Prevalence and Risk Factors of Sarcopenia among Older Adults Aged ≥65 Years Admitted to Daycare Centers of Taiwan: Using AWGS 2019 Guidelines.

Sarcopenia is a geriatric syndrome which is likely to cause disability, body unbalance, and mortality and thus can lead to heavy healthcare expenditure and caregiver burden. Although some studies have addressed the prevalence of sarcopenia for older adults, there are limited studies conducted in daycare centers. The present study aimed to (i) estimate the prevalence of sarcopenia and (ii) explore associated factors of sarcopenia and standing balance among older adults admitted to daycare centers in Taiwan. The cross-sectional study collected data on demographics, health status, handgrip strength, gait speed (GS), skeletal muscle mass, Taiwan-Mini Nutritional Assessment Short-Form (TW-MNA-SF), and Short Physical Performance Battery from daycare centers in northern Taiwan. The definition of sarcopenia followed the Asian Working Group for Sarcopenia 2019 guidelines. Among 173 participants ≥65 year-old, 50.9% had confirmed sarcopenia, 47.4% possible sarcopenia, and 1.7% normal. Results showed that calf circumference, TW-MNA-SF, dementia, and body mass index (BMI) were associated with sarcopenia. Moreover, BMI, GS, and sarcopenia were associated factors of standing balance. The study estimated a high prevalence of sarcopenia in daycare centers and identified some significant factors of sarcopenia and standing balance. Early nutritional and physiotherapy interventions could benefit older adults to prevent sarcopenia or unbalance.

Selective serotonin reuptake inhibitor, fluoxetine, impairs E-cadherin-mediated cell adhesion and alters calcium homeostasis in pancreatic beta cells.

Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed drugs for mood disorders. Long term use of SSRIs is associated with an increased risk of diabetes, but the underlying mechanism(s) remains elusive. E-cadherin-mediated cell-cell adhesion and elevated [Ca2+]i are important for insulin release and pancreatic ß cell functions. This study aims to investigate whether a SSRI, fluoxetine (Prozac), induces pancreatic ß cell dysfunction through affecting E-cadherin and/or [Ca2+]i. Here we show that fluoxetine significantly reduces glucose stimulated insulin secretion (GSIS). MIN6 cells, an established murine immortalized ß cell line, form smaller colonies of loosely packed cells with reduced cell-cell contact after fluoxetine treatment. Immunofluorescence staining reveals that fluoxetine increases cytoplasmic accumulation of E-cadherin and reduces the membrane-localized E-cadherin probably due to increase of its endocytosis. Fluoxetine inhibits spreading of ß cells on E-cad/Fc coated slides and also disrupts E-cadherin-mediated actin filaments. Additionally, fluoxetine significantly suppresses endoplasmic reticulum (ER) calcium release and store-operated calcium entry (SOCE) activation, probably through reduction of ER calcium storage and inhibition of stromal interaction molecule 1 (STIM1) trafficking. These data suggest that exposure to fluoxetine results in impaired ß cell functions, occurring in concert with reduction of E-cadherin-dependent cell adhesion and alterations of calcium homeostasis.