Reduced hepatocellular lipid accumulation and energy metabolism in patients with long standing type 1 diabetes mellitus

The prevalence of obesity and metabolic syndrome increases in patients with type 1 diabetes mellitus (T1DM). In the general population this is linked with ectopic lipid accumulation in liver (HCL) and skeletal muscle (IMCL), representing hallmarks in the development of insulin resistance. Moreover, hepatic mitochondrial activity is lower in newly diagnosed patients with T1DM. If this precedes later development of diabetes related fatty liver disease is currently not known. This study aims to investigate energy metabolism in liver (k(ATP)) and skeletal muscle (k(CK)) and its impact on HCL, IMCL, cardiac fat depots and heart function in 10 patients with long standing T1DM compared to 11 well-matched controls by (31)P/(1)H magnetic resonance spectroscopy. HCL was almost 70% lower in T1DM compared to controls (6.9 ± 5% vs 2.1 ± 1.3%; p = 0.030). Also k(ATP) was significantly reduced (0.33 ± 0.1 s(−1) vs 0.17 ± 0.1 s(−1); p = 0.018). In T1DM, dose of basal insulin strongly correlated with BMI (r = 0.676, p = 0.032) and HCL (r = 0.643, p = 0.045), but not with k(ATP). In the whole cohort, HCL was significantly associated with BMI (r = 0.615, p = 0.005). In skeletal muscle k(CK) was lower in patients with T1DM (0.25 ± 0.05 s(−1) vs 0.31 ± 0–04 s(−1); p = 0.039). No significant differences were found in IMCL. Cardiac fat depots as well as heart function were not different. Our results in patients with long standing T1DM show that HCL is lower compared to matched controls, despite reduced energy metabolism in liver and skeletal muscle.