Published online May 15, 2015. doi: 10.4239/wjd.v6.i4.626
Peer-review started: September 4, 2014
First decision: November 14, 2014
Revised: January 30, 2015
Accepted: February 9, 2015
Article in press: February 11, 2015
Published online: May 15, 2015
Processing time: 253 Days and 20.1 Hours
Under normal metabolic conditions insulin stimulates microvascular perfusion (capillary recruitment) of skeletal muscle and subcutaneous adipose tissue and thus increases blood flow mainly after meal ingestion or physical exercise. This helps the delivery of insulin itself but also that of substrates and of other signalling molecules to multiple tissues beds and facilitates glucose disposal and lipid kinetics. This effect is impaired in insulin resistance and type 2 diabetes early in the development of metabolic dysregulation and reflects early-onset endothelial dysfunction. Failure of insulin to increase muscle and adipose tissue blood flow results in decreased glucose handling. In fat depots, a blunted postprandial blood flow response will result in an insufficient suppression of lipolysis and an increased spill over of fatty acids in the circulation, leading to a more pronounced insulin resistant state in skeletal muscle. This defect in blood flow response is apparent even in the prediabetic state, implying that it is a facet of insulin resistance and exists long before overt hyperglycaemia develops. The following review intends to summarize the contribution of blood flow impairment to the development of the atherogenic dysglycemia and dyslipidaemia.
Core tip: Insulin resistance and type 2 diabetes present with diminished glucose transport and disposal in muscles and fat and inadequate inhibition of lipolysis after meal ingestion or during physical exercise. This defect lies mainly in the cellular and subcellular level of insulin action. However, the resistance in the haemodynamic properties of insulin is another facet of type 2 diabetes and the metabolic syndrome. In this review, we intend to summarize the contribution of this impairment to the development of the atherogenic dysglycemia and dyslipidaemia.