Review article

Metabolic Insulin Resistance Syndrome and Metabolism of Carbohydrates

Željko Metelko
Neva Crkvenčić

Abstract

Insulin resistance represents the inability
of insulin to produce its usual biological effects at concentrations
effective in healthy subjects. These effects include
the effects on the metabolism of glucose, metabolism of
lipids, vascular and platelet function and regulation of the
autonomic nervous system. Physical inactivity, unhealthy
diet and sedentary lifestyle signifi cantly contribute to the
development of obesity, insulin resistance and type 2 diabetes.
Insulin resistance in type 2 diabetes is characterized by
the impaired ability of insulin to inhibit hepatic glucose production
and stimulate glucose uptake by skeletal muscle.
Insulin also fails to suppress lipolysis in adipose tissue thus
increasing the concentration of non-esterifi ed fatty-acids
(NEFA) that stimulate gluconeogenesis, triglyceride synthesis
and glucose production in the liver while further impairing
glucose utilization by skeletal muscle. Insulin resistance
in skeletal muscle is a result of multiple postreceptor
site defects: decreased activation of insulin receptor
substrate-1 (IRS-1) and phosphatidylinositol (PI)3-kinase,
impaired translocation of glucose transporter (GLUT 4),
and decreased glycogen synthesis. Insulin resistance in the
liver is manifested by the failure of insulin to suppress both
glucose output and very low density lipoprotein (VLDL) production.
Insulin resistance is characterized by the increase
in triglycerides and low density (LDL) lipoprotein, decrease
in high density (HDL) lipoprotein, decreased vasodilatation
of peripheral arteries and increased sympathetic nervous
system which may lead to procoagulant changes. Microvascular
complications are related to glycaemia, while macrovascular
complications are related to other risk factors
(hypertension, obesity, dyslipidaemia) as well.

Keywords

metabolic syndrome; insulin resistance; type 2 diabetes; glucose metabolism; obesity; impaired β cell function; lipids; hemorheology; diabetes complications

Hrčak ID:

18999

URI

https://hrcak.srce.hr/18999

Publication date:

15.11.2004.

Article data in other languages: croatian

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