Nutmeg extract potentially alters characteristics of white adipose tissue in rats.

BACKGROUND: Browning of white adipose tissue (WAT) is a promising approach to obesity treatment. During browning, WAT transforms into beige adipose tissue through stimulation of the peroxisome proliferator activated receptor γ (PPARγ). Nutmeg, one of the Indonesian herbs, reportedly has dual roles as a PPARα/γ partial agonist. Even though nutmeg has been traditionally used in body weight reduction, there is limited information regarding the potential role of nutmeg in browning of WAT. OBJECTIVES: In this study, we explored the effect of nutmeg seed extract (NuSE) as a potential inductor of WAT browning. METHODS: Twelve male Wistar rats, 5-6 weeks old, were divided into control and nutmeg groups. The rats in nutmeg group were given NuSE for 12 weeks by oral gavage. After 12 weeks, the rat's inguinal WAT and brown adipose tissue (BAT) were collected, weighed and stored at - 80°C until use. RESULTS: We observed that even though NuSE did not reduce the final body weight, it significantly reduced body weight gain. NuSE also increased protein levels of peroxisome proliferator activated receptor γ coactivator 1α (PGC-1α) and uncoupling protein 3 (UCP3) significantly and tended to increase UCP2 and UCP1 levels. Furthermore, NuSE induced macroscopic and microscopic morphological changes of inguinal WAT, marked by significantly increased adipocyte numbers and decreased adipocyte size. CONCLUSIONS: Even though NuSE did not increase UCP1 significantly, it potentially alters inguinal WAT characteristics and leads to browning through PGC-1α and UCP3 induction. However, UCP3's specific mechanism in WAT browning remains unclear. Our findings could contribute to obesity treatment in the future.

Effects of Selenium Supplementation on the Diabetic Condition Depend on the Baseline Selenium Status in KKAy Mice.

Oxidative stress in obesity leads to insulin resistance in type 2 diabetes. Some selenoproteins possess antioxidant properties, suggesting that selenium (Se) may protect against type 2 diabetes; however, evidence from epidemiological studies is contradictory. We hypothesized that Se status before supplementation (baseline) contributes to the supplementation outcome. This study aimed to clarify the influence of baseline Se status on the effect of Se supplementation on the diabetic condition. Six-week-old KKAy mice were fed a diet without supplemental Se or with 0.1 ppm Se in the form of L-selenomethionine (SeM) for 2 weeks to create low-Se and sufficient-Se baseline statuses, respectively. For the next 4 weeks, low-Se mice were given a SeM (0.5 ppm Se)-supplemented diet, and sufficient-Se mice were given either a SeM (0.5 ppm Se)- or sodium selenite (0.5 ppm Se)-supplemented diet; control groups continued on baseline diets. Serum Se concentrations, glutathione peroxidase (GPx) activities, adiponectin levels, glucose tolerance, and insulin sensitivity were analyzed. All mice became diabetic during the 2-week baseline induction period. At the end of the supplementation period, Se-receiving groups demonstrated significantly higher Se concentrations and GPx activities than their respective controls. Sufficient-Se mice receiving SeM had lower blood glucose levels and better insulin sensitivity than control and sodium selenite-receiving mice, whereas low-Se mice receiving SeM showed no such improvements compared with their controls. Our results suggest that Se supplementation in the form of SeM may help prevent type 2 diabetes aggravation in people taking the 55 µg/day Se recommended dietary allowance.

Iron, zinc, vitamin A and selenium status in a cohort of Indonesian infants after adjusting for inflammation using several different approaches.

Inflammation confounds the interpretation of several micronutrient biomarkers resulting in estimates that may not reflect the true burden of deficiency. We aimed to assess and compare the micronutrient status of a cohort of Indonesian infants (n 230) at aged 6, 9 and 12 months by ignoring inflammation (unadjusted) and adjusting four micronutrient biomarkers for inflammation with C-reactive protein (CRP) and α-1-glycoprotein (AGP) using the following methods: (1) arithmetic correction factors with the use of a four-stage inflammation model; and (2) regression modelling. Prevalence of infants with any inflammation (CRP>5 mg/l and/or AGP>1 g/l) was about 25% at each age. Compared with unadjusted values, regression adjustment at 6, 9 and 12 months generated the lowest (P50 % across all ages. In conclusion, without inflammation adjustment, Fe deficiency was grossly under-estimated and vitamin A and Zn deficiency over-estimated, highlighting the importance of correcting for the influence of such, before implementing programmes to alleviate micronutrient malnutrition. However, further work is needed to validate the proposed approaches with a particular focus on assessing the influence of varying degrees of inflammation (i.e. recurrent acute infections and low-grade chronic inflammation) on each affected nutrient biomarker.

Consumption of fortified infant foods reduces dietary diversity but has a positive effect on subsequent growth in infants from Sumedang district, Indonesia.

Stunting and underweight among under-five children in Indonesia are common, raising public health concerns. Whether inappropriate complementary feeding (CF) practices compromise optimal growth during late infancy in Indonesia is uncertain. Therefore we characterized and evaluated CF practices in Indonesian infants and investigated their relationship with subsequent growth. We enrolled breastfed infants at 6 months of age (n = 230); and followed them at 9 (n = 202) and 12 months of age (n = 190). We collected socio-demographic and anthropometric data and two-day in-home weighed food records. Relations between WHO CF indicators, sentinel foods, and energy and micronutrient intakes at 9 months and growth at 12 months were explored using multiple linear regression. Stunting and underweight increased from 15.8% and 4.4% at 6 months to 22.6% and 10.5% at 12 months, respectively. Median intakes of calcium, iron, zinc, and riboflavin were below WHO recommendations. Infants consuming fortified infant foods (FIFs) at 9 months had diets with a lower dietary diversity (DD) score (2.3 vs.3.0), energy density, median energy (250 vs. 310 kcal/d) and protein (6.5 vs. 9.1 g/d) intake than non-consumers (p<0.01), despite higher intakes of calcium, iron, and vitamins A and C (p<0.001). Positive relations existed for 9-month consumption of iron-rich/iron fortified infant foods with length-for-age Z-score (LAZ) at 12 months (ß = 0.22; 95% CI: 0.01, 0.44; P = 0.04), and for fortified infant foods alone with both LAZ (ß = 0.29; 95% CI: 0.09, 0.48; P = 0.04) and weight-for-age Z-score (ß = 0.14; 95% CI: 0.02, 0.26; P = 0.02) at 12 months. The positive association of FIFs with subsequent growth may be attributed to their content of both powdered cow's milk and multi-micronutrient fortificants. Nonetheless, mothers should not be encouraged to over-rely on FIFs as they reduce DD.