Diabetes Mellitus Clinical Trial
Official title:
Hepatic Metabolic Changes in Response to Glucagon Infusion
The objective of the study is to investigate how exogenously administered glucagon affects hepatic lipid, glucose and protein metabolism as well as appetite, food intake and resting energy expenditure.
Most research has focused on the role of the pancreatic hormone, insulin, and insulin
signalling (or lack of) in the development of NAFLD. However, increasing evidence suggest
that the other major gluco-regulatory pancreatic hormone glucagon is also implicated in lipid
metabolism and recent human data from studies investigating the effect of glucagon receptor
antagonism suggest that glucagon signalling may be essential for maintaining a fat-free
liver. This, combined with observations of increased degree of hepatic steatosis in patients
after total pancreatectomy, who are devoid of pancreatic glucagon and typically are lean and
peripherally insulin sensitive, suggests that glucagon may play a hitherto unrecognised role
in the pathophysiology of NAFLD.
The hypothesis of the study is that exogenously delivered glucagon will drive hepatic
metabolism in a lipolytic direction and increase resting energy expenditure without affecting
appetite and food intake.
The acute effects of exogeneous glucagon infusion on hepatic lipid metabolism will be
evaluated in patients after total pancreatectomy (no endogenous pancreatic hormones), in
patients with type 1 diabetes (no endogenous insulin production) and in healthy controls
(preserved endogenous pancreatic hormones).
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