Study of pancreatic β-cell dysfunction and heart failure in type 2 diabetes mellitus

Objective To investigate the clinical features and related hormone changes of diabetic cardiac insufficiency and pancreatic β-cell dysfunction in type 2 diabetes mellitus(T2DM). Methods From January to April 2008, 96 patients with T2DM(group A) and 35 healthy volunteers with a normal glucose tolerance (NGT) (group B) were enrolled in this study. According to the course of T2DM and symptom of heart failure, the patients in group A were divided into three groups: group A1: newly-diagnosed T2DM or course of T2DM 2 years without obvious signs and symptoms of heart failure, n=32; group A3: course of T2DM>2 years with obvious clinical signs and symptoms of heart failure, n=31. The serum fasting plasma glucose (FPG), fasting insulin(FINS), true insulin(TI), proinsulin(PI) and brain natriuretic peptide(BNP) were detected in all the subjects. The ratio between early diastolic peak flow velocity and atrium peak flow velocity(E/A), the lateral wall of mitral annular movement(e/a), pulmonary venous peak systolic velocities and diastolic velocities (S/D) and left ventricular ejection fraction(LVEF) stage in all subjects were examined by echocardiogram. Variance analysis was used for data analysis among the 4 groups. Results The Homa-Is decreased with the progression of T2DM (group B: 110.0±76.3, group A1: 45.0±22.7, group A2: 15.0±14.0, group A3: 5.8±2.4; F=6.34, P<0.05); it indicated that the secretary function of β-cell declined significantly with the progress of T2DM. The serum level of BNP was significantly increased accompanied the function declines of pancreatic β-cell (group B: (75±19) ng/L, group A1: (810±185) ng/L, group A2: (1060±264) ng/L, group A3: (2071±785) ng/L; F=8.89, P<0.05). The serum level of TI and PI in group A3 were all significantly lower than those in group B, A1 and A2 (all P<0.05). The values of E/A, e/a, S/D and LVEF in group A were all significantly lower than those in group B (all P<0.05). Conclusion With the functional declines of pancreatic β-cell in T2DM, the myocardial contractility and diastolic function declines, meanwhile the TI and PI secretion reduces, and these changes finally induce metabolic disorders which can aggravate heart failure. Key words: Diabetes mellitus, type 2; Insulin-secreting cells; Heart failure