Effect of n-3 fatty acids supplementation during life style modification in women with overweight.

OBJECTIVE: The marine n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) exert numerous beneficial effects on health, but their potency to defend against development of peripheral insulin resistance of healthy person with overweight remains poorly characterized. We aimed to evaluate the effect of a combination intervention using EPA + DHA and the lifestyle modification (LSM) in women with overweight. METHOD: In a parallel-group, three-arm, randomized trial (UMIN Clinical Trials Registry - R000031131), 34 women were assigned to a 12-week-intervention using corn oil (1.5 g/day; placebo); LSM and corn oil (1.5 g/day; LSM); or LSM and EPA + DHA concentrate (1.5 g/day, containing ~ 0.6 g EPA + DHA; LSM & n-3). At baseline and after intervention, anthropometric measurements including bioelectrical impedance analysis, spiroergometry, 24-hours dietary recall, and various metabolic markers, adiponectin and cytokines were evaluated in serum using standard procedures. Data from 29 women were used for the final evaluation. Wilcoxon two-sided rank-sum test was used to inspect the differences between LSM and LSM & n-3, and placebo groups, with a p-value of ≤ 0.05. All computations were performed with MATLAB Statistics Toolbox. RESULTS: In comparison with placebo, LSM and LSM & n-3 decreased body weight, waist circumference, and body fat, and increased VO2max/kg. LSM & n-3 increased adiponectin levels in comparison to LSM. Fasting insulin, IL8, and cholesterol were decreased by LSM, but were unchanged by LSM & n-3. IL6 was not affected in LSM & n-3, while it was increased in LSM. Other inflammatory markers, as well as leptin, LIF, follistatin, BDNF, and fasting triacylglycerol were not significantly affected by any of the interventions. CONCLUSION: Besides preventing a modest negative effect of LSM on IL6 and adiponectin level, the combination of LSM and EPA + DHA supplementation could be probably used to improve the functional capacity of adipose tissue in women with overweight.

Obesogens in Foods.

Obesogens, as environmental endocrine-disrupting chemicals, are supposed to have had an impact on the prevalence of rising obesity around the world over the last forty years. These chemicals are probably able to contribute not only to the development of obesity and metabolic disturbances in individuals, but also in their progeny, having the capability to epigenetically reprogram genetically inherited set-up points for body weight and body composition control during critical periods of development, such as fetal, early life, and puberty. In individuals, they may act on myriads of neuro-endocrine-immune metabolic regulatory pathways, leading to pathophysiological consequences in adipogenesis, lipogenesis, lipolysis, immunity, the influencing of central appetite and energy expenditure regulations, changes in gut microbiota-intestine functioning, and many other processes. Evidence-based medical data have recently brought much more convincing data about associations of particular chemicals and the probability of the raised risk of developing obesity. Foods are the main source of obesogens. Some obesogens occur naturally in food, but most are environmental chemicals, entering food as a foreign substance, whether in the form of contaminants or additives, and they are used in a large amount in highly processed food. This review article contributes to a better overview of obesogens, their occurrence in foods, and their impact on the human organism.

Chronic DDE Exposure Modifies Mitochondrial Respiration during Differentiation of Human Adipose-Derived Mesenchymal Stem Cells into Mature Adipocytes.

The contribution of environmental pollutants to the obesity pandemic is still not yet fully recognized. Elucidating possible cellular and molecular mechanisms of their effects is of high importance. Our study aimed to evaluate the effect of chronic, 21-day-long, 2,2-bis (4-chlorophenyl)-1,1-dichlorethylenedichlorodiphenyldichloroethylene (p,p'-DDE) exposure of human adipose-derived mesenchymal stem cells committed to adipogenesis on mitochondrial oxygen consumption on days 4, 10, and 21. In addition, the mitochondrial membrane potential (MMP), the quality of the mitochondrial network, and lipid accumulation in maturing cells were evaluated. Compared to control differentiating adipocytes, exposure to p,p'-DDE at 1 µM concentration significantly increased basal (routine) mitochondrial respiration, ATP-linked oxygen consumption and MMP of intact cells on day 21 of adipogenesis. In contrast, higher pollutant concentration seemed to slow down the gradual increase in ATP-linked oxygen consumption typical for normal adipogenesis. Organochlorine p,p'-DDE did not alter citrate synthase activity. In conclusion, in vitro 1 µM p,p'-DDE corresponding to human exposure is able to increase the mitochondrial respiration per individual mitochondrion at the end of adipocyte maturation. Our data reveal that long-lasting exposure to p,p'-DDE could interfere with the metabolic programming of mature adipocytes.