Wheat germ supplementation has modest effects on gut health markers but improves glucose homeostasis markers in adults classified as overweight: A randomized controlled pilot study.

Wheat germ (WG), a by-product of flour milling, is rich in bioactive substances that may help improve health complications associated with increased adiposity. This study investigated the effects of WG on gut health, metabolic, and inflammatory markers in adults classified as overweight. We hypothesized that WG, because of its many bioactive components, would improve gut health and metabolic, and inflammatory markers in overweight adults. Forty adults (18-45 years old) and with a body mass index between 25 and 30 kg/m2 participated in this single-blinded randomized controlled pilot study. Participants consumed the study supplements containing 30 g of either cornmeal (control, CL) or WG daily for 4 weeks. Primary outcome variables were gut health markers including gut microbiota, gut integrity markers, and fecal short-chain fatty acids, whereas secondary outcome variables included metabolic and inflammatory parameters assessed at baseline and at the end of supplementation. Thirty-nine participants (n = 19 and 20 for CL and WG group, respectively) completed the study. The genus Faecalibacterium was significantly higher in the WG group compared to CL post-supplementation but no significant changes in other gut health markers, short-chain fatty acids, inflammatory markers, and lipid profiles were observed. Compared with baseline, WG improved markers of glucose homeostasis including insulin (P = .02), homeostatic model assessment of insulin resistance (P = .03), glycated hemoglobin (P = .07), and the pro-inflammatory adipokine, resistin (P = .04). However, these parameters after intervention were not different with control. Our findings suggest that WG supplementation have modest effects on gut health but may provide an economical option for individuals to improve glycemic control.

Impact of Short-Term Creatine Supplementation on Muscular Performance among Breast Cancer Survivors.

Breast cancer (BC) is one of the most common cancers in the United States. Advances in detection and treatment have resulted in an increased survival rate, meaning an increasing population experiencing declines in muscle mass and strength. Creatine supplementation has consistently demonstrated improvements in strength and muscle performance in older adults, though these findings have not been extended to cancer populations. PURPOSE: The purpose of this study was to investigate the effects of short-term creatine supplementation on muscular performance in BC survivors. METHODS: Using a double-blind, placebo-controlled, randomized design, 19 female BC survivors (mean ± SD age = 57.63 ± 10.77 years) were assigned to creatine (SUPP) (n = 9) or dextrose placebo (PLA) (n = 10) groups. The participants completed two familiarization sessions, then two test sessions, each separated by 7 days, where the participants supplemented with 5 g of SUPP or PLA 4 times/day between sessions. The testing sessions included sit-to-stand power, isometric/isokinetic peak torque, and upper/lower body strength via 10 repetition maximum (10RM) tests. The interaction between supplement (SUPP vs. PLA) and time (Pre vs. Post) was examined using a group × time ANOVA and effect sizes. RESULTS: No significant effects were observed for sit-to-stand power (p = 0.471; ηp2 = 0.031), peak torque at 60°/second (p = 0.533; ηp2 = 0.023), peak torque at 120°/second (p = 0.944; ηp2 < 0.001), isometric peak torque (p = 0.905; ηp2 < 0.001), 10RM chest press (p = 0.407; ηp2 = 0.041), and 10RM leg extension (p = 0.932; ηp2 < 0.001). However, a large effect size for time occurred for the 10RM chest press (ηp2 = 0.531) and leg extension (ηp2 = 0.422). CONCLUSION: Seven days of creatine supplementation does not influence muscular performance among BC survivors.

Postprandial triglycerides across the aging spectrum: A secondary analysis utilizing an abbreviated fat tolerance test.

BACKGROUND & AIMS: Elevated postprandial triglycerides are an independent cardiovascular disease risk factor and observed in older adults. However, differences in postprandial triglycerides across the spectrum of adulthood remain unclear. METHODS AND RESULTS: We performed a secondary analysis of six studies where adults (aged 18-84 years; N = 155) completed an abbreviated fat tolerance test (9 kcal/kg; 70% fat). Differences in postprandial triglycerides were compared in those ≥50 and <50 years and by decade of life, adjusting for sex and BMI. Compared to those <50 years, participants ≥50 years had higher fasting, 4 h, and Δ triglycerides from baseline (p's < 0.05). When examining triglyceride parameters by decade, no differences were observed for fasting triglycerides, but 50 s, 60 s, and 70s-80 s displayed greater 4 h and Δ triglycerides versus 20 s (p's ≤ 0.001). The frequency of adverse postprandial triglyceride responses (i.e., ≥220 mg/dL) was higher in participants ≥50 versus <50 years (p < 0.01), and in 60 s compared to all other decades (p = 0.01). CONCLUSION: Older age was generally associated with higher postprandial triglycerides, with no divergence across the spectrum of older adulthood. In our sample, postprandial triglyceride differences in older and younger adults were driven by those >50 years relative to young adults in their 20 s. REGISTRATION: N/A (secondary analysis).

Investigation of an individual with background levels of exhaled isoprene: a case study.

Isoprene is one of the most abundant and most frequently evaluated volatile organic compounds in exhaled breath. Recently, several individuals with background levels of exhaled isoprene have been identified. Here, case study data are provided for an individual, identified from a previous study, with this low prevalence phenotype. It is hypothesized that the individual will illustrate low levels of exhaled isoprene at rest and during exercise. At rest, the subject (7.1 ppb) shows background (µ= 14.2 ± 7.0 ppb) levels of exhaled isoprene while the control group illustrates significantly higher quantities (µ= 266.2 ± 72.3 ppb) via proton transfer reaction mass spectrometry (PTR-MS). The result, background levels of isoprene at rest, is verified by thermal desorption gas chromatography mass spectrometry (TD-GC-MS) collections with the individual showing -3.6 ppb exhaled isoprene while the room background containedµ= -4.1 ± 0.1 ppb isoprene. As isoprene has been shown previously to increase at the initiation of exercise, exercise bike experiments were performed with the individual identified with low isoprene, yielding low and invariant levels of exhaled isoprene (µ= 6.6 ± 0.1 ppb) during the exercise while control subjects illustrated an approximate 2.5-fold increase (preµ= 286.3 ± 43.8 ppb, exerciseµ= 573.0 ± 147.8 ppb) in exhaled isoprene upon exercise start. Additionally, exhaled breath bag data showed a significant decrease in isoprene (delta post/pre, p = 0.0078) of the control group following the exercise regimen. Finally, TD-GC-MS results for exhaled isoprene from the individual's family (mother, father, sister and maternal grandmother) illustrated that the mother and father exhibited isoprene values (28.5 ppb, 77.2 ppb) below control samples 95% confidence interval (µ= 166.8 ± 43.3 ppb) while the individual's sister (182.0 ppb) was within the control range. These data provide evidence for a large dynamic range in exhaled isoprene in this family. Collectively, these results provide additional data surrounding the existence of a small population of individuals with background levels of exhaled isoprene.

Barriers and Facilitators for Population Genetic Screening in Healthy Populations: A Systematic Review.

Studies suggest that 1-3% of the general population in the United States unknowingly carry a genetic risk factor for a common hereditary disease. Population genetic screening is the process of offering otherwise healthy patients in the general population testing for genomic variants that predispose them to diseases that are clinically actionable, meaning that they can be prevented or mitigated if they are detected early. Population genetic screening may significantly reduce morbidity and mortality from these diseases by informing risk-specific prevention or treatment strategies and facilitating appropriate participation in early detection. To better understand current barriers, facilitators, perceptions, and outcomes related to the implementation of population genetic screening, we conducted a systematic review and searched PubMed, Embase, and Scopus for articles published from date of database inception to May 2020. We included articles that 1) detailed the perspectives of participants in population genetic screening programs and 2) described the barriers, facilitators, perceptions, and outcomes related to population genetic screening programs among patients, healthcare providers, and the public. We excluded articles that 1) focused on direct-to-consumer or risk-based genetic testing and 2) were published before January 2000. Thirty articles met these criteria. Barriers and facilitators to population genetic screening were organized by the Social Ecological Model and further categorized by themes. We found that research in population genetic screening has focused on stakeholder attitudes with all included studies designed to elucidate individuals' perceptions. Additionally, inadequate knowledge and perceived limited clinical utility presented a barrier for healthcare provider uptake. There were very few studies that conducted long-term follow-up and evaluation of population genetic screening. Our findings suggest that these and other factors, such as prescreen counseling and education, may play a role in the adoption and implementation of population genetic screening. Future studies to investigate macro-level determinants, strategies to increase provider buy-in and knowledge, delivery models for prescreen counseling, and long-term outcomes of population genetic screening are needed for the effective design and implementation of such programs. Systematic Review Registration: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020198198.

The reliability of an abbreviated fat tolerance test: A comparison to the oral glucose tolerance test.

BACKGROUND & AIMS: Postprandial lipemia (PPL) is predictive of cardiovascular disease risk, but the current method for assessing PPL is a burdensome process. Recently, the validity of an abbreviated fat tolerance test (AFTT) has been demonstrated. As a continuation of this research, the purpose of this study was to determine the reliability of the AFTT and compare it to the reliability of the oral glucose tolerance test (OGTT). METHODS: In this randomized crossover trial, 20 healthy adults (10 male and 10 female) completed 2 AFTTs and 2 OGTTs, each separated by a 1-week washout. For the AFTT, triglycerides (TG) were measured at baseline and 4 h post-consumption of a high-fat meal, during which time participants were able to leave the lab. For the OGTT, we measured blood glucose at baseline and 2 h post-consumption of a 75-g pure glucose solution, and participants remained in the lab. To determine reliability, we calculated within-subject coefficient of variation (WCV) and intraclass correlation coefficient (ICC). RESULTS: The mean 4-h TG WCV for the AFTT was 12.6%, while the mean 2-h glucose WCV for the OGTT was 10.5%. ICC values for 4-h TG and TG change were 0.79 and 0.71, respectively, while ICC values for 2-h glucose and glucose change were 0.66 and 0.56, respectively. CONCLUSIONS: Based on WCV and ICC, the TG response to an AFTT was similarly reliable to the glucose response to an OGTT in our sample of healthy adults, supporting the AFTT's potential as a standard clinical test for determining PPL. However, reliability of the AFTT needs to be further tested in individuals at greater risk for cardiometabolic disease.

Postprandial Metabolism and Vascular Function: Impact of Aging and Physical Activity Level.

The consumption of a high-fat meal can induce postprandial lipemia and endothelial dysfunction. The authors assessed the impact of age and physical activity on metabolic and vascular outcomes following meal consumption in healthy adults. The authors recruited four groups: younger active (age 22.1 ± 1.4 years; n = 9), younger inactive (age 22.6 ± 3.7 years; n = 8), older active (age 68.4 ± 7.7 years; n = 8), and older inactive (age 67.7 ± 7.2 years; n = 7). The metabolic outcomes were measured at the baseline and hourly for 6 hr post high-fat meal consumption (12 kcal/kg; 63% fat). Flow-mediated dilation was measured at the baseline, 2 hr, and 4 hr postmeal. The total area under the curve for triglycerides was significantly lower in the more active groups, but did not differ based on age (younger active = 6.5 ± 1.4 mmol/L × 6 hr, younger inactive = 11.7 ± 4.8, older active = 6.8 ± 2.7, older inactive = 12.1 ± 1.7; p = .0004). After adjusting for artery diameter, flow-mediated dilation differed between groups at the baseline (younger active = 4.8 ± 1.6%, younger inactive = 2.5 ± 0.5, older active = 3.4 ± 0.9, older inactive = 2.2 ± 0.4; p < .001) and decreased significantly across groups 4 hr postmeal (mean difference = 0.82; 95% CI [0.02, 1.6]; p = .04). These findings highlight the beneficial effect of regular physical activity on postprandial lipemia, independent of age.

Targeted transgenesis identifies Gαs as the bottleneck in ß2-adrenergic receptor cell signaling and physiological function in airway smooth muscle.

G protein-coupled receptors are the most pervasive signaling superfamily in the body and act as receptors to endogenous agonists and drugs. For ß-agonist-mediated bronchodilation, the receptor-G protein-effector network consists of the ß2-adrenergic receptor (ß2AR), Gs, and adenylyl cyclase, expressed on airway smooth muscle (ASM). Using ASM-targeted transgenesis, we previously explored which of these three early signaling elements represents a limiting factor, or bottleneck, in transmission of the signal from agonist binding to ASM relaxation. Here we overexpressed Gαs in transgenic mice and found that agonist-promoted relaxation of airways was enhanced in direct proportion to the level of Gαs expression. Contraction of ASM from acetylcholine was not affected in Gαs transgenic mice, nor was relaxation by bitter taste receptors. Furthermore, agonist-promoted (but not basal) cAMP production in ASM cells from Gαs-transgenic mice was enhanced compared with ASM from nontransgenic littermates. Agonist-promoted inhibition of platelet-derived growth factor-stimulated ASM proliferation was also enhanced in Gαs mouse ASM. The enhanced maximal ß-agonist response was of similar magnitude for relaxation, cAMP production, and growth inhibition. Taken together, it appears that a limiting factor in ß-agonist responsiveness in ASM is the expression level of Gαs. Gene therapy or pharmacological means of increasing Gαs (or its coupling efficiency to ß2AR) thus represent an interface for development of novel therapeutic agents for improvement of ß-agonist therapy.