Reduced Lower-Limb Muscle Strength in Type 2 Diabetes Patients with Arthritis Is Associated with Impaired Beta-Cell Function

Abstract

Insulin levels might affect the integrity of musculoskeletal structures. We hypothesized that in type 2 diabetes patients (T2D) with arthritis musculoskeletal impairment is associated with insulin secretion. This analysis of the German Diabetes Study comprised T2D with (T2D+A (n[m/f]=12[4/8], age 63±9 years, BMI 34.8±7.2 kg/m2) or without arthritis (T2D-A: 22[12/10], 59±13 years, 32.8±6.5 kg/m2) and healthy controls (CON: 18[10/8], 42±16 years, 25.3±4.1 kg/m2). Group comparison analyses were adjusted for age, sex and BMI. T2D duration was <5 years. Beta-cell function was assessed from C-peptide levels during glucagon stimulation test (GST) and intravenous glucose tolerance tests (IVGTT), insulin sensitivity (IS) from hyperinsulinemic-euglycemic clamps. Isometric knee extension force (KEF) was assessed with a dynamometer and range of motion (ROM) was measured using a goniometer. IS was comparable in T2D+A and T2D-A (3.5±0.7 vs. 5.1±2.4 mg*kg-¹*min-¹), but lower than in CON (11.5±3.3 mg*kg-¹*min-¹, p<0.05). Hemoglobin A1c (HbA1c) was similar in T2D+A and T2D-A (53±6 vs. 51±11 mmol/mol), but higher than in CON (33±3 mmol/mol, p<0.05). In T2D+A, C-peptide secretion (IVGTT) was 43% and 63% lower (p<0.05) than in T2D-A and in CON, respectively. C-peptide secretion (IVGTT) correlated inversely with HbA1c levels in T2D+A (r=-0.81, p<0.05) and T2D-A (r=-0.60, p<0.05). In T2D+A, KEF was 60% lower than in CON (19±11 kg vs. 47±12 kg, p<0.05) and correlated negatively with C-peptide secretion (GST; r=-0.99, p<0.05). ROM was 8% and 19% lower (p<0.05) in T2D+A than in T2D-A and CON, respectively. Within T2D+A, ROM was negatively correlated with insulin secretion (IVGTT; r=-0.64, p<0.05). In conclusion, musculoskeletal impairment is associated with decreased beta-cell function in T2D patients suffering from arthritis, possibly mediated by chronic hyperglycemia. Disclosure O.P. Zaharia: None. D. Pesta: None. P. Bobrov: None. Y. Kupriyanova: None. K. Bódis: None. V. Burkart: None. J. Hwang: None. K. Müssig: None. M. Roden: Speaker's Bureau; Self; Boehringer Ingelheim GmbH. Research Support; Self; Boehringer Ingelheim GmbH. Consultant; Self; Poxel SA. Research Support; Self; Danone Nutricia Early Life Nutrition, GlaxoSmithKline plc., Nutricia Advanced Medical Nutrition, Sanofi. J. Szendroedi: None.