Interplay between Myokine Profile and Glycemic Control in Type 2 Diabetes Mellitus Patients with Heart Failure

Abstract

Type 2 diabetes mellitus (T2DM) remains a powerful predictor of progressive heart failure (HF), but it is not clear whether altered glycemic control interferes with HF progression via an impaired profile of circulating myokines. The aim was to investigate plausible effects of glucose control on a myokine signature in T2DM patients affected by chronic HF. We selected 372 T2DM patients from the local database and finally included 314 individuals suffering from chronic HF and subdivided them into two groups according to glycosylated hemoglobin (HbA1c) levels (<6.9% and ≥7.0%). Echocardiography and Doppler examinations along with biomarker measurements were performed at the baseline of the study. The results showed that irisin levels were significantly lower in patients with HbA1c ≥ 7.0% than in those with HbAc1 < 6.9%, whereas concentrations of apelin, myostatin and adropin did not significantly differ between these two groups. We also identified numerous predictors of poor glycemic control, but only N-terminal brain natriuretic propeptide (odds ratio [OR] = 1.07; 95% confidence interval [CI] = 1.02–1.10, p = 0.04) and irisin (OR = 1.09; 95% CI = 1.04–1.17, p = 0.001) remained independent predictors of the dependent variable. In conclusion, we found that decreased levels of irisin were associated with poor glycemic control in T2DM patients with HF regardless of clinical conditions and other biomarkers.

Adropin Predicts Chronic Kidney Disease in Type 2 Diabetes Mellitus Patients with Chronic Heart Failure

“…Another study reported that elevated serum levels of adropin correlated with a low risk of carotid atherosclerosis in T2DM patients [ 25 ]. Yet, elevated serum adropin levels after treatment with sitagliptin or SGLT2 inhibitors were strongly associated with improvements in fasting blood glucose, glycosylated haemoglobin (HbA1c), insulin sensitivity, and NP levels [ 26 , 27 ]. Along with it, aerobic exercise training was able to increase plasma levels of adropin in connection with blood pressure reduction by increasing nitric oxide production and bioavailability [ 28 ].…”

“…Along with it, aerobic exercise training was able to increase plasma levels of adropin in connection with blood pressure reduction by increasing nitric oxide production and bioavailability [ 28 ]. On the contrary, in patients with cardiac dysfunction, the serum levels of adropin increased significantly according to the New York Heart Association (NYHA) class of HF and demonstrated a tendency to decrease during treatment with hydralazine combined with sodium nitroprusside and SGLT2 inhibitors [ 27 , 29 , 30 , 31 ]. Although low levels of adropin predicted CKD in T2DM and high levels of adropin were associated with HF, there is no certain evidence that adropin has a discriminative value for CKD in HF patients with T2DM [ 32 ].…”