Prevention of Metabolic Complications of Glucocorticoid Excess
Status:
Completed
Trial end date:
2015-01-01
Target enrollment:
Participant gender:
Summary
According to current estimates, nearly 1% of the general population is treated with long-term
glucocorticoids. Chronic hypercortisolism leads to a phenotype that resembles the metabolic
syndrome. The investigators have shown that inhibition of adenosine-monophosphate-activated
protein kinase (AMPK) activity in adipose tissue plays a role in corticosteroid-mediated
insulin resistance. Metformin, one of the mainstay therapies for type 2 diabetes, is a known
activator of AMPK, which mediates its beneficial effects on glucose and lipid metabolism. The
investigators have shown in an animal model that metformin - via altering AMPK activity -
prevents the development of the metabolic complications of glucocorticoid excess, and the
investigators wish to confirm this in a human study. The aim of this prospective, randomised,
double-blind, placebo-controlled study is to investigate the effect of metformin treatment on
metabolic parameters in patients on long-term high-dose glucocorticoids. The study is part of
the investigators translational project and could rapidly lead to immediate patient benefit,
improving quality of life and reducing health care costs for the NHS.
Phase:
Phase 2/Phase 3
Details
Lead Sponsor:
Barts & The London NHS Trust
Collaborator:
Barts and the London School of Medicine and Dentistry