22:5 omega-3) and docosahexaenoic acid (DHA, C22:6 omega-3) regulate different metabolic processes to maintain homeostasis. Thus, we will describe some aspects of these fatty acids—from their structural function in cell membranes to their role as regulators of gene expression, mainly in lipid metabolism. However, further studies are required in order to elucidate these actions and to have a better understanding in regard to the beneficial effects of omega-3 LC-PUFAs in the pathogenesis of several diseases as well as their functions as nutrients with protective action to avoid or delay development of these diseases. Furthermore, it is necessary to highlight the lack of comprehensive studies including nutritional, biochemical, genetic and immune aspects in order to identify specific molecular mechanisms involved in the beneficial effects of consumption of DHA (C22:6 omega-3) and EPA (C22:5 omega-3) and their metabolic derivatives on health promotion.
Pub.: 02 May '17, Pinned: 30 Sep '17