Browsing by Subject "diet"
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Item Craniofacial Bone Mineral Density in Mice with Osteogenesis Imperfecta(2019-05) McBride, Alexandra H.; Menegaz, Rachel A.; Muchlinski, Magdalena N.; Maddux, Scott D.Osteogenesis imperfecta (OI) is a rare genetic disorder characterized by the abnormal synthesis and assembly of type I collagen, a major organic component of bone. Clinical manifestations of the severe OI type III include small body size, limb deformities, and low bone mineral density (BMD) within the post-cranial skeleton. OI type III often co-occurs with craniofacial defects, such as dentinogenesis imperfecta (DI). The goals of this study are: (1) to examine whether type I collagen defects, as seen in OI type III, affect BMD within the craniofacial skeleton; (2) to determine whether BMD varies among specific region of the craniofacial skeleton; (3) to examine whether diet-related variation in biomechanical loading is related to higher craniofacial BMD. The homozygous recessive murine mouse (OIM-/-) is a model for OI Type III. Similar to human OI patients, OIM-/- mice exhibit low post-cranial BMD, smaller body size, and DI. OIM-/- mice and WT littermates were weaned at 21 days and raised on either hard (high loading) or soft (low loading) diets. This resulted in four genotype x diet treatment groups: OIM-soft (n=3), OIM-hard (n=6), WT-soft (n=3), and WT-hard (n=9). Micro-CT scans were collected at 16 weeks (skeletal maturity). BMD was measured using Bruker CTAnalyzer software for eight regions of interest (ROIs) within the mandible (TMJ, corpus at the second molar, and symphysis), facial skeleton (nasal bone, maxilla at the second molar, premaxilla at the incisor), and cranial vault (frontal and parietal bones). Pairwise Mann-Whitney U tests were used to statistically compare BMD between genotypes (α = 0.100). When controlling for diet, WT mice had significantly greater BMD values than OIM mice at each ROI except at the maxilla at M2. Although variation between treatment groups, a general trend for increased BMD in "high" strain regions, such as the mandibular symphysis or the maxillary incisor, existed. Lastly, WT mice raised on a hard diet were observed to have the highest BMD measurements across each region the craniofacial skeleton, however no significant differences were observed between OIM-/- mice raised on hard versus soft diets. These results suggest that craniofacial BMD is generally lower in individuals with type I collagen defects, consistent with the post-cranial presentation. Additionally, regions associated with high strain during routine masticatory loading exhibited increased BMD as compared to regions of the skull that experience relatively "low" strain during chewing. While diet-associated loading may influence craniofacial BMD, in this study type I collagen status appears to be the primary determinant of BMD.Item Effects of a Synthetic Amino Acid Diet: Insights from the Guy Microbiome, Inflammation, and Behavior(2021-05) Mancilla, Viviana J.; Allen, Michael S.; Jones, Harlan P.; Phillips, Nicole R.; Planz, John V.; Ellis, DorettePhenylketonuria (PKU) is an inborn error of phenylalanine metabolism primarily treated through a phenylalanine-restrictive diet and frequently supplemented with an amino acid formula to maintain proper nutrition. PKU patients often report high levels of anxiety along with symptoms of gastrointestinal distress (i.e., chronic diarrhea, constipation, cramps); symptoms previously associated with gut microbiome dysbiosis. Little is known of the effects of these dietary interventions on the gut microbiome of PKU patients, particularly in adults. The gut microbiome is a collection of microbes residing primarily in the large intestine. The colon is a major production site for short chain fatty acids (SCFAs) through anaerobic fermentation by commensal bacteria. SCFAs provide a source of energy for the colonocytes, as well as provide anti-inflammatory benefits. The production of SCFA appears to be dependent on the availability of soluble fibers and members of the gut microbiota capable of fermentation. We characterized the gut microbiome of adults with PKU for the first time and identified signs of dysbiosis. We then focused on the synthetic, low fiber, nature of the amino acid diet in a murine model. In this interdisciplinary study, we monitored the effect of a consuming synthetic diet on the composition of the murine gut microbiome over the course of 13 weeks, beginning at weaning. At the conclusion of the feeding period, mice we observed for anxiolytic behavior, locomotion, and cognition. We also searched for markers of inflammation through colon shrinkage, changes in cytokine levels within several tissues, and determined the concentration of SCFAs in the colon at the conclusion of the feeding period. The gut microbiome of mice fed the synthetic diet experienced significant deviation from the control group which affected relative abundance of beneficial bacteria. Mice on the synthetic diet were found to have shorter colons, lower concentration of SCFAs in the colon, and demonstrated elevated exploratory behavior.Item Physical Culture Classics: Pertinant Statements by the Masters(E.R. Dumont, 1909-01-01) Fleming, WilliamItem Physical Culture Classics: Strength From Exercise and Diet(E.R. Dumont, 1909-01-01) McFadden, Bernarr; Treloar, Albert; Merrilles, Charles; Fleming, WilliamItem The Adult Phenylketonuria (PKU) Gut Microbiome(MDPI, 2021-03-04) Mancilla, Viviana J.; Mann, Allison E.; Zhang, Yan; Allen, Michael S.Phenylketonuria (PKU) is an inborn error of phenylalanine metabolism primarily treated through a phenylalanine-restrictive diet that is frequently supplemented with an amino acid formula to maintain proper nutrition. Little is known of the effects of these dietary interventions on the gut microbiome of PKU patients, particularly in adults. In this study, we sequenced the V4 region of the 16S rRNA gene from stool samples collected from adults with PKU (n = 11) and non-PKU controls (n = 21). Gut bacterial communities were characterized through measurements of diversity and taxa abundance. Additionally, metabolic imputation was performed based on detected bacteria. Gut community diversity was lower in PKU individuals, though this effect was only statistically suggestive. A total of 65 genera across 5 phyla were statistically differentially abundant between PKU and control samples (p < 0.001). Additionally, we identified six metabolic pathways that differed between groups (p < 0.05), with four enriched in PKU samples and two in controls. While the child PKU gut microbiome has been previously investigated, this is the first study to explore the gut microbiome of adult PKU patients. We find that microbial diversity in PKU children differs from PKU adults and highlights the need for further studies to understand the effects of dietary restrictions.Item The Association of Multimorbidity With Whole Health Activities Among Adults in the United States: Evidence From the NHIS and BRFSS(Academic Consortium for Integrative Medicine & Health, 2023-05-08) Neba, Rolake A.; Warner, Mayela; Manning, Sydney E.; Wiener, R. Constance; Sambamoorthi, UshaBACKGROUND: Whole health is a holistic approach encompassing integrative medicine, emotional, and spiritual health and is critical to improving health outcomes among individuals with multimorbidity. OBJECTIVE: To examine the prevalence of Whole Health activities and the association of multimorbidity and Whole Health activities using nationally representative datasets. METHODS: As no single dataset has information on Whole Health self-care activities, data from the 2017 National Health Interview Survey (n = 25 134) was used to measure participants' mind-body therapy usage, sleep, mental health, and physical activity. We used the 2017 Behavioral Risk Factor Surveillance System (n = 347 029) to assess regular vegetable and/or fruit consumption. RESULTS: A significantly lower percentage of adults with multimorbidity had adequate sleep (58.2%vs.67.1%), no psychological distress (71.8%vs.82.1%), adequate physical activity (48.2%vs.62.1%), and regular vegetable and/or fruit consumption (54.2%vs.56.6%) compared to those without multimorbidity. Although lower percentages of adults with multimorbidity utilized mind-body therapies (22.9%vs.25.2%), the association was reversed when adjusted for socioeconomic factors. In the fully adjusted models, adults with multimorbidity were more likely to use mind-body therapies (AOR = 1.19, 95%CI = 1.09, 1.31). Furthermore, when adjusting for other independent variables, the associations of multimorbidity with sleep, psychological distress, and diet were exacerbated, and the association of multimorbidity with physical activity was attenuated. CONCLUSION: Adults with multimorbidity were less likely to engage in most of the Whole Health activities except mind-body therapies compared to the no multimorbidity group. Findings suggest that adjustment for other factors such as age and socioeconomic status changed the magnitude and direction of the association of multimorbidity with Whole Health activities.Item The Effect of Dietary Loading on Structural Determinants of Force Production in the Rat Masseter(2020-05) Rossiter, Jeffrey A.; Menegaz, Rachel A.; Maddux, Scott D.; Reeves, Rustin E.Rossiter, Jeffrey A., The Effect of Dietary Loading on Structural Determinants of Force Production in the Rat Masseter. Master of Science in Medical Sciences - Anatomy, May 2020. Biomechanical loading associated with feeding is known to direct cranial bone growth, however less is known about its effects on masticatory muscle growth and performance. Peak muscle contractile forces are determined by a combination of factors including total muscle mass, fiber length, and fiber type. Here, we test two hypotheses: that mechanically challenging diets will (1) increase the physiological cross-sectional area (PCSA), an estimate of maximum contractile force at tetanus, and (2) increase the number and proportion of type II (fast-twitch) muscle fibers in the masseter of the rat. Sprague-Dawley rats were raised on either a hard/tough (overuse) diet or a soft (underuse) diet (n=5/cohort). The superficial masseters were dissected and photographed using a trifocal stereo microscope, and muscle fiber length (6/individual) were measured using ImageJ. Muscle volumes were calculated from in-situ diffusible iodine-based contrast-enhanced μCT scans. Muscles were stained using an IHC protocol for the fast isoform of myosin heavy chain, allowing the number and areas of type II (stained) and type I (unstained) fibers to be quantified in ImageJ. Results from this study do not support our hypotheses, most likely due to the small sample sizes (n=5/treatment group) available for this study. Paradoxical results were found, with rats raised on a soft diet tending to have longer superficial masseter muscle fibers and more type II muscle fibers with larger cross-sectional areas in the posterior masseter. Rats raised on a hard diet tend to have larger masseter muscle volumes. However, these trends were not statistically significant (p > 0.05). Mechanically challenging diets tend to be associated with greater masticatory muscle volumes and thus increased PCSA. The fiber type results from the posterior masseter (with more deep masseter fibers) were the opposite of those previous results from the middle masseter (with more superficial masseter fibers) in the same animals. Future studies with increased sample sizes are needed to better understand the structural determinants of force production in the rat masseter.Item The Role of Advanced Glycation End Products in Brain Aging(2007-10-01) Thangthaeng, Nopporn; Michael J. Forster; Tina MachuThangthaeng, Nopporn, The Role of Advanced Glycation End Products in Brain Aging. Doctor of Philosophy (Biomedical Sciences), October, 2007, 178 pp., 9 tables, 6 figures, bibliography, 213 titles. Glycoxidation is a process of post-translational modification of proteins, involving both glycation and oxidation that ultimately generated advanced glycation end products (AGEs). Glycoxidation, which pay promote oxidative stress and disrupt protein structure and function, is hypothesized to be responsible for pathological conditions related to aging, diabetes, neurodegenerative diseases, and degenerative ophthalmic diseases. Previous studies have demonstrated that AGEs accumulate in the brains of aged animals and humans, yet few studies have directly addressed the possibility that AGEs are a cause of age-related brain dysfunction. Therefore, the overall purpose of the present studies was to examine the role AGEs in normal brain again and the associated decline in cognitive and psychomotor function. In order to achieve the goals, two different approaches were taken. The first approach involved (i) determining whether or not AGEs accumulated in different regions of the brain as a function of age and (ii) determining whether these changes were correlated with individual differences in the ability of old mice to perform in tests of cognitive and psychomotor function. Age-associated accumulation of CML, a predominant form of AGEs in vivo, and expression of receptor for AGEs (RAGE) protein, inferred from densitometry quantification of immunoblots in different regions of the brain, were assessed by comparing groups of 8-or 25-month old mice. The 25-month-old mice were administered a series of behavioral tests to assess cognitive and psychomotor function prior to assessment of glycation status. In the second approach, groups of mature (6 mos) and older mice (18 mos) were fed with a control diet or a diet enriched with galactose (49% of caloric content), an intervention that was expected to promote formation of AGEs. The mice were subsequently tested for impairment of their cognitive and psychomotor functions after 8 weeks on the assigned diet. Upon completion of the behavioral tests (after 14 weeks on diet), amounts of CML and RAGE protein were assessed through densitometric analyses of the immunoblots. The main findings from the first approach were that (i) there was a robust increase in CML content and expression of RAGE protein in the aged mouse brain that occurred in a region-specific manner; (ii) the relative amounts of CML and RAGE were not closely associated with the degree of age-related impairment of mice tested for brain function. The main findings from the second approach were that high dietary galactose: (i) failed to induce aged-like behavioral impairments in young/mature mice; (ii) exacerbated age-related impairment of some psychomotor functions and (iii) had no significant effects on glycation status or oxidative damage. Comparison of the experimental outcomes from the first and second approaches was complicated by a difference in the fat content of the diets fed to the mice in the two studies, which had an apparent effect on the amounts of AGEs and protein oxidation present in young mice. However, considering the results of the two studies independently warrants the following conclusions: (i) Amounts of AGEs do not predict individualized brain aging as assessed by neurobehavioral impairment and may instead by largely reflective of chronological age. (ii) Diets enriched with galactose may produce deleterious effects in older mice that do not involve a change in oxidative damage or glycation status. Overall, these studies provide little support for a specific role of glycoxidation in normal brain aging. It is impossible that the extent of accrual of AGEs in the normally aging brain is insufficient to affect cellular function, whereas larger accumulations of AGEs may be associated with various pathological conditions discussed in the literature.