Metabolic Vascular Syndrome: New Insights into a Multidimensional Network of Risk Factors and Diseases

Abstract

Background: Since 1981, we have used the term metabolic syndrome to describe an association of a dysregulation in lipid metabolism (high triglycerides, low high-density lipoprotein cholesterol, disturbed glucose homeostasis (enhanced fasting and/or prandial glucose), gout, and hypertension), with android obesity being based on a common soil (overnutrition, reduced physical activity, sociocultural factors, and genetic predisposition). We hypothesized that main traits of the syndrome occur early and are tightly connected with hyperinsulinemia/insulin resistance, procoagulation, and cardiovascular diseases.

Methods: To establish a close link between the traits of the metabolic vascular syndrome, we focused our literature search on recent original work and comprehensive reviews dealing with the topics metabolic syndrome, visceral obesity, fatty liver, fat tissue inflammation, insulin resistance, atherogenic dyslipidemia, arterial hypertension, and type 2 diabetes mellitus.

Results: Recent research supports the concept that the metabolic vascular syndrome is a multidimensional and interactive network of risk factors and diseases based on individual genetic susceptibility and epigenetic changes where metabolic dysregulation/metabolic inflexibility in different organs and vascular dysfunction are early interconnected.

Conclusion: The metabolic vascular syndrome is not only a risk factor constellation but rather a life-long abnormality of a closely connected interactive cluster of developing diseases which escalate each other and should continuously attract the attention of every clinician.

Keywords: Common soil; Insulin resistance; Metabolic syndrome; Metabolic vascular syndrome; Obesity; Type 2 diabetes.

Figures

Fig. 1

Historic description of the metabolic syndrome (adapted from [1]).

Fig. 2

The multidimensional network of the metabolic vascular syndrome.

Fig. 3

Selective vascular insulin resistance (adapted from [21]).

Fig. 4

Effects of visceral obesity and ectopic fat depots on liver, vasculature, and muscle. RAS = Renin-angiotensin system; SNS = sympathetic nervous system; VAT = visceral adipose tissue; FFA = free fatty acids; IL6 = interleukin 6; CRP = C-reactive protein; ATII = angiotensin II; PA-I = plasminogen activator inhibitor.