Prevalence of food insecurity in NCAA Division III collegiate athletes.

Objective: Prevalence of food insecurity in NCAA DIII student-athletes was assessed via an anonymous, online survey (n = 787) in February of 2020. Participants: Participants were mainly female, 18-21 years old, self-identified as white, lived on campus and had a campus meal plan. Methods: Food security was assessed using an anonymous, online survey based off of the USDA 6-item short form food security survey. Results: Overall prevalence of food insecurity was 14.7% with Hispanic students, Black students, those without a meal plan, recipients of a Pell grant, first generation college students and those experiencing food insecurity prior to enrolling in college being at higher risk. A majority of respondents felt lack of access to food impacted their academic and athletic performance, as well as overall health and cited timing of practices and games overlapping with dining hall hours as a key contributor. Conclusion: Based off of these results, educational programs and resources should be targeted toward these high-risk groups to help ensure consistent access to safe and healthy food for student-athletes.

Significant differences in dietary intake of NCAA Division III soccer players compared to recommended levels.

Objective: This study evaluated dietary intake patterns of NCAA Division III soccer players compared to recommended levels. Participants: NCAA Division III soccer players (n = 75). Methods: Actual dietary intake was determined by the analysis of a 3-day food record. Results: Results indicate that total energy, carbohydrate, and dietary fiber intake was significantly below the recommended levels. In addition, added sugar and total fat consumption were significantly above recommended levels. Potassium, magnesium, and vitamin D levels were consumed in levels significantly below the recommended levels. Sodium, iron, and vitamin C were consumed in significantly higher levels than the recommended target. Female athletes had significantly higher intakes of added sugar, saturated fat and vitamin C compared to male athletes. Female athletes had significantly lower intakes of calcium, potassium, sodium, iron, magnesium and vitamin D compared to male athletes. Conclusion: Based on the results of the present study, increased efforts should be put into development of nutrition education programs for NCAA Division III athletes.

Implementation of an Educational Fueling Station for a National Collegiate Athletic Association Division III Athletic Program.

ABSTRACT: Gomez-Hixson, K, and Brown, ML. Implementation of an educational fueling station for a NCAA division III athletic program. J Strength Cond Res 35(8): 2346-2350, 2021-The purpose of this project was to evaluate the effectiveness and sustainability of an educational fueling station for National Collegiate Athletic Association (NCAA) Division III student-athletes. Subjects included student-athletes participating in the fall 2018 athletic season (n = 82). Once the mobile fueling station was established, the athletes were informed of the mobile fueling station policies and educated on the appropriate use and timing of the fueling station. The fueling station remained in operation until the end of the 2018 fall athletic season, after which the effectiveness and athlete acceptance of the mobile fueling station was assessed. An anonymous online survey was used as the assessment tool and was created by the authors based on the information pertinent to our institution and mobile fueling station goals and objectives. An itemized inventory usage tracking system was used to calculate actual costs. Data analysis was limited to basic descriptive statistics including the overall response rate and the frequency and percentage of responses to the survey questions. Outcome assessment indicated that 97% of athletes found that the foods provided helped their performance; 95% felt they were properly oriented to the fueling station, and 51% used the fueling station 1-2 times per week on game days. Furthermore, inventory tracking revealed that the operational costs came in under the projected budget. Overall, the mobile fueling station was successfully implemented for student-athletes within a NCAA Division III university and demonstrated feasibility and sustainability within a low-budget athletic program. Establishing proof of concept led to the permanent adoption of the mobile fueling station.

FSTL3-Neutralizing Antibodies Enhance Glucose-Responsive Insulin Secretion in Dysfunctional Male Mouse and Human Islets.

Diabetes is caused by insufficient insulin production from pancreatic beta cells or insufficient insulin action, leading to an inability to control blood glucose. While a wide range of treatments exist to alleviate the symptoms of diabetes, therapies addressing the root cause of diabetes through replacing lost beta cells with functional cells remain an object of active pursuit. We previously demonstrated that genetic deletion of Fstl3, a critical regulator of activin activity, enhanced beta cell number and glucose-responsive insulin production. These observations suggested the hypothesis that FSTL3 neutralization could be used to therapeutically enhance beta cell number and function in humans. To pursue this possibility, we developed an FSTL3-neutralizing antibody, FP-101, and characterized its ability to prevent or disrupt FSTL3 from complexing with activin or related ligands. This antibody was selective for FSTL3 relative to the closely related follistatin, thereby reducing the chance for off-target effects. In vitro assays with FP-101 and activin revealed that FP-101-mediated neutralization of FSTL3 can enhance both insulin secretion and glucose responsiveness to nonfunctional mouse and human islets under conditions that model diabetes. Thus, FSTL3 neutralization may provide a novel therapeutic strategy for treating diabetes through repairing dysfunctional beta cells.

A Decade Later: Revisiting the TGFß Family's Role in Diabetes.

In 2010, we published a review summarizing the role of the transforming growth factor-beta (TGFß) family of proteins in diabetes. At that time there were still many outstanding questions that needed to be answered. In this updated review, we revisit the topic and provide new evidence that supports findings from previous studies included in the 2010 review and adds to the knowledge base with new findings and information. The most substantial contributions in the past 10 years have been in the areas of human data, the investigation of TGFß family members other than activin [e.g., bone morphogenetic proteins (BMPs), growth and differentiation factor 11 (GDF11), nodal], and the expansion of ß-cell number through various mechanisms including transdifferentiation, which was previously believed to not be possible.

Creation of a Dual-Purpose Collegiate Athlete Nutrition Advising Program and Educational Curriculum.

The intent of this article is to describe the process of creating a dual-purpose athlete nutrition advising program at the collegiate level. The first goal was to help student athletes enhance their performance through optimal fuel and hydration. The second goal was to provide experiential learning for nutrition students. This program provided a platform for nutrition students to gain hands-on experience assessing, monitoring, and educating athletes in relation to nutrition for performance. The implication for practice is based on recent growth and increased interest in the performance nutrition field that drives the need for more formal training programs.

Activin Enhances α- to ß-Cell Transdifferentiation as a Source For ß-Cells In Male FSTL3 Knockout Mice.

Diabetes results from inadequate ß-cell number and/or function to control serum glucose concentrations so that replacement of lost ß-cells could become a viable therapy for diabetes. In addition to embryonic stem cell sources for new ß-cells, evidence for transdifferentiation/reprogramming of non-ß-cells to functional ß-cells is accumulating. In addition, de-differentiation of ß-cells observed in diabetes and their subsequent conversion to α-cells raises the possibility that adult islet cell fate is malleable and controlled by local hormonal and/or environmental cues. We previously demonstrated that inactivation of the activin antagonist, follistatin-like 3 (FSTL3) resulted in ß-cell expansion and improved glucose homeostasis in the absence of ß-cell proliferation. We recently reported that activin directly suppressed expression of critical α-cell genes while increasing expression of ß-cell genes, supporting the hypothesis that activin is one of the local hormones controlling islet cell fate and that increased activin signaling accelerates α- to ß-cell transdifferentiation. We tested this hypothesis using Gluc-Cre/yellow fluorescent protein (YFP) α-cell lineage tracing technology combined with FSTL3 knockout (KO) mice to label α-cells with YFP. Flow cytometry was used to quantify unlabeled and labeled α- and ß-cells. We found that Ins+/YFP+ cells were significantly increased in FSTL3 KO mice compared with wild type littermates. Labeled Ins+/YFP+ cells increased significantly with age in FSTL3 KO mice but not wild type littermates. Sorting results were substantiated by counting fluorescently labeled cells in pancreatic sections. Activin treatment of isolated islets significantly increased the number of YFP+/Ins+ cells. These results suggest that α- to ß-cell transdifferentiation is influenced by activin signaling and may contribute substantially to ß-cell mass.

Activins A and B Regulate Fate-Determining Gene Expression in Islet Cell Lines and Islet Cells From Male Mice.

TGFß superfamily ligands, receptors, and second messengers, including activins A and B, have been identified in pancreatic islets and proposed to have important roles regulating development, proliferation, and function. We previously demonstrated that Fstl3 (an antagonist of activin activity) null mice have larger islets with ß-cell hyperplasia and improved glucose tolerance and insulin sensitivity in the absence of altered ß-cell proliferation. This suggested the hypothesis that increased activin signaling influences ß-cell expansion by destabilizing the α-cell phenotype and promoting transdifferentiation to ß-cells. We tested the first part of this hypothesis by treating α- and ß-cell lines and sorted mouse islet cells with activin and related ligands. Treatment of the αTC1-6 α cell line with activins A or B suppressed critical α-cell gene expression, including Arx, glucagon, and MafB while also enhancing ß-cell gene expression. In INS-1E ß-cells, activin A treatment induced a significant increase in Pax4 (a fate determining ß-cell gene) and insulin expression. In sorted primary islet cells, α-cell gene expression was again suppressed by activin treatment in α-cells, whereas Pax4 was enhanced in ß-cells. Activin treatment in both cell lines and primary cells resulted in phosphorylated mothers against decapentaplegic-2 phosphorylation. Finally, treatment of αTC1-6 cells with activins A or B significantly inhibited proliferation. These results support the hypothesis that activin signaling destabilized the α-cell phenotype while promoting a ß-cell fate. Moreover, these results support a model in which the ß-cell expansion observed in Fstl3 null mice may be due, at least in part, to enhanced α- to ß-cell transdifferentiation.

Comparative Analysis of the Mitochondrial Physiology of Pancreatic ß Cells.

The mitochondrial metabolism of ß cells is thought to be highly specialized. Its direct comparison with other cells using isolated mitochondria is limited by the availability of islets/ß cells in sufficient quantity. In this study, we have compared mitochondrial metabolism of INS1E/ß cells with other cells in intact and permeabilized states. To selectively permeabilize the plasma membrane, we have evaluated the use of perfringolysin-O (PFO) in conjunction with microplate-based respirometry. PFO is a protein that binds membranes based on a threshold level of active cholesterol. Therefore, unless active cholesterol reaches a threshold level in mitochondria, they are expected to remain untouched by PFO. Cytochrome c sensitivity tests showed that in PFO-permeabilized cells, the mitochondrial integrity was completely preserved. Our data show that a time-dependent decline of the oligomycin-insensitive respiration observed in INS1E cells was due to a limitation in substrate supply to the respiratory chain. We predict that it is linked with the ß cell-specific metabolism involving metabolites shuttling between the cytoplasm and mitochondria. In permeabilized ß cells, the Complex l-dependent respiration was either transient or absent because of the inefficient TCA cycle. The TCA cycle insufficiency was confirmed by analysis of the CO2 evolution. This may be linked with lower levels of NAD+, which is required as a co-factor for CO2 producing reactions of the TCA cycle. ß cells showed comparable OxPhos and respiratory capacities that were not affected by the inorganic phosphate (Pi) levels in the respiration medium. They showed lower ADP-stimulation of the respiration on different substrates. We believe that this study will significantly enhance our understanding of the ß cell mitochondrial metabolism.

Effects of patient health literacy, patient engagement and a system-level health literacy attribute on patient-reported outcomes: a representative statewide survey.

BACKGROUND: The effects of health literacy are thought to be based on interactions between patients' skill levels and health care system demands. Little health literacy research has focused on attributes of health care organizations. We examined whether the attribute of individuals' experiences with front desk staff, patient engagement through bringing questions to a doctor visit, and health literacy skills were related to two patient-reported outcomes. METHODS: We administered a telephone survey with two sampling frames (i.e., household landline, cell phone numbers) to a randomly selected statewide sample of 3358 English-speaking adult residents of Missouri. We examined two patient-reported outcomes - whether or not respondents reported knowing more about their health and made better choices about their health following their last doctor visit. Multivariable logistic regression models were used to examine the independent contributions of predictor variables (i.e., front desk staff, bringing questions to a doctor visit, health literacy skills). RESULTS: Controlling for self-reported health, having a personal doctor, time since last visit, number of chronic conditions, health insurance, and sociodemographic characteristics, respondents who had a good front desk experience were 2.65 times as likely (95% confidence interval [CI]: 2.13, 3.30) and those who brought questions were 1.73 times as likely (95% CI: 1.32, 2.27) to report knowing more about their health after seeing a doctor. In a second model, respondents who had a good front desk experience were 1.57 times as likely (95% CI: 1.26, 1.95) and those who brought questions were 1.66 times as likely (95% CI: 1.29, 2.14) to report making better choices about their health after seeing a doctor. Patients' health literacy skills were not associated with either outcome. CONCLUSIONS: Results from this representative statewide survey may indicate that one attribute of a health care organization (i.e., having a respectful workforce) and patient engagement through question asking may be more important to patient knowledge and health behaviors than patients' health literacy skills. Findings support focused research to examine the effects of organizational attributes on patient health outcomes and system-level interventions that might enhance patient health.

Effects of activin A on survival, function and gene expression of pancreatic islets from non-diabetic and diabetic human donors.

Emerging evidence suggests that activin with its associated receptors, second messengers, and antagonists would be excellent targets for therapeutic drug development in the treatment of diabetes. We undertook the current study to investigate the ability to extrapolate findings from rodent studies to human islets in which data thus far has been scarce. We tested the hypothesis that human islets synthesize activin and that activin participates in the regulation of islet ß-cells. Human islets from 33 separate isolations were categorized based on functional status, culture status and diabetic status. Statistical comparisons were made by ANOVA with Tukey post-hoc adjustment for multiple comparisons. Experiments investigating activin utilized qPCR, FACS cell sorting, immunofluorescent antibody staining, functionality assays, viability assays and protein secretion assays. We have defined the transcript expression patterns of activin and the TGFß superfamily in human islets. We found INHBA (the gene encoding activin A) to be the most highly expressed of the superfamily in normal, cultured islets. We elucidated a link between the islet microenvironment and activin A. We found differential ligand expression based on diabetic, culture and functional status. Further, this is also the first report that links direct effects of activin A with the ability to restore glucose-stimulated insulin secretion in human islets from type 2 diabetic donors thereby establishing the relevance of targeting activin for therapeutic drug development.

Increased activin bioavailability enhances hepatic insulin sensitivity while inducing hepatic steatosis in male mice.

The development of insulin resistance is tightly linked to fatty liver disease and is considered a major health concern worldwide, although their mechanistic relationship remains controversial. Activin has emerging roles in nutrient homeostasis, but its metabolic effects on hepatocytes remain unknown. In this study, we investigated the effects of increased endogenous activin bioactivity on hepatic nutrient homeostasis by creating mice with inactivating mutations that deplete the circulating activin antagonists follistatin-like-3 (FSTL3) or the follistatin 315 isoform (FST315; FST288-only mice). We investigated liver histology and lipid content, hepatic insulin sensitivity, and metabolic gene expression including the HepG2 cell and primary hepatocyte response to activin treatment. Both FSTL3-knockout and FST288-only mice had extensive hepatic steatosis and elevated hepatic triglyceride content. Unexpectedly, insulin signaling, as assessed by phospho-Akt (a.k.a. protein kinase B), was enhanced in both mouse models. Pretreatment of HepG2 cells with activin A increased their response to subsequent insulin challenge. Gene expression analysis suggests that increased lipid uptake, enhanced de novo lipid synthesis, decreased lipolysis, and/or enhanced glucose uptake contribute to increased hepatic triglyceride content in these models. However, activin treatment recapitulated only some of these gene changes, suggesting that increased activin bioactivity may be only partially responsible for this phenotype. Nevertheless, our results indicate that activin enhances hepatocyte insulin response, which ultimately leads to hepatic steatosis despite the increased insulin sensitivity. Thus, regulation of activin bioactivity is critical for maintaining normal liver lipid homeostasis and response to insulin, whereas activin agonists may be useful for increasing liver insulin sensitivity.

Differential synthesis and action of TGFß superfamily ligands in mouse and rat islets.

Members of the TGFß superfamily, including activins and TGFß, modulate glucose-stimulated insulin secretion (GSIS) in vitro using rat islets while genetic manipulations that reduce TGFß superfamily signaling in vivo in mice produced hypoplastic islets and/or hyperglycemia. Moreover, deletion of Fstl3, an antagonist of activin and myostatin, resulted in enlarged islets and ß-cell hyperplasia. These studies suggest that endogenous TGFß superfamily ligands regulate ß-cell generation and/or function. To test this hypothesis, we examined endogenous TGFß ligand synthesis and action in isolated rat and mouse islets. We found that activin A, TGFß1, and myostatin treatment enhanced rat islet GSIS but none of the ligands tested enhanced GSIS in mouse islets. However, follistatin inhibited GSIS, consistent with a role for endogenous TGFß superfamily ligands in regulating insulin secretion. Endogenous expression of TGFß superfamily members was different in rat and mouse islets with myostatin being highly expressed in mouse islets and not detectable in rats. These results indicate that TGFß superfamily members directly regulate islet function in a species-specific manner while the ligands produced by islets differ between mice and rats. The lack of in vitro actions of ligands on mouse islets may be mechanical or result from species-specific actions of these ligands.

Ion release from a novel orthodontic resin bonding agent for the reduction and/or prevention of white spot lesions. An in vitro study.

OBJECTIVE: To measure ion release from four sol-gel bioactive glass-containing orthodontic resin bonding agents (BAG-Bonds) following immersion into simulated body fluid (SBF) at pH values of 4 and 7. MATERIALS AND METHODS: Four BAG-Bonds, two containing fluoride, were developed. Prepared in our laboratory, the BAG-Bonds were composed of a mixture of resin monomers and bioactive glasses (BAGs). Workability of the final BAG-Bonds determined the amount of filler added to each, and this varied according to BAG composition. Commercially available Transbond-XT was used as the control. Three disks (10 mm × 2 mm) of each material were individually suspended in 3.5 mL of SBF at pH 4 and pH 7. SBF was analyzed to measure pH and ions released at 1 hour, 10 hours, and 100 hours. Calcium was measured by atomic absorption analysis, phosphate by ultraviolet visible spectrometry, and fluoride by an ion-specific electrode. The data were compared using a three-way analysis of variance, with P ≤ .05. RESULTS: Significant differences in calcium and phosphate ion release were found between the four BAG-Bonds and the control at multiple time points. Significant changes in pH were also found. There was no measureable release of fluoride from any of the materials. CONCLUSIONS: The BAG-Bonds showed the capacity for buffering acidic oral environments and significant release of calcium ions into their surrounding environment, and they hold the potential to be biomimetic bonding agents that may reduce white spot lesion formation.

Follistatin and follistatin like-3 differentially regulate adiposity and glucose homeostasis.

Transforming growth factor-ß superfamily ligands, including activin and myostatin, modulate body composition, islet function, and glucose homeostasis. Their bioactivity is controlled by the antagonists follistatin (FST) and FST like-3 (FSTL3). The hypothesis tested was that FST and FSTL3 have distinct roles in regulating body composition, glucose homeostasis, and islet function through regulation of activin and myostatin bioactivity. Three genetic mutant mouse lines were created. FSTL3 knockout (FSTL3 KO), a mouse line producing only the FST288 isoform (FST288-only) and a double mutant (2xM) in which the lines were crossed. FST288-only males were lighter that wild-type (WT) littermates while FSTL3 KO and 2xM males had reduced perigonadal fat pad weights. However, only 2xM mice had increased whole body fat mass and decreased lean mass by quantitative nuclear magnetic resonance (qNMR). Fasting glucose levels in FSTL3 WT and KO mice were lower than FST mice in younger animals but were higher in older mice. Serum insulin and pancreatic insulin content in 2xM mice was significantly elevated over other genotypes. Nevertheless, 2xM mice were relatively insulin resistant and glucose intolerant compared to FST288-only and WT mice. Fractional islet area and proportion of ß-cells/islet were increased in FSTL3 KO and 2xM, but not FST288-only mice. Despite their larger size, islets from FSTL3 KO and 2xM mice were not functionally enhanced compared to WT mice. These results demonstrate that body composition and glucose homeostasis are differentially regulated by FST and FSTL3 and that their combined loss is associated with increased fat mass and insulin resistance despite elevated insulin production.

Emerging roles for the TGFbeta family in pancreatic beta-cell homeostasis.

Loss of functional beta-cells is the primary cause of type 2 diabetes, so that there is an acute need to understand how beta-cell number and function are regulated in the adult under normal physiological conditions. Recent studies suggest that members of the transforming growth factor (TGF)-beta family regulate beta-cell function and glucose homeostasis. These factors are also likely to influence beta-cell proliferation and/or the incorporation of new beta-cells from progenitors in adults. Soluble TGFbeta antagonists also appear to have important roles in maintaining homeostasis, and the coordinated activity of TGFbeta family members is likely to regulate the differentiation and function of adult beta-cells, raising the possibility of developing new diabetes therapies based on TGFbeta agonists or antagonists.

Revascularization and remodelling of pancreatic islets grafted under the kidney capsule.

The revascularization and the structural changes resulting from interactions between the graft and the host were investigated in transplanted pancreatic islets under the kidney capsule. Islets were isolated from mice pancreata and transplanted in syngeneic diabetic animals. Graft-bearing kidneys were collected on different days post-transplant and processed for light microscopy, immunohistochemistry and transmission electron microscopy. A numerical analysis was performed in order to compare the percentage number of the different types of cells in native islets and at different time points after the transplant. Recipient animals reversed diabetes within 4 days. An intraperitoneal glucose tolerance test was performed to determine islet functionality under stressful conditions. During the initial few days post-transplant, the islets showed peculiar shapes and the graft tended to aggregate along the vessels. Starting at days 4-7 post-transplant, islets were revascularized from vessels connected to both the cortical and the capsular vascular network of the kidney. From day 7-14 post-transplant, the vessels progressively appeared more similar in features and size to those of in situ pancreatic islets. Both the percentage number of the different cell types and the distribution of Alpha, Beta and Delta cells inside the graft were significantly different as compared with intact islets, demonstrating quantitative and structural changes after the engraftment. No concomitant proliferation of Beta cells was detected using a bromodeoxyuridin staining method. Despite the fact that quick revascularization preserved a large mass of tissue, the remodelling process of the graft and the newly formed vascularization led to a different organization of the endocrine tissue as compared with intact in situ islets. This constitutes the morphological basis for alterations of the normal intercellular interactions and may explain the altered secretory cell function often observed in transplant.

Heparin-induced thrombocytopenia following pancreatectomy and islet auto-transplantation.

We report the case of a female with chronic pancreatitis who underwent multiple surgical procedures leading to total resection of the pancreas with successful islet auto-transplantation. Postoperatively, she developed heparin-induced thrombocytopenia. Heparinization prior to islet infusion is currently recommended to prevent portal vein thrombosis. Antibodies against heparin are not standard pre-operative testing for islet transplantation. Timely screening for heparin-dependent anti-platelet antibody should be kept in consideration for elective surgical cases (especially following previous surgeries) including pancreatic islet allo- and auto-transplantation.