Obesity is a risk factor for several comorbidities and complications, including iron deficiency anemia. Iron deficiency anemia is a serious global public health problem, with a worldwide prevalence. The high prevalence of obesity in combination with iron deficiency incidence observed in different age and sex categories suggests an association between obesity and iron status. Obesity may disrupt iron homeostasis, resulting in iron deficiency anemia. The association between obesity and iron deficiency may be due to increased hepcidin levels mediated by chronic inflammation. Hepcidin is a small peptide hormone that functions as a negative regulator of intestinal iron absorption. Significant body weight loss in overweight and obese individuals decreases chronic inflammation and serum hepcidin levels, resulting in improved iron status due to increased iron absorption. However, further randomized controlled trials are required to confirm this effect. Contents 1. Introduction 2. Iron metabolism 3. Hepcidin and iron homeostasis 4. Obesity and low-grade chronic inflammation 5. Association between overweight and obesity, and iron status 6. Effect of weight loss on iron status 7. Future research and clinical implications 8. Conclusions

The epidemic of obesity in developed countries is commonly associated with poor dietary habit and sedentary lifestyle. However, other determinants, including education background and family income, may contribute towards the problem especially in developing countries. This study aimed to determine the influence of socioeconomic status (SES) on obesity among 12-year-old school adolescents in Terengganu, Malaysia. Body weight and height were measured and BMI was categorised based on WHO z-score cut-off points. Information was obtained from self-reported questionnaire on parents’ education background, family income and occupation. A total of 3,798 school adolescents aged 12 years (44% boys and 56% girls) were recruited. There was no significant difference in BMI status between boys and girls, or between rural and urban participants. There were significant differences between BMI categories and gender, household income and SES level within rural areas. In the urban areas, significant differences were found between BMI categories and gender, parents’ occupational and educational level, household income and size, and SES level. A logistic regression model found several SES factors to be predictors of obesity in this population, namely, gender, household size, father’s occupation level, household income level and SES level. Each component of SES has been significantly associated with the BMI category of school adolescents, particularly in the urban areas. This suggests the requirement of multifaceted approaches, including the role of family, society and authorities, in the effort to curtail adolescent obesity.

BackgroundResearch suggests that physical activity plays a role to improve health related- quality of life (QoL), however studies examining the association between physical activity and HRQOL are limited in the paediatric literature. The aim of this study is to explore the relationship between physical activity and HRQoL among Malaysian children.MethodsParticipants (n = 78 normal weight; 78 obese children) aged 9–11 years completed a validated quality of life (QoL) inventory and wore an accelerometer to objectively measure physical activity for 1 week.ResultsPsychosocial Health domain and Total QoL (all p < 0.05) were significantly lower for obese compared to normal weight children. Children who spent more time in sedentary behaviour had significantly lower QoL on Psychosocial Health domain and Total QoL except for the Physical Health domain. There was also a strong positive correlation between QoL and moderate-vigorous physical activity (MVPA) indicating that children who are physically active have a better quality of life.ConclusionsPhysical activity promotion should be emphasised to improve QoL in children.

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Dietary sugars are linked to the development of non-alcoholic fatty liver disease (NAFLD) and dyslipidaemia, but it is unknown if NAFLD itself influences the effects of sugars on plasma lipoproteins. To study this further, men with NAFLD (n = 11) and low liver fat 'controls' (n = 14) were fed two iso-energetic diets, high or low in sugars (26% or 6% total energy) for 12 weeks, in a randomised, cross-over design. Fasting plasma lipid and lipoprotein kinetics were measured after each diet by stable isotope trace-labelling. There were significant differences in the production and catabolic rates of VLDL subclasses between men with NAFLD and controls, in response to the high and low sugar diets. Men with NAFLD had higher plasma concentrations of VLDL 1 -triacylglycerol (TAG) after the high (P<0.02) and low sugar (P<0.0002) diets, a lower VLDL 1 -TAG fractional catabolic rate after the high sugar diet (P<0.01), and a higher VLDL 1 -TAG production rate after the low sugar diet (P<0.01), relative to controls. An effect of the high sugar diet, was to channel hepatic TAG into a higher production of VLDL 1 -TAG (P<0.02) in the controls, but in contrast, a higher production of VLDL 2 -TAG (P<0.05) in NAFLD. These dietary effects on VLDL subclass kinetics could be explained, in part, by differences in the contribution of fatty acids from intra-hepatic stores, and de novo lipogenesis. The present study provides new evidence that liver fat accumulation leads to a differential partitioning of hepatic TAG into large and small VLDL subclasses, in response to high and low intakes of sugars.