Supplementation of Juçara Berry (Euterpe edulis Mart.) Modulates Epigenetic Markers in Monocytes from Obese Adults: A Double-Blind Randomized Trial.

Nutrigenomics is an emerging field in obesity since epigenetic markers can be modified by environmental factors including diet. Considering juçara composition-rich in anthocyanins, monounsaturated fatty acids (MUFAs) and fibers-it has the potential for epigenetic modulation. We evaluated the juçara supplementation modulating the serum fatty acids profile and epigenetic markers in monocytes of adult obese humans. It was a randomized double-blind, controlled trial with 27 obese (Body mass index between 30.0 and 39.9 kg/m²) participants of both genders aged from 31 to 59 years, divided into juçara group (5 g juçara freeze-dried pulp) or placebo group (5 g of maltodextrin) for 6 weeks. Before and after supplementation, blood samples were collected. The serum and monocytes cells obtained were cultured and stimulated with lipopolysaccharides as proinflammatory stimulus. After 24 h of incubation, the cells and supernatants were collected and analyzed. Juçara improved the serum fatty acids profile on unsaturated fatty acids levels. The epigenetic markers evaluated were improved post-treatment. Also, the methylated DNA level was increased after treatment. We find that juçara supplementation is a predictor of methyl CpG binding proteins 2 (MeCP2) in monocytes. Concluding, juçara supplementation improved the serum fatty acids profile, modulating the epigenetic markers in monocytes from obese individuals.

Programming mediated by fatty acids affects uncoupling protein 1 (UCP-1) in brown adipose tissue.

Brown adipose tissue (BAT) has recently been given more attention for the part it plays in obesity. BAT can generate great amounts of heat through thermogenesis by the activation of uncoupling protein 1 (UCP-1), which can be regulated by many environmental factors such as diet. Moreover, the build-up of BAT relates to maternal nutritional changes during pregnancy and lactation. However, at present, there is a limited number of studies looking at maternal nutrition and BAT development, and it seems that the research trend in this field has been considerably declining since the 1980s. There is much to discover yet about the role of different fatty acids on the development of BAT and the activation of UCP-1 during the fetal and the postnatal periods of life. A better understanding of the impact of nutritional intervention on the epigenetic regulation of BAT could lead to new preventive care for metabolic diseases such as obesity. It is important to know in which circumstances lipids could programme BAT during pregnancy and lactation. The modification of maternal dietary fatty acids, amount and composition, during pregnancy and lactation might be a promising strategy for the prevention of obesity in the offspring and future generations.

Leptin as a cardiovascular risk marker in metabolically healthy obese: Hyperleptinemia in metabolically healthy obese.

Adipokines contribute to the inflammatory process which can lead to obesity-associated cardiometabolic complications. Metabolically healthy obese individuals seem to be protected or more resistant to develop these complications and it is intriguing why some individuals develop comorbidities and others do not. Thus, we questioned whether the differences between metabolically healthy and unhealthy obese relied on the alterations in metabolic profile, characterized by serum leptin and adiponectin. A total of 142 obese adults were divided into 2 groups - metabolically healthy obese (MHO) or unhealthy obese (MUO) - and they were evaluated for anthropometric measures, body composition, blood pressure, dietary intakes and plasma levels of leptin and adiponectin. Leptin/adiponectin ratio (L/A) was calculated. Age, BMI and blood pressure were higher in the MUO. No differences in anthropometric measurements, body composition, dietary intake and dietary quality were observed between groups. Leptin were significantly higher in the MUO (53.07 ± 34.56 versus 36.27 ± 24.02 ng/ml in the MHO, r < 0.04). The logistic regression analysis demonstrated that leptin was an important factor associated with not being healthy, independent of age, body weight and BMI. There were no differences between groups for adiponectin and L/A. Leptin correlated positively with body weight (r = 0.25, r < 0.05), BMI (r = 0.38, r < 0.05) and BF (r = 0.74, r < 0.05), and negatively with FFM (r = -0.74, r < 0.05). Our findings suggest that leptin is an important cardiovascular disease marker to obese population and can contribute to evaluate metabolic risks in these individuals.