Total parenteral nutrition after surgery rapidly increases serum leptin levels

Citation
A. Elimam et al., Total parenteral nutrition after surgery rapidly increases serum leptin levels, EUR J ENDOC, 144(2), 2001, pp. 123-128
Citations number
54
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
EUROPEAN JOURNAL OF ENDOCRINOLOGY
ISSN journal
08044643 → ACNP
Volume
144
Issue
2
Year of publication
2001
Pages
123 - 128
Database
ISI
SICI code
0804-4643(200102)144:2<123:TPNASR>2.0.ZU;2-C
Abstract
Objective: In humans, leptin is regulated by long-term changes in energy in take. However, short-term regulation of serum leptin by nutrients has been difficult to show. The aim of this study was to investigate whether short p eriods of fasting and stress sensitise the leptin response to nutrients. Subjects and experimental protocol: Fourteen patients of normal weight unde rgoing elective open cholecystectomy were randomised into two groups. One g roup received saline infusion during surgery and for 24 h postoperatively. The other group also received saline during the surgical procedure, but tot al parenteral nutrition (TPN) was started immediately after surgery, Blood samples were drawn before as well as 2, 4, 8, 16, and 24 h after the start of surgery to determine the serum levels of leptin and other hormones. Results: Postoperative TPN induced a significant rise in serum leptin withi n 6 h, reaching a more than fourfold increase within 14 h (P < 0.001). Seru m glucose and insulin levels increased within 2 h. Growth hormone and IGF-1 serum levels also increased significantly in the group receiving TPN. Seru m cortisol levels increased postoperatively in both groups, which may expla in why no significant reduction in serum leptin was observed in the group r eceiving saline. Free tri-iodothyronine (T3) decreased in both groups, whil e catecholamines were similar in the groups. Conclusion: During fasting and surgical stress, nutrients rapidly increased the serum leptin levels in humans in a manner similar to that previously r eported in rodents. This may be mediated by increases in serum glucose, ins ulin and cortisol.