Document Detail


Short-term hypocaloric nutrition but not bed rest decrease insulin sensitivity and IGF-I bioavailability in healthy subjects: the importance of glucagon.
MedLine Citation:
PMID:  9433709     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Hyperinsulinemic, normoglycemic clamps were performed before and after 24 h of either hypocaloric nutrition or bed rest in healthy subjects. Decreased insulin sensitivity and insulin-like growth factor-I (IGF-I) bioavalibility, as measured by the serum IGF-I/insulin-like growth factor binding protein-1 (IGFBP-1) ratio, was found after fasting, whereas no metabolic changes were found after bed rest. Glucagon seems to be a key regulator of IGFBP-1 after brief hypocaloric nutrition. Hypocaloric nutrition and immobilization may add to the catabolic response to surgery and other trauma. Presently, six healthy subjects were studied before and after a 24-h period of hypocaloric nutrition (200 kcal/24 h, fast) or immobilization (bed rest) using the hyperinsulinemic (0.8 mU.kg-1.min-1), normoglycemic (4.5 mmol/L) clamp, indirect calorimetry, and circulating levels of substrates and hormones. After fast, body weight decreased (P < 0.05), and nitrogen balance was negative (-10 +/- 1 g urea nitrogen/24 h). Basal levels of free fatty acids, glucagon, and IGFBP-1 increased (P < 0.05), whereas c-peptide levels and the IGF-I/IGFBP-1 ratio decreased (P < 0.05). However, no change was found in basal levels of IGF-1 or substrate oxidation. Furthermore, changes (%) in basal levels of glucagon after fast correlated to IGFBP-1 (r = 1.0, P < 0.05), whereas the suppressibility of IGFBP-1 by insulin was maintained at normal levels. During clamps, glucose infusion rates (GIR) decreased after fast (-43 +/- 13%, mean +/- SEM, P < 0.001). Although not significantly, clamp levels of fat oxidation tended to increase and glucose oxidation tended to decrease. Levels of IGFBP-1 during clamps were higher as compared with the control clamp (P < 0.05). No adverse metabolic changes were seen after bed rest, and no change in GIR during clamps were seen as compared with the control measurement (0 +/- 14%). After brief hypocaloric nutrition, insulin sensitivity is reduced, whereas IGF-I bioavalibility is reduced by an increase in levels of IGFBP-1. Glucagon seems to contribute to the increase in IGFBP-1 during these conditions.
Authors:
J Nygren; A Thorell; K Brismar; F Karpe; O Ljungqvist
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Nutrition (Burbank, Los Angeles County, Calif.)     Volume:  13     ISSN:  0899-9007     ISO Abbreviation:  Nutrition     Publication Date:    1997 Nov-Dec
Date Detail:
Created Date:  1998-02-27     Completed Date:  1998-02-27     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8802712     Medline TA:  Nutrition     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  945-51     Citation Subset:  IM    
Affiliation:
Department of Surgery, Gustaf V Research Institute, Karolinska Hospital, Stockholm, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Adult
Bed Rest / adverse effects*
Biological Availability
Blood Glucose / analysis,  metabolism
C-Peptide / blood,  metabolism
Calorimetry, Indirect
Cohort Studies
Fasting / adverse effects*
Fatty Acids, Nonesterified / blood,  metabolism
Glucagon / blood*,  metabolism
Glucose / administration & dosage
Glucose Clamp Technique
Glycerol / blood,  metabolism
Humans
Hydrocortisone / blood,  metabolism
Insulin / blood*,  metabolism
Insulin-Like Growth Factor Binding Protein 1 / blood,  metabolism
Insulin-Like Growth Factor I / analysis,  metabolism*
Male
Oxidation-Reduction
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/C-Peptide; 0/Fatty Acids, Nonesterified; 0/Insulin-Like Growth Factor Binding Protein 1; 11061-68-0/Insulin; 50-23-7/Hydrocortisone; 50-99-7/Glucose; 56-81-5/Glycerol; 67763-96-6/Insulin-Like Growth Factor I; 9007-92-5/Glucagon

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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