Substrate Metabolism, Growth Hormone Signaling, and Insulin Sensitivity During Fasting
Status:
Completed
Trial end date:
2016-11-01
Target enrollment:
Participant gender:
Summary
Background: Calorie restriction increases longevity in many species and attenuate the
development of chronic disorders including type 2 diabetes, cardiovascular diseases and
cancer. In mice reduced activity of insulin-like growth factor I (IGF-I) and/or insulin is
associated with extended longevity. Growth hormone (GH) is the main regulator of IGF-I
production, but the molecular mechanism whereby GH switches from IGF-I stimulation (protein
anabolism) to fatty acid oxidation (fatty acid catabolism) as well as induction of insulin
resistance during fasting remains enigmatic.
Hypotheses: The changes of the global set of metabolites, induction of insulin resistance,
and the shift in metabolism from protein anabolism to lipolysis together with the potentially
favorable effect of calorie restriction during fasting depend on preserved fasting-induced GH
secretion.
Aim: The investigators wish to provide knowledge on changes in metabolites and shift in
signaling pathways that take place at the transition to the fasting state among healthy
overweight and obese subjects. Furthermore the investigators wish to determine the effect of
GH on the adaption of the metabolism to a fasting state.