Browsing by Author "Wilson, Hannah E."

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    Sexual and reproductive health considerations in the care of young adults with inflammatory bowel disease: A multidisciplinary conversation
    (Elsevier, 2023-12-07) Reed, Sydney; Bugwadia, Amy K.; Dave, Sneha; Wilson, Hannah E.; Ramesh, Prathikka; Michel, Hilary K.; Anatomy, Cell Biology and Physiology, School of Medicine
    The effects of inflammatory bowel disease (IBD) and the medications used to treat it on sexual and reproductive health can be significant, impacting the quality of life of patients across gender identities. This article presents insights from a roundtable discussion facilitated by the Crohn's and Colitis Young Adults Network (CCYAN) between young adult patients with IBD and medical professionals, including physicians, nurses, psychologists, and trainees/medical students. It underscores the distinction between sexual and reproductive health, emphasizing the need to address both aspects comprehensively. The discussion identified key themes, including sexual dysfunction and well-being in IBD patients; discussing sexual health with young adult IBD patients; current research in reproductive health: gaps and opportunities; discussing reproductive health with young adult IBD patients; and providing resources and comprehensive multidisciplinary care.
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    The Dietary Fiber Inulin Slows Progression of Chronic Kidney Disease–Mineral Bone Disorder (CKD-MBD) in a Rat Model of CKD
    (Oxford University Press, 2023-12-07) Biruete, Annabel; Chen, Neal X.; Metzger, Corinne E.; Srinivasan, Shruthi; O’Neill, Kalisha; Fallen, Paul B.; Fonseca, Austin; Wilson, Hannah E.; de Loor, Henriette; Evenepoel, Pieter; Swanson, Kelly S.; Allen, Matthew R.; Moe, Sharon M.; Anatomy, Cell Biology and Physiology, School of Medicine
    Chronic kidney disease (CKD)–mineral bone disorder (CKD‐MBD) leads to fractures and cardiovascular disease. Observational studies suggest beneficial effects of dietary fiber on both bone and cardiovascular outcomes, but the effect of fiber on CKD‐MBD is unknown. To determine the effect of fiber on CKD‐MBD, we fed the Cy/+ rat with progressive CKD a casein‐based diet of 0.7% phosphate with 10% inulin (fermentable fiber) or cellulose (non‐fermentable fiber) from 22 weeks to either 30 or 32 weeks of age (~30% and ~15% of normal kidney function; CKD 4 and 5). We assessed CKD‐MBD end points of biochemistry, bone quantity and quality, cardiovascular health, and cecal microbiota and serum gut‐derived uremic toxins. Results were analyzed by two‐way analysis of variance (ANOVA) to evaluate the main effects of CKD stage and inulin, and their interaction. The results showed that in CKD animals, inulin did not alter kidney function but reduced the increase from stage 4 to 5 in serum levels of phosphate and parathyroid hormone, but not fibroblast growth factor‐23 (FGF23). Bone turnover and cortical bone parameters were similarly improved but mechanical properties were not altered. Inulin slowed progression of aorta and cardiac calcification, left ventricular mass index, and fibrosis. To understand the mechanism, we assessed intestinal microbiota and found changes in alpha and beta diversity and significant changes in several taxa with inulin, together with a reduction in circulating gut derived uremic toxins such as indoxyl sulfate and short‐chain fatty acids. In conclusion, the addition of the fermentable fiber inulin to the diet of CKD rats led to a slowed progression of CKD‐MBD without affecting kidney function, likely mediated by changes in the gut microbiota composition and lowered gut‐derived uremic toxins.
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    The uremic toxin indoxyl sulfate decreases osteocyte RANKL/OPG and increases Wnt inhibitor RNA expression that is reversed by PTH
    (Oxford University Press, 2024-10-29) Chen, Neal X.; O’Neill, Kalisha D.; Wilson, Hannah E.; Srinivasan, Shruthi; Bonewald, Lynda; Moe, Sharon M.; Medicine, School of Medicine
    Renal osteodystrophy (ROD) leads to increased fractures, potentially due to underlying low bone turnover in chronic kidney disease (CKD). We hypothesized that indoxyl sulfate (IS), a circulating toxin elevated in CKD and a ligand for the aryl hydrocarbon receptor (AhR), may target the osteocytes leading to bone cell uncoupling in ROD. The IDG-SW3 osteocytes were cultured for 14 days (early) and 35 days (mature osteocytes) and incubated with 500 μM of IS after dose finding studies to confirm AhR activation. Long-term incubation of IS for 14 days led to decreased expression of Tnfsf11/Tnfrsf11b ratio (RANKL/OPG), which would increase osteoclast activity, and increased expression of Wnt inhibitors Sost and Dkk1, which would decrease bone formation in addition to decreased mineralization and alkaline phosphatase (ALP) activity. When osteocytes were incubated with IS and the AhR translocation inhibitor CH223191, mineralization and ALP activity were restored. However, the Tnfsf11/Tnfrsf11b ratio and Sost, Dkk1 expression were not altered compared with IS alone, suggesting more complex signaling. In both early and mature osteocytes, co-culture with parathyroid hormone (PTH) and IS reversed the IS-induced upregulation of Sost and Dkk1, and IS enhanced the PTH-induced increase of the Tnfsf11/Tnfrsf11b ratio. Co-culture of IS with PTH additively enhanced the AhR activity assessed by Cyp1a1 and Cyp1b1 expression. In summary, IS in the absence of PTH increased osteocyte messenger RNA (mRNA) Wnt inhibitor expression in both early and mature osteocytes, decreased mRNA expression ofTnfsf11/Tnfrsf11b ratio and decreased mineralization in early osteocytes. These changes would lead to decreased resorption and formation resulting in low bone remodeling. These data suggest IS may be important in the underlying low turnover bone disease observed in CKD when PTH is not elevated. In addition, when PTH is elevated, IS interacts to further increase Tnfsf11/Tnfrsf11b ratio for osteoclast activity in both early and mature osteocytes, which would worsen bone resorption.