Skeletal muscle microvascular exchange capacity is associated with hyperglycaemia in subjects with central obesity
M Turzyniecka1, S H Wild, A J Krentz
1School of Medicine, University of Southampton, Southampton, UK.
Insights
Skeletal muscle microvascular function, measured as K(f), is strongly linked to glycated haemoglobin (HbA(1c)) levels. This finding suggests K(f) is a key indicator for glycaemic control in individuals at risk for Type 2 diabetes.
Area of Science:
- Endocrinology
- Metabolic Health
- Vascular Physiology
Background:
- Poor glycaemic control elevates microvascular disease risk in organs like eyes and kidneys.
- The link between glycated haemoglobin (HbA(1c)) and skeletal muscle microvascular function remains underexplored.
- Central obesity and prediabetes increase the risk of Type 2 diabetes.
Purpose of the Study:
- To investigate the association between HbA(1c) and skeletal muscle microvascular exchange capacity (K(f)).
- To assess the relationship in individuals with central obesity at risk for Type 2 diabetes.
Main Methods:
- Study included 47 participants (28 women, 19 men) with central obesity, without diabetes.
- Measurements included insulin sensitivity (hyperinsulinaemic-euglycaemic clamp), body composition (MRI), cardiorespiratory fitness (VO(2) max), physical activity (METS), and skeletal muscle microvascular capacity (K(f)) via plethysmography.
- Regression modeling was used to analyze associations.
Main Results:
- HbA(1c) variance was initially explained by age, sex, and fasting plasma glucose (r(2) = 0.31).
- Adding K(f) significantly increased explained variance in HbA(1c) (r(2) = 0.57, P = 0.0001).
- Skeletal muscle microvascular capacity (K(f)) showed a strong, independent negative association with HbA(1c) (standardized B = -0.45, P = 0.001).
Conclusions:
- A significant inverse relationship exists between skeletal muscle microvascular exchange capacity (K(f)) and HbA(1c).
- K(f) independently predicts HbA(1c) levels, comparable in influence to fasting plasma glucose.
- Skeletal muscle microvascular function is a crucial factor in glycaemic regulation, particularly in at-risk populations.
Aims:
Poor glycaemic control is associated with increased risk of microvascular disease in various organs including the eye and kidney, but the relationship between glycated haemoglobin (HbA(1c)) and microvascular function in skeletal muscle has not been described. We tested the association between HbA(1c) and a measure of microvascular exchange capacity (K(f)) in skeletal muscle in people with central obesity at risk of developing Type 2 diabetes.
Methods:
Microvascular function was measured in 28 women and 19 men [mean (+/- sd) age 51 +/- 9 years] with central obesity who did not have diabetes. We estimated insulin sensitivity by hyperinsulinaemic-euglycaemic clamp, visceral and total fatness by magnetic resonance imaging, fitness (VO(2) max by treadmill testing), physical activity energy expenditure [metabolic equivalents of tasks (METS) by use of the SenseWear Pro armband] and skeletal muscle microvascular exchange capacity (K(f)) by venous occlusion plethysmography.
Results:
In regression modelling, age, sex and fasting plasma glucose accounted for 30.5% of the variance in HbA(1c) (r(2) = 0.31, P = 0.001). Adding K(f) to this model explained an additional 26.5% of the variance in HbA(1c) (r(2) = 0.57, P = 0.0001 and K(f) was strongly and independently associated with HbA(1c) (standardized B coefficient -0.45 (95% confidence interval -0.19, -0.06), P = 0.001).
Conclusions:
We found a strong negative independent association between a measure of skeletal muscle microvascular exchange capacity (K(f)) and HbA(1c). K(f) was associated with almost as much of the variance in HbA(1c) as fasting plasma glucose.
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