Insulin resistance is a condition that is characterised by a desensitisation of the insulin receptor to the hormone insulin. Insulin resistance is present in the metabolic syndrome, a disorder of metabolic dysfunction that can increase the risk of developing obesity and cardiovascular disease. Many of the abnormalities seen in the metabolic syndrome are likely caused by dysfunction of the insulin system as a direct result of insulin resistance. Haemodynamic-metabolic coupling is a term that refers to the regulation of metabolism and haemodynamic functions in the post prandial state, where both food ingestion and subsequent insulin release regulate blood flow and other vascular parameters. Evidence suggests that insulin resistance may have detrimental effects on normal vascular function particularly during the fasting state. These haemodynamic disturbances, may in turn explain some of the reason that metabolic syndrome is associated with an increased risk of cardiovascular disease.
For example, researchers1 have investigated the fasting and postprandial cardiac responses of 66 subjects with and without insulin resistance. Insulin resistance was determine by using the insulin sensitivity index and cardiac response was measured using continuous impedance cardiography. This method was chosen because of its non-invasive nature that allowed continual monitoring. Fasting conditions increased systolic and diastolic blood pressure and the systemic vascular resistance index in the insulin resistance subjects, compared to their non-insulin resistance counterparts. In the postprandial state, acute vasodilatation occurred in both the insulin resistance and non-insulin resistant subjects to the same degree, but subsequent recovery of vascular tone was impaired in the insulin resistant subjects. Dysfunction to haemodynamics was directly correlated with metabolic disturbance in the fasting state, but postprandially, there was no significant difference between insulin resistance and non-insulin resistant subjects.
The insulin resistant subjects in this study experienced a disturbed vasodialatory response 30 to 180 min post ingestion of a mixed meal, which is typical of an exaggerated insulin response and defective glucose clearance. This might suggest a dysfunction in the metabolic-haemodynamic coupling in subjects with insulin resistance. The higher systolic and diastolic blood pressure seen in insulin resistance subjects are consistent with increased arterial stiffness and endothelial dysfunction that affects vasodilatation and pulse wave velocity. The mixed meal used in this study to elicit the effects was reasonable high in carbohydrate content. A meal with a lower carbohydrate content may therefore have affected the haemodynamic parameters in a less significant manner if the insulin and glucose area under the curve had been reduced. The haemodynamic disturbance seen in subjects with insulin resistance may therefore contribute to the increased risk of cardiovascular disease seen in these individuals.
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