Insulin resistance and adipocyte function in metabolic syndrome
Research type
Research Study
Full title
Understanding the mechanisms of insulin resistance and adipocyte function in Type 2 Diabetes in subjects with metabolic syndrome
IRAS ID
205445
Contact name
Shaun Bolton
Contact email
Sponsor organisation
University Hospitals Birmingham NHS Foundation Trust
Duration of Study in the UK
1 years, 0 months, 0 days
Research summary
Obesity rates in the general population are steadily increasing, with the latest WHO data showing that in Europe over 50% of both men and women are overweight or obese, and about 23% of women and 20% of men are obese. Obesity is one of the key risk factors in the development of insulin resistance and type 2 diabetes, as well as cardiovascular diseases and cancer. The relationship between obesity and adverse health outcomes is clear at a population level, but the exact pathophysiological mechanism linking obesity to the development of insulin resistance is still a matter of intense research. Central to the development of insulin resistance in obese patients is adipose tissue dysfunction. We have recently undertaken a detailed metabolic characterisation of subjects with Alström syndrome who may serve as a model for understanding insulin resistance and its complications. Alström syndrome is a rare (1 per million) autosomal recessive (OMIM 203800) monogenic metabolic syndrome characterised by childhood onset obesity, extreme insulin resistance, acanthosis nigricans, diabetes, dyslipidaemia, hypertension and non-alcoholic fatty liver disease.
Understanding the adipose tissue dysfunction in monogenic metabolic syndrome and comparing with a “common obesity” will allow us to better define the pathophysiological mechanisms that underpin insulin resistance and obesity-associated complications. This rare natural model of adipose tissue dysfunction and insulin resistance can be highly informative as to the pathways that might be deregulated in adipose tissue in common obesity.
This study aims to understand the mechanisms contributing to adipose tissue dysfunction in Alstrom syndrome and determine whether similar pathophysiological mechanisms between Alstrom syndrome and “common obesity” contribute to the development of obesity-related complications by comparing the adipose tissue phenotype of AS patients with BMI-matched controls, as well as a control cohort, spanning various degrees of obesity and metabolic complications.
REC name
West Midlands - Solihull Research Ethics Committee
REC reference
16/WM/0400
Date of REC Opinion
18 Nov 2016
REC opinion
Further Information Favourable Opinion