Abstract
The oxidative stress associated with glucose variability might be responsible for neuronal damage while autonomic neuropathy (AN) has a detrimental effect on metabolism. The aim of the study was to find relationship between AN and GV in type 1 diabetic patients and to identify further factors that affect GV. Twenty type 1 diabetic patients were involved (age: 39.5 ± 3.4 years, duration of diabetes: 17.5 ± 2.5 years; HbA1c: 8.1 ± 0.2%, mean ± SE). AN was assessed by the cardiovascular reflex tests. The interstitial glucose levels were determined following insertion of a subcutaneous electrode during the continuous glucose monitoring (CGM) method on six consecutive days. GV was characterized by calculation of four parameters. SD of interstitial glucose values correlated positively with the overall AN score and the degree of the orthostatic reduction of systolic blood pressure (AN-score-SD ρ = 0.47, p < 0.05; orthostasis-SD: ρ = 0.51, p < 0.05). Mean absolute glucose (MAG) correlated with three parameters of AN (AN-score-MAG: ρ = 0.62, p < 0.01; 30/15 ratio-MAG: ρ = -0.50, p < 0.05; orthostasis-MAG: ρ = 0.59, p < 0.01). The HbA1c also correlated with two parameters of GV (HbA1c-continuous overlapping net glycemic action: ρ = 0.56, p < 0.05; HbA1c-MAG: ρ = 0.45, p < 0.05). The frequency of hypoglycemia did not exhibit any correlation with measures of GV. Severity of glucose variability but not overall glucose load correlates with both parasympathetic and sympathetic dysfunctions in type 1 diabetes. Higher HbA1c is associated with more severe glucose variability. The observed correlation between increased glucose variability and the severity of AN necessitates the further exploration of this relationship.
Highlights
Large prospective trials provided clear evidence two decades ago that long-term hyperglycemia due to less intensive treatment is associated with micro- and macrovascular complications in patients with diabetes [1, 2]
The glucose variability (GV) parameters were compared and no significant difference was proven between the groups with a tendency of higher GV parameters in the autonomic neuropathy (AN) group (CONGA: 7.6 ± 0.55 vs 8.5 ± 0.56 mmol/L, p = 0.235; SD: 3.3 ± 0.15 vs 3.67 ± 0.18 mmol/L, p = 0.129, mean amplitude of glycemic excursions (MAGE): 5.9 ± 0.4 vs 6.2 ± 0.16 mmol/L, p = 0.678; mean absolute glucose (MAG): 2.16 ± 0.3 vs 2.33 ± 0.09 mmol/L, p = 0.06; patients without AN vs patients with AN, mean ± SE)
The AN scores calculated from the cardiovascular reflex tests (CRT)-s expressing the overall severity of cardiovascular AN correlated positively with the SD of continuously measured interstitial glucose levels (ρ = 0.47, p < 0.05; Figure 1) showing that higher glucose variability expressed with SD was associated with more severe cardiovascular AN in this group of type 1 diabetic patients
Summary
Large prospective trials provided clear evidence two decades ago that long-term hyperglycemia due to less intensive treatment is associated with micro- and macrovascular complications in patients with diabetes [1, 2]. Reduced beta-cell function is one of the most important risk factors of GV and an inverse relationship between residual C-peptide levels and glucose variability has been shown in type 1 diabetic patients [10]. In type 1 diabetic patients, hyperglycemia is primarily related to the loss of endogenous insulin secretion, while the impaired glucagon response to hypoglycemia explains the susceptibility to abnormally low glucose values [12]. These observations suggest the hypothesis of a more pronounced GV in type 1 than in type 2 diabetic subjects. We investigated further possible pathogenetic factors of GV including HbA1c, body mass index (BMI), gender, age, daily insulin dose, diabetes duration, and frequency of hypoglycemia
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