Intracellular Counter-regulatory Mechanisms Following Low Blood Glucose
Status:
Completed
Trial end date:
2014-04-01
Target enrollment:
Participant gender:
Summary
Diabetes mellitus type I (DMI) is characterized by lack of endogenous insulin and these
patients are 100% dependent on insulin substitution to survive. Diabetes mellitus type II
(DMII) is characterized by reduced insulin sensitivity and sometimes also reduced insulin
production, thus patients with DMII might also be dependent on insulin substitution.
Insulin is produced in- and secreted from the pancreas when blood glucose concentration rises
during- and after a meal. Insulin increases cellular uptake of glucose leading to lower blood
glucose concentration. Substitution with insulin is/can be necessary in DM, but at the same
time it induces the risk of hypoglycemia. This makes treatment with insulin a balancing act
between hyper- and hypoglycemia.
A hypoglycemic episode is a dreaded consequence of insulin overdosing, and also a very
frequent reason for hospital admission in patients with DM. Examples of hypoglycemic symptoms
may be; shaking, a sense of hunger, sweating, irritability progressing to lack of relevant
cerebral responses and eventually coma, convulsions and possibly death. People with diabetes
lose the ability to sense of low blood glucose with time, because of a lack of appropriate
counter-regulatory responses, hereby increasing the risk of severe hypoglycemia.
Understanding normal physiologic counter regulatory mechanisms during hypoglycemia is of
major importance to patients with DM and has the potential to change medical treatment in
diabetes, to reduce the risk of hypoglycemia.
Hypothesis: Hypoglycemia counteracts insulin signaling via hormone-dependent intracellular
counter-regulatory mechanisms, involving phosphorylation of specific signaling proteins.
Aim: To define counter-regulatory mechanisms in muscle- and fat tissue during hypoglycemia,
and to investigate the effect of insulin on lipid metabolism in healthy- and type I diabetic
subjects.