Kyushu University · Medicine
Professor Maki Yokomoto-Umakoshi’s research lab focuses on the pathophysiological roles of adrenal hormones, particularly cortisol and DHEA-S, in age-related disorders such as sarcopenia, osteoporosis, and vascular dysfunction. The lab employs genetic epidemiology approaches, including Mendelian randomization, to investigate causal relationships between hormonal imbalances and musculoskeletal and metabolic health. A key research direction involves understanding the bone-vascular axis in glucocorticoid excess states, including Cushing’s syndrome and malignant pheochromocytoma/paraganglioma, where bone metastasis and skeletal-related events significantly impact patient quality of life. The lab also explores the protective effects of DHEA-S on bone mineral density and fracture risk.
Figures are computed from collected data and may differ slightly.
Abstract Context Prolonged exposure to pathological cortisol, as in Cushing’s syndrome causes various age-related disorders, including sarcopenia. However, it is unclear whether mild cortisol excess, for example, accelerates sarcopenia due to aging or chronic stress. Objective We used Mendelian randomization (MR) analysis to assess whether cortisol was causally associated with muscle strength and mass. Methods Three single-nucleotide polymorphisms associated with plasma cortisol concentrations i
Diabetes mellitus is associated with an increased risk of falls, which increases the incidence of osteoporotic fractures and accordingly decreases quality of life. However, the association between fall risk and diabetic complications is not completely understood. Therefore, the aim of this study was to examine the association between fall risk and osteoporotic fractures in patients with type 2 diabetes mellitus (T2DM). We enrolled 194 Japanese patients with T2DM and assessed their fall risk usin
DHEAS was associated with increased BMD and decreased fracture. DHEAS may play a protective role in decreasing fracture risk, mainly by increasing bone mass.
JSPS KAKENHI, Secom Science and Technology Foundation, Takeda Science Foundation, Japan Foundation for Applied Enzymology, AMED-CREST, JSTA-STEP, JST-Moonshot, and Ono Medical Research Foundation.
In endogenous glucocorticoid excess, bone and vascular diseases frequently coexisted, and deteriorated bone quality, not bone loss, was related to arterial stiffness. Thus, glucocorticoid excess may perturb the bone-vascular axis.
Malignant pheochromocytoma (PHEO) and paraganglioma (PGL) (PHEO and PGL: PPGL) are frequently associated with bone metastasis. Bone metastasis requires long-term management and may lead to skeletal-related events (SREs) that remarkably reduce patients' quality of life (QOL). The aim of this study was to elucidate the risk factors for developing bone metastasis in patients with PPGL. The medical records of 40 consecutive adult patients with malignant PPGL at the National Hospital Organization Kyo
Plasma steroid profiles differed between those with and without DM in men with NFAI. 11β-hydroxytestosterone was associated with hyperglycemia and indicators related to pancreatic β-cell dysfunction, independently of cortisol.
Abstract Context: Many endocrine diseases are known to cause secondary osteoporosis, which is potentially reversible by treatment of the underlying disease itself. Pheochromocytoma (PHEO) and paraganglioma (PGL) (PHEO and PGL: PPGLs) are the rare catecholamine-producing neuroendocrine tumors, which are associated with low bone mineral density (BMD). However, PPGLs have not been recognized as a cause of secondary osteoporosis. Indeed, even the prevalence of osteoporotic fracture in patients with
Adrenal hormones are essential for maintaining physiological homeostasis; however, imbalances in their production can significantly impact bone metabolism. This review examines how adrenal hormone dysregulation affects bone health, focusing on the following three key pathological conditions: autonomous cortisol secretion, primary aldosteronism, and pheochromocytoma/paraganglioma. Each disorder exerts distinct effects on bone metabolism, contributing to reduced bone mass, deteriorated bone qualit
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