Effects of inulin supplementation on body composition and metabolic outcomes in children with obesity.

Inulin might improve body composition in obese children. We aimed to determine the effects of inulin supplementation on body composition and metabolic outcomes in obese children. A randomized, double-blinded placebo-controlled study was conducted in obese Thai children aged 7-15 years. Participants were assigned to 3 treatment groups for 6 months: 13 g of extracted inulin powder from Thai Jerusalem artichoke, isocaloric maltodextrin, and dietary fiber advice groups. Body composition was assessed by bioelectrical impedance analysis. One-hundred and fifty-five children completed the study (mean age 10.4 ± 2.2 years, BMI z-score 3.2 ± 1.0, 59% male). The drop-out rate was 6%. The inulin extract yielded more than 90% compliance without significant gastrointestinal side effects. All three groups demonstrated a significant decrease in BMI z-score, fat mass index (FMI), and trunk FMI, but the differences between groups were not observed. Fat-free mass index significantly increased only in the inulin group (16.18 ± 1.90 vs. 16.38 ± 1.98 kg/m2, P = 0.009). There were no significant differences in the metabolic profiles between groups. Despite showing no substantial effect on adiposity, inulin may increase fat-free mass in obese children. Further research in the change of gut microbiota composition is needed to determine inulin's impact on host-microbe interaction in pediatric obesity.

The functional starter and its genomic insight for histamine degradation in fish sauce.

Histamine is a biogenic amine significantly formed in fish sauce leading to a major concern in consumers. This study aimed to identify a halophilic bacterium for histamine degradation in fish sauce, and understand its genomic insight to enhance histamine degradation activity. We discovered the novel halophilic bacterium, Bacillus piscicola FBU1786, degrading histamine and other biogenic amines. Its histamine breakdown was growth-associated in a wide range of NaCl concentrations, pH, and temperature from 4% to 18%, 6.0 to 9.0, and 30 to 45 °C, respectively. Genome sequencing revealed the presence of Cu2+-binding oxidase-encoding genes and their heterologous expression with Cu2+ supplementation triggered histamine degradation in E. coli. The degree of histamine breakdown in B. piscicola FBU1786 could be enhanced by Cu2+ addition. Histamine degradation of the culture was evaluated in raw fish sauce mixtures to partially mimic the condition during fish sauce fermentation. Histamine degradation was suppressed to the extent of raw fish sauce, but could be restored by Cu2+ supplementation. Together, this study disclosed B. piscicola FBU1786 with the potent histamine degradation activity, identified Cu2+-binding oxidases responsible for histamine breakdown, and enhanced histamine degradation of the culture using Cu2+ supplementation.

Polymethoxyflavones from Kaempferia parviflora ameliorate skin aging in primary human dermal fibroblasts and ex vivo human skin.

Skin aging is accompanied by an increase in the number of senescent cells, resulting in various pathological outcomes. These include inflammation, impaired barrier function, and susceptibility to skin disorders such as cancer. Kaempferia parviflora (Thai black ginger), a medicinal plant native to Thailand, has been shown to counteract inflammation, cancer, and senescence. This study demonstrates that polymethoxyflavones (5,7-dimethoxyflavone, 5,7,4'-trimethoxyflavone, and 3,5,7,3',4'-pentamethoxyflavone) purified from K. parviflora rhizomes suppressed cellular senescence, reactive oxygen species, and the senescence-associated secretory phenotype in primary human dermal fibroblasts. In addition, they increased tropocollagen synthesis and alleviated free radical-induced cellular and mitochondrial damage. Moreover, the compounds mitigated chronological aging in a human ex vivo skin model by attenuating senescence and restoring expression of essential components of the extracellular matrix, including collagen type I, fibrillin-1, and hyaluronic acid. Finally, we report that polymethoxyflavones enhanced epidermal thickness and epidermal-dermal stability, while blocking age-related inflammation in skin explants. Our findings support the use of polymethoxyflavones from K. parviflora as natural anti-aging agents, highlighting their potential as active ingredients in cosmeceutical and nutraceutical products.

Alterations of mineralized matrix by lead exposure in osteoblast (MC3T3-E1) culture.

The present study investigated the effect of lead (Pb) on bone ultrastructure and chemistry using an in vitro bone model. MC3T3-E1 preosteoblasts were differentiated and treated with lead acetate at 0.4, 2, 10, and 50 µM. No abnormalities in either cell growth or bone nodule formation were observed with the treated dose of lead acetate. However, Pb treatments could significantly increase Pb accumulation in differentiated osteoblast cultures and upregulate expression of Divalent metal transporter 1 (Dmt1) in a dose dependent manner. Pb treatments also altered the expression of osteogenic genes, including secreted phosphoprotein 1, osteocalcin, type I collagen, and osteoprotegerin. Moreover, in mineralized osteoblast cultures, Pb was found to be mainly deposited as Pb salts and oxides, respectively. Ultrastructure analysis revealed Pb localizing with calcium and phosphorus in the mineralized matrix. In mineralizing osteoblast cells, Pb was found in the intracellular calcified vesicles which is one of the bone mineralization mechanisms. Pb was also present in mineral deposits with various shapes and sizes, such as small and large globular or needle-like mineral deposits representing early to mature stages of mineral deposits. Furthermore, Pb was found more in the globular deposits than the needle shaped mineral crystals. Taken together, our observations revealed how Pb incorporates into bone tissue, and showed a close association with bone apatite.

ZNT7 binds to CD40 and influences CD154-triggered p38 MAPK activity in B lymphocytes-a possible regulatory mechanism for zinc in immune function.

Zinc deficiency impairs the immune system leading to frequent infections. Although zinc is known to play critical roles in maintaining healthy immune function, the underlying molecular targets are largely unknown. In this study, we demonstrate that zinc is important for the CD154-CD40-mediated activation of downstream signaling pathways in human B lymphocytes. CD40 is a receptor localized on the cell surface of many immune cells, including B lymphocytes. It binds to CD154, a membrane protein expressed on antigen-activated T helper (Th) lymphocytes. This CD154-CD40 interaction leads to B-cell activation. We showed that cellular zinc deficiency impaired the CD154-CD40-mediated p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation. We also showed that zinc supplemental treatment of B lymphocytes had limited effect on this CD40-mediated p38 MAPK signaling. Most importantly, we demonstrated that the zinc transporter protein zinc transporter 7 (ZNT7) interacted with CD40 using immunoprecipitation analyses. ZNT7 knockdown in B lymphocytes had a negative effect on the cell surface expression of CD40. Consequently, the CD40-mediated p38 MAPK signaling transduction was down-regulated in ZNT7 KD B lymphocytes. Conversely, this p38 MAPK signaling activity was up-regulated by overexpression (OE) of ZNT7 in B lymphocytes. Moreover, we found that ZNT7 knockdown in B lymphocytes constitutively up- and down-regulated the inhibitor of i kappa B kinase and AKT serine/threonine kinase phosphorylation, respectively, which implies the activation of survival signaling in ZNT7 KD B cells. We conclude that CD40 is the target molecule for ZNT7 in regulation of immune function of B lymphocytes.