At a glance
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Metabolic Signalling in Muscle- and Adipose Tissue Following Insulin Withdrawal and Growth Hormone Injection in Type I Diabetes Mellitus, a Clinical Experimental Study.
In Brief
A clinical study evaluating Insulin withdrawal and Norditropin for Diabetes Mellitus Type I and Ketoacidosis. Completed, enrolled 9 participants across 1 site.
Detailed 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
Study Details
Timeline
Interventions
Withdrawal of usual (evening) insulin, replaced by Insuman Rapid (10% of the amount of usual evening insulin) as a continuous IV- administration overnight until 8 o'clock on the study day.
0,4 mg of GH administered at 7.05 A.M. on the study day.