Metabolic syndrome

Han, T. S. and Lean, M. E.J. (2015) Metabolic syndrome. Medicine, 43(2), pp. 80-87. (doi:10.1016/j.mpmed.2014.11.006)

Full text not currently available from Enlighten.

Abstract

The metabolic syndrome is a condition characterized by the co-existence of several major risk factors for cardiovascular disease (CVD) – high blood pressure, hyperglycaemia, and dyslipidaemia (reduced high-density lipoprotein cholesterol or raised triglycerides). These components are related to insulin resistance and appear to be aetiologically linked, probably by genetic factors. In recent years genome-wide association studies (GWAS) have provided new insights into the genetic basis of obesity and metabolic syndrome. The appearance of the metabolic syndrome phenotype is provoked by weight gain, particularly if there was poor intra-uterine growth, and specifically by intra-abdominal fat accumulation with a large waist circumference. The metabolic syndrome is highly prevalent among individuals with partial lipodystrophy and spinal cord injury, suggesting that a lack of subcutaneous adipose tissue and muscle atrophy play critical roles in metabolic disturbances. Sleep disorders may cause metabolic disturbances by inducing neurohumoral changes and perhaps altered muscle fibre adaptation. Developing the metabolic syndrome doubles the risk of CVD and type 2 diabetes, but offers an effective treatment approach. Reducing weight by 5–10 kg, by diet and exercise or with anti-obesity drugs, reduces CVD risk substantially and reduces diabetes risk by over 50%. Some new anti-diabetic agents have been found to improve insulin resistance, and to reduce lipids and weight, and could potentially be used to treat metabolic syndrome.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Lean, Professor Michael
Authors: Han, T. S., and Lean, M. E.J.
College/School:College of Medical Veterinary and Life Sciences > School of Medicine, Dentistry & Nursing
Journal Name:Medicine
Publisher:Elsevier
ISSN:1357-3039
ISSN (Online):1878-9390
Published Online:24 December 2014

University Staff: Request a correction | Enlighten Editors: Update this record