Alterations in heart rate variability during everyday life are linked to insulin resistance. A role of dominating sympathetic over parasympathetic nerve activity?

Abstract

AimsTo evaluate the role of the autonomic nervous system (ANS) in the development of insulin resistance (IR) and assess the relationship between IR and activity of ANS using power spectrum analysis of heart rate variability (HRV).Subjects and methodsTwenty-three healthy first-degree relatives of patients with type 2 diabetes (R) and 24 control subjects without family history of diabetes (C) group-matched for age, BMI and sex were included. Insulin sensitivity (M value) was assessed by hyperinsulinemic (56 mU/m2/min) euglycemic clamp. Activity of the ANS was assessed using power spectrum analysis of HRV in long-term recordings, i.e., 24-h ECG monitoring, and in short-term recordings during manoeuvres activating the ANS. Computed tomography was performed to estimate the amount and distribution of abdominal adipose tissue.ResultsInsulin sensitivity (M value, mg/kg lbm/min) did not differ significantly between the R and C groups. Total spectral power (Ptot) and very low-frequency (PVLF) power was lower in R than C during 24 h ECG-recordings (p = 0.02 and p = 0.03). The best fit multiple variable linear regression model (r2 = 0.37, p < 0.001 for model) indicated that body composition (BMI) and long-term low to high frequency (LF/HF) power ratio (std β = −0.46, p = 0.001 and std β = −0.28, p = 0.003, respectively) were significantly and independently associated with the M value.ConclusionAltered heart rate variability, assessed by power spectrum analysis, during everyday life is linked to insulin resistance. The data suggest that an increased ratio of sympathetic to parasympathetic nerve activity, occurring via both inherited and acquired mechanisms, could potentially contribute to the development of type 2 diabetes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0411-8) contains supplementary material, which is available to authorized users.

Heart Rate, Autonomic Function, and Future Changes in Glucose Metabolism in Individuals Without Diabetes: The Whitehall II Cohort Study

“…Autonomic imbalance has been observed in individuals with prediabetes(10) and the metabolic syndrome (11; 12) and is associated with incident diabetes (13; 14), suggesting that alterations in autonomic function may contribute to the pathogenesis of diabetes. Similar associations have been found in the offspring of type 2 diabetes patients (15) implying that a pathological interplay between autonomic neuropathy and glucose metabolism exists not only in diabetes but also in individuals with increased risk of the disease. Indeed, some cross-sectional cohort studies have shown that CAN assessed by heart rate variability (HRV) is associated with lower insulin sensitivity in non-diabetic individuals (16; 17).…”

WITHDRAWN: Nicotinamide Attenuates Streptozotocin-Induced Diabetes Complications and Increases Survival Rate in Rats: Role of Autonomic Nervous System.

“…Lin et al (2008) showed early cardiac autonomic dysfunction and barore ex impairment in diabetic rats pre-treated with N; however, rats were anesthetized during the evaluation [15]. In young adults with diabetic parents compared to non-diabetic parents, autonomic alterations were observed despite differences in baseline glycemia levels [16].…”

Altered Glucose Uptake in Muscle, Visceral Adipose Tissue, and Brain Predict Whole-Body Insulin Resistance and may Contribute to the Development of Type 2 Diabetes: A Combined PET/MR Study

“…VAT may, for example, influence whole-body glucose tolerance by release of free fatty acids and adipokines like leptin, omentin, resistin, visfatin, and interleukin-6 that signal to other tissues [20]. Additionally, altered glucose uptake in the brain may influence autonomic output to peripheral tissues, which in turn has been shown to affect glucose homeostasis and diabetes susceptibility [21,22]. Furthermore, the adipose tissue and brain may interact with each other through neuroendocrine pathways and autonomic nervous system feedback loops [23], and differences in VAT-brain interactions may contribute to alterations in whole-body insulin sensitivity.…”