Metabolic Signalling in Muscle- and Adipose-tissue Following Insulin Withdrawal and Growth Hormone Injection.
Status:
Completed
Trial end date:
2015-09-01
Target enrollment:
Participant gender:
Summary
Diabetes mellitus type I (DM I) is characterized by lack of endogenous insulin and these
patients are 100% dependent on insulin substitution to survive.
Insulin is a potent anabolic hormone with its primary targets in the liver, the skeletal
muscle-tissue and - adipose-tissue.
Severe lack of insulin leads to elevated blood glucose levels, dehydration, electrolyte
derangement, ketosis and thus eventually ketoacidosis.
Insulin signalling pathways are well-known.
Growth hormone (GH) is also a potent anabolic hormone, responsible for human growth and
preservation of protein during fasting. GH (in concert with lack of insulin) induces
lipolysis during fasting. It is not known how GH exerts its lipolytic actions.
The aim is to define insulin and growth hormone (GH) signalling pathways in 3 different
states in patients with DM I.
And to test whether ATGL-related lipolysis in adipose tissue contributes to the development
of ketosis.
1. Good glycemic control
2. Lack of insulin (ketosis/ketoacidosis)
3. Good glycemic control and GH injection