BackgroundNon-alcoholic fatty liver disease (NAFLD) is caused by multiple factors including hepatic oxidative stress, lipotoxicity, and mitochondrial dysfunction. Obesity is among the risk factors for NAFLD alongside type 2 diabetes mellitus and hyperlipidemia. α- mangostin (α-MG) extracts from the pericarps of mangosteen (Garcinia mangostana Linn.) may regulate high fat diet-induced hepatic steatosis; however the underlying mechanisms remain unknown. The aim of this study was to investigate the regulatory effect of α-MG on high fat diet-induced hepatic steatosis and the underlying mechanisms related to mitochondrial functionality and apoptosis in vivo and in vitro.MethodsSprague Dawley (SD) rats were fed on either AIM 93-M control diet, a high-fat diet (HFD), or high-fat diet supplemented with 25 mg/day mangosteen pericarp extract (MGE) for 11 weeks. Thereafter, the following were determined: body weight change, plasma free fatty acids, liver triglyceride content, antioxidant enzymes (superoxide dismutase, SOD; glutathione, GSH; glutathione peroxidase, GPx; glutathione reductase GRd; catalase, CAT) and mitochondrial complex enzyme activities. In the in vitro study, primary liver cells were treated with 1 mM free fatty acid (FFA) (palmitate: oleate acid = 2:0.25) to induce steatosis. Thereafter, the effects of α-MG (10 μM, 20 μM, 30 μM) on total and mitochondria ROS (tROS, mitoROS), mitochondria bioenergetic functions, and mitochondrial pathway of apoptosis were examined in the FFA-treated primary liver cells.ResultsThe MGE group showed significantly decreased plasma free fatty acids and hepatic triglycerides (TG) and thiorbarbituric acid reactive substances (TBARS) levels; increased activities of antioxidant enzymes (SOD, GSH, GPx, GRd, CAT); and enhanced NADH-cytochrome c reductase (NCCR) and succinate-cytochrome c reductase (SCCR) activities in the liver tissue compared with HFD group. In the in vitro study, α-MG significantly increased mitochondrial membrane potential, enhanced cellular oxygen consumption rate (OCR), decreased tROS (total ROS) and mitoROS (mitochondrial ROS) levels ; reduced Ca2+ and cytochrome c (cyt c) release from mitochondria, and reduced caspases 9 and 3 activities compared with control group.ConclusionThese findings demonstrate α-MG attenuated hepatic steatosis in high fat-diet fed rats potentially through enhanced cellular antioxidant capacity and improved mitochondrial functions as well as suppressed apoptosis of hepatocytes. The findings of study represent a novel nutritional approach on the use of α-MG in the prevention and management of NAFLD.

Inflammatory bowel diseases (IBD) are characterized by wasting and chronic intestinal inflammation triggered by various cytokine-mediated pathways. In recent years, it was shown that T helper 17 (Th17) cells are involved in the pathogenesis of IBD, which makes them an attractive therapeutic target. Th17 cells preferentially produce interleukin (IL)-17A–F as signature cytokines. The role of the interplay between host genetics and intestinal microbiota in the pathogenesis of IBD was demonstrated. Probiotics are live microorganisms that when orally ingested in adequate amounts, confer a health benefit to the host by modulating the enteric flora or by stimulating the local immune system. Several studies indicated the effectiveness of probiotics in preventing and treating IBD (ulcerative colitis, and Crohn’s disease). Furthermore, there is mounting evidence of probiotics selectively targeting the Th17 lineage in the prevention and management of inflammatory and autoimmune diseases such as IBD. This review highlights critical roles of Th17 cells in the pathogenesis of IBD and the rationale for using probiotics as a novel therapeutic approach for IBD through manipulation of Th17 cells. The potential molecular mechanisms by which probiotics modulate Th17 cells differentiation and production are also discussed.

Whether being overweight or obese is associated with increased risk of iron deficiency anemia (IDA) remains controversial. We evaluated the dietary intakes and risk for IDA in relation to body mass index (BMI). One thousand two hundred and seventy-four females aged ≥19 years, enrolled in the third Nutrition and Health Survey in Taiwan (NAHSIT) 2005–2008, were selected. Half of the women were either overweight (24.0%) or obese (25.3%). The overall prevalence of anemia, iron deficiency and IDA among adult women was 19.5%, 8.6% and 6.2%. BMI showed a protective effect on IDA: overweight (odds ratio, OR: 0.365 (0.181–0.736)) and obese (OR: 0.480 (0.259–0.891)) when compared with normal weight. Univariate analysis identified increased IDA risk for overweight/obese women who consumed higher dietary fat but lower carbohydrate (CHO) (OR: 10.119 (1.267–80.79)). No such relationship was found in IDA women with normal weight (OR: 0.375 (0.036–4.022)). Analysis of interaction(s) showed individuals within the highest BMI tertile (T3) had the lowest risk for IDA and the risk increased with increasing tertile groups of fat/CHO ratio; OR 0.381 (0.144–1.008; p = 0.051), 0.370 (0.133–1.026; p = 0.056) and 0.748 (0.314–1.783; p = 0.513); for T1, T2 and T3, respectively. In conclusion, a protective effect of BMI on IDA may be attenuated in women who had increased fat/CHO ratio.

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Aflatoxins are toxic secondary metabolites produced by fungi and contaminate various agricultural commodities either before harvest or under post-harvest conditions. Acute aflatoxin poisoning leading to casepatients and deaths has continued to occur in several parts of Kenya. However, there is emerging evidence implicating chronic aflatoxins exposure as an important factor in infant growth stunting and immune suppression. The consumption of smaller dosages overtime produces no obvious symptoms as would happen with acute dosage. Thus, it has not attracted much attention in Kenya in terms of public health priorities. Aflatoxins have been detected mainly in the staple foods such as cereals and legumes commodities, which form the main gruel ingredients used to compose weaning foods in most rural households. This suggests that children may be more exposed to mycotoxins than the rest of the population and this could be the reason for increased cases of infant malnutrition and mortality in certain areas in Kenya. The extent to which stunted growth and immune suppression contribute to the overall burden of infectious disease merits consideration. Therefore, this paper discusses dietary chronic mycotoxins exposure in Kenya and emerging public health concerns of stunted growth and immune suppression as reported in various related animal and human studies. It also highlights several factors that may enhance the dietary mycotoxins exposure especially amongst children and further explores various localized control measures and research areas within the context of food scarcity and extreme poverty experienced in rural Kenya. This paper aims at reinforcing that presence of mycotoxins within the food system should be addressed as an urgent food safety issue as they place a significant hindrance towards the attainment of the Millennium Development Goals (MDGs) 4 and 6 on reduction of child mortality and combating of diseases, respectively.