Iodine, an essential micronutrient, is required to produce thyroid hormones. Iodine deficiency disorders (IDD) comprise a range of adverse maternal and fetal outcomes, with the most significant irreversible effect resulting from neurodevelopmental deficits in fetal brain caused by deficient iodine status during early pregnancy. The objective of this scoping review was to summarize the studies that assessed iodine status of women of reproductive age in the USA. A systematic review of literature using the PRISMA Extension for Scoping Reviews (PRISMA-ScR) statement was conducted. PubMed, Medline, CINAHL, EMBASE, EBSCOHost, Cochrane, ERIC, Google Scholar, and Web of Science databases were searched, 1652 records were identified. One thousand six hundred forty-one records that did not satisfy the inclusion/exclusion criteria and quality review were excluded, and 11 peer-reviewed articles were determined to be eligible for this scoping review. Despite the USA being considered iodine sufficient for the general population, the US dietary iodine intakes have decreased drastically since the 1970s, with iodine deficiency reemerging in vulnerable groups such as women of reproductive age. Although data to conduct a scoping review of iodine status among women of reproductive age in the USA was scarce, majority of the articles reviewed demonstrate emergent iodine deficiency in this population of women of reproductive age, indicating alarm for a public health concern needing immediate attention.
Skeletal muscle physiology is regulated by microRNA that are localized within skeletal muscle (myomiRs). This study investigated how the expression of myomiRs and genes regulating skeletal muscle mass and myogenesis are influenced in response to acute and consecutive days of exercise-related signaling using the exercise mimetic, formoterol, in vitro. Human skeletal muscle cells were proliferated and differentiated for 6 days. Experimental conditions included: (a) control, (b) acute formoterol stimulation (AFS), and (c) consecutive days of formoterol stimulation (CFS). For AFS, myotubes were treated with 30 nM of formoterol for three hours on day 6 of differentiation, and this was immediately followed by RNA extraction. For CFS, myotubes were treated with 30 nM of formoterol for three hours on two or three consecutive days, with RNA extracted immediately following the final three-hour formoterol treatment. We observed increased myomiR expression for both AFS and CFS. AFS appeared to promote myogenesis, but this effect was lost with CFS. Additionally, we observed increased expression of genes involved in metabolism, mitochondrial biogenesis, and muscle protein degradation in response to AFS. myomiR and gene expression appear to be sensitive to acute and long-term exercise-related stimuli, and this likely contributes to the regulation of skeletal muscle mass.
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