Leptin response to endogenous acute stress is independent of pituitary function.
There are close interactions between the adipocyte-derived hormone, leptin, and the anterior pituitary, especially the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the relationship between the sympathetic adrenergic system and serum leptin levels, dependent on the function of anterior pituitary hormone axes, in 27 patients without a history of a hormone-secreting pituitary adenoma or other underlying endocrine disease. Based on responses in a routine insulin hypoglycemia test (ITT), the patients were classified as hypopituitary (HP; n=15), growth hormone deficient (GHD; n=6) or controls (CTR; 6 patients with normal responses). Nadir plasma glucose was 1.5+/-0.1 mmol/l at the time of maximum hypoglycemia. Each group had a significant increase in plasma epinephrine; however the magnitude of change was significantly higher in GHD (6.066+/-1.633 nmol/l) compared with HP patients (1.781+/-0.492 nmol/l) (P<0.01). The rise in norepinephrine was delayed (60 min) in the HP and CTR groups. However, in GHD patients there was a considerable increase at the time of hypoglycemia which was significantly different from HP (P<0.001) and CTR (P<0.05) patients. The increase in catecholamines was followed by a quick and significant decrease in serum leptin levels 45 min after an i.v. bolus injection of insulin in HP patients (-4.7+/-2.5%, P<0.05), which was significantly sustained after 60 min (-5.6+/-2.5%, P<0.05). In CTR patients there was a significant decrease in serum leptin levels 60 min after i.v. insulin (-14.4+/-6.9%, P<0.05), while no significant response was observed in the GHD group, although 5 of 6 patients had decreased levels at 45 and 60 min. No differences between the groups were found by ANOVA. In conclusion, an acute increase in endogenous circulating catecholamines is associated with a quick decrease in serum leptin levels. Intact anterior pituitary function seems not to be essential for this hitherto poorly understood mechanism.
Schafroth
U
U
Department of Endocrinology, National University Hospital, Sognsvannsveien 20, 0027 Oslo, Norway. urs.schafroth@rikshospitalet.no
Godang
K
K
Ueland
T
T
Bollerslev
J
J
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D004837:Epinephrine / Q000097:blood; D005260:Female; D019382:Human Growth Hormone / Q000097:blood / Q000172:deficiency; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007018:Hypopituitarism / Q000503:physiopathology; D007328:Insulin; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D007700:Kinetics; D020738:Leptin / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D010900:Pituitary Diseases / Q000503:physiopathology*; D010903:Pituitary Gland, Anterior / Q000503:physiopathology*
D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine