Elevated heart rate predicts β cell function in non-diabetic individuals: the RISC cohort.

Abstract

Elevated heart rate has been associated with insulin resistance and incident type 2 diabetes but its relationship with β-cell function is not known. Our aim was to investigate whether baseline heart rate is associated with β-cell function and hyperglycaemia. We used the prospective RISC cohort with 1005 non-diabetic individuals who had an oral glucose tolerance test (OGTT) at baseline and after 3 years. Impaired glucose regulation was defined as a fasting plasma glucose ≥ 6.1 mmol/l or a 2-h plasma glucose ≥ 7.8 mmol/l. Insulin sensitivity was assessed by the OGIS index and insulin secretion and β-cell glucose sensitivity at both baseline and 3 years. Baseline heart rate was positively related to both fasting (P < 0.0001) and 2 h glucose levels (P = 0.02) at year 3 and predicted the presence of impaired glucose regulation at year 3 in a logistic regression model adjusting for insulin sensitivity at inclusion (OR/10 beats per min: 1.31; 95% CI (1.07-1.61); P = 0.01). Baseline heart rate was associated with lower insulin sensitivity (β = -0.11; P < .0001), a decrease in both β-cell glucose sensitivity (β = -0.11; P = 0.003) and basal insulin secretion rate (β = -0.11; P = 0.002) at 3 years in an adjusted multivariable regression model. Baseline heart rate predicted the 3-year decrease in β-cell glucose sensitivity (β = -0.10; P = 0.007) and basal insulin secretion (β = -0.12; P = 0.007). Heart rate predicts β-cell function and impaired glucose regulation at 3 years in non-diabetic individuals, independently of the level of insulin sensitivity. These findings suggest a possible effect of the sympathetic nervous system on β-cell dysfunction, which deserves further investigation.