ABSTRACT
Fucoidan is a sulfated polysaccharide found in a range of brown algae species. Growing evidence supports the long-term supplementation of fucoidan as an ergogenic aid to improve skeletal muscle performance. The aim of this study was to investigate the effect of fucoidan on the skeletal muscle of mice. Male BL/6 mice (N = 8-10) were administered a novel fucoidan blend (FUC, 400 mg/kg/day) or vehicle (CON) for 4 weeks. Treatment and control experimental groups were further separated into exercise (CON+EX, FUC+EX) or no-exercise (CON, FUC) groups, where exercised groups performed 30 min of treadmill training three times per week. At the completion of the 4-week treatment period, there was a significant increase in cross-sectional area (CSA) of muscle fibers in fucoidan-treated extensor digitorum longus (EDL) and soleus fibers, which was accompanied by a significant increase in tibialis anterior (TA) muscle force production in fucoidan-treated groups. There were no significant changes in grip strength or treadmill time to fatigue, nor was there an effect of fucoidan or exercise on mass of TA, EDL, or soleus muscles. In gastrocnemius muscles, there was no change in mRNA expression of mitochondrial biogenesis markers PGC-1α and Nrf-2 in any experimental groups; however, there was a significant effect of fucoidan supplementation on myosin heavy chain (MHC)-2x, but not MHC-2a, mRNA expression. Overall, fucoidan increased muscle size and strength after 4 weeks of supplementation in both exercised and no-exercised mice suggesting an important influence of fucoidan on skeletal muscle physiology.
Subject(s)
Anabolic Agents/administration & dosage , Muscle Contraction/drug effects , Muscle Strength/drug effects , Muscle, Skeletal/drug effects , Physical Endurance/drug effects , Polysaccharides/administration & dosage , Skeletal Muscle Enlargement/drug effects , Administration, Oral , Animals , Male , Mice, Inbred C57BL , Mitochondria, Muscle/drug effects , Mitochondria, Muscle/genetics , Mitochondria, Muscle/metabolism , Mitochondrial Proteins/genetics , Mitochondrial Proteins/metabolism , Muscle, Skeletal/metabolism , Time FactorsABSTRACT
The fungus Aspergillus fumigatus is a ubiquitous opportunistic human pathogen capable of causing a life-threatening disease called invasive aspergillosis, or IA, with an associated 40-90% mortality rate in immunocompromised patients. Of the approximately 250 species known in the genus Aspergillus, A. fumigatus is responsible for up to 90% of IA infections. This study focuses on examining the role of the putative polysaccharide synthase cpsA gene in A. fumigatus virulence. Additionally, we evaluated its role in cellular processes that influence invasion and colonization of host tissue. Importantly, our results support that cpsA is indispensable for virulence in A. fumigatus infection of non-neutropenic hosts. Our study revealed that cpsA affects growth and sporulation in this fungus. Absence of cpsA resulted in a drastic reduction in conidiation, and forced overexpression of cpsA produced partially fluffy colonies with low sporulation levels, suggesting that wild-type cpsA expression levels are required for proper conidiation in this fungus. This study also showed that cpsA is necessary for normal cell wall integrity and composition. Furthermore, both deletion and overexpression of cpsA resulted in a reduction in the ability of A. fumigatus to adhere to surfaces, and caused increased sensitivity to oxidative stress. Interestingly, metabolomics analysis indicated that cpsA affects A. fumigatus secondary metabolism. Forced overexpression of cpsA resulted in a statistically significant difference in the production of fumigaclavine A, fumigaclavine B, fumigaclavine C, verruculogen TR-2, and tryprostatin A.
Subject(s)
Aspergillus fumigatus/enzymology , Aspergillus fumigatus/pathogenicity , Fungal Proteins/metabolism , Glycosyltransferases/metabolism , Adhesiveness , Animals , Aspergillus fumigatus/growth & development , Cell Wall/metabolism , Disease Models, Animal , Female , Humans , Metabolomics , Mice, Inbred ICR , Osmotic Pressure , Oxidative Stress , Spores, Fungal/physiology , VirulenceABSTRACT
Iodine insufficiency is now a prominent issue in the UK and other European countries due to low intakes of dairy products and seafood (especially where iodine fortification is not in place). In the present study, we tested a commercially available encapsulated edible seaweed (Napiers Hebridean Seagreens® Ascophyllum nodosum species) for its acceptability to consumers and iodine bioavailability and investigated the impact of a 2-week daily seaweed supplementation on iodine concentrations and thyroid function. Healthy non-pregnant women of childbearing age, self-reporting low dairy product and seafood consumption, with no history of thyroid or gastrointestinal disease were recruited. Seaweed iodine (712 µg, in 1 g seaweed) was modestly bioavailable at 33 (interquartile range (IQR) 28-46) % of the ingested iodine dose compared with 59 (IQR 46-74) % of iodine from the KI supplement (n 22). After supplement ingestion (2 weeks, 0·5 g seaweed daily, n 42), urinary iodine excretion increased from 78 (IQR 39-114) to 140 (IQR 103-195) µg/l (P< 0·001). The concentrations of thyroid-stimulating hormone increased from 1·5 (IQR 1·2-2·2) to 2·1 (IQR 1·3-2·9) mIU/l (P< 0·001), with two participants having concentrations exceeding the normal range after supplement ingestion (but normal free thyroxine concentrations). There was no change in the concentrations of other thyroid hormones after supplement ingestion. The seaweed was palatable and acceptable to consumers as a whole food or as a food ingredient and effective as a source of iodine in an iodine-insufficient population. In conclusion, seaweed inclusion in staple foods would serve as an alternative to fortification of salt or other foods with KI.
