Open AccessIrisin is a predictor of sarcopenic obesity in type 2 diabetes mellitus
Author(s) -
Ayten Oğuz,
Murat Şahin,
Dilek Tüzün,
Ergül Kurutaş,
Cansu Ülgen,
Ozlem Bozkus,
Kamile Gül
Publication year - 2021
Publication title -
medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 148
eISSN - 1536-5964
pISSN - 0025-7974
DOI - 10.1097/md.0000000000026529
Subject(s) - medicine , sarcopenia , bioelectrical impedance analysis , myostatin , sarcopenic obesity , body mass index , percentile , endocrinology , type 2 diabetes mellitus , diabetes mellitus , obesity , skeletal muscle , statistics , mathematics
We aimed to evaluate sarcopenia and sarcopenic obesity (SO) in patients with type 2 diabetes mellitus (T2DM), possible relationships with serum irisin and myostatin levels, and the effect of glycemic control on SO. Ninety T2DM patients were included in this a cross-sectional study. Sarcopenia was determined by evaluating muscle mass (bioelectrical impedance analysis), muscle strength (HGS), and gait speed (GS). Patients with muscle mass loss with functionally reduced muscle strength and/or performance were considered sarcopenic. In addition, participants were divided into 3 groups according to the FM (fat mass)/FFM (fat-free mass) ratio [group 1:5th-50th percentiles; group 2:50th-95th percentiles and group 3: ≥95 percentiles (sarcopenic obese)]. Irisin, myostatin levels and metabolic parameters were measured in all patients. The prevalence of sarcopenia and SO was 25.6% and 35.6%, respectively. Irisin levels were lower in sarcopenic patients, while glycosylated hemoglobin (A1c), body mass index (BMI), FM, and FM index were higher ( P < .05). From group 1 to group 3, BMI, FM, FM index, GS, myostatin, and A1c increased, and muscle mass percentage, HGS, and irisin decreased ( P < .05). A positive correlation was found between FM/FFM and myostatin and a negative correlation between FM/FFM and irisin (r = 0.303, P = .004 vs. r = −0.491, P < .001). Irisin remained an important predictor of SO, even after adjusting for confounding variables (OR:1.105; 95% CI:0.965–1.338, P = .002). The optimal cut-off value for irisin to predict SO was 9.49 ng/mL (specificity = 78.1%, sensitivity = 75.8%). In addition, A1c was an independent risk factor for SO development (OR:1.358, P = .055). This study showed that low irisin levels (<9.49ng/mL) and poor glycemic control in T2DM patients were an independent risk factor, especially for SO.