The GH/IGF-I axis in obesity: influence of neuro-endocrine and metabolic factors.
In this review we propose an integrated neuro-endocrine-metabolic point of view on the alterations (adaptations?) of GH/IGF-1 axis in obesity, summarizing the evidence from the literature, particularly focusing the data on humans and adding where possible results from our studies in this field. It is well-known that GH secretion is deeply impaired in overweight patients: we reviewed the multiple mechanisms underlying this issue, considering either central (CNS-related, such as impairment of GHRH tone or increased somatostatin release) or peripheral (ie metabolic: insulin, free fatty acids, glucose) factors. A central point of the debate about GH insufficiency in obesity is if it represents a simple adaptive phenomenon or reflects a true impairment of the axis activity. Evaluation of IGF-I levels and generation in obesity was the mean used to address this question: a bulk of evidence on IGF-I balance in human obesity has been provided, but the matter is still uncertain and unsolved.
Maccario
M
M
Department of Internal Medicine, University of Turin, Italy.
Grottoli
S
S
Procopio
M
M
Oleandri
S E
SE
Rossetto
R
R
Gauna
C
C
Arvat
E
E
Ghigo
E
E
D001786:Blood Glucose / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D019382:Human Growth Hormone / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D009490:Neurosecretory Systems / Q000503:physiopathology*; D009765:Obesity / Q000503:physiopathology*
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I