Effects of short-term caloric restriction on circulating free IGF-I, acid-labile subunit, IGF-binding proteins (IGFBPs)-1-4, and IGFBPs-1-3 protease activity in obese subjects.
OBJECTIVE
Decreased levels of GH and total IGF-I have been reported in obesity. It has been hypothesized that increased free (biologically active) IGF-I levels generated from IGF-binding protein (IGFBP) protease activity could be the mechanism for the low GH release in dieting obese subjects. However, no published data exist on free IGF-I levels, acid labile subunit (ALS), or IGFBP protease activity in relation to GH release during a hypocaloric diet. The main purpose of this study was to determine free IGF-I, ALS, IGFBPs-1-4, and IGFBPs-1-3 protease activity in relation to 24-h GH release before and after a short-term very low-calorie diet (VLCD).


METHODS
Six obese subjects before weight loss, five after an average weight loss of 36.1 kg, and five age-and sex-matched lean controls underwent a 4-day VLCD. All subjects were studied on two occasions, once during normal basic diet and again during the last day of the VLCD (1.6 MJ).


METHODS
Free IGF-I was determined by a non-competitive immunoradiometric assay.


RESULTS
Free IGF-I levels decreased in concert with increased ALS and unchanged blunted GH release after a VLCD in the obese subjects. IGFBPs-1-3 proteolytic activity was found to be unchanged by hypocaloric diet in all groups.


CONCLUSIONS
We conclude that free IGF-I decreases after a short-term hypocaloric diet in obese subjects with no concomitant change in 24-h GH release. Circulating free IGF-I per se cannot be the main mechanism of the attenuated GH release in dieting obese subjects.
Rasmussen
Michael Højby
MH
Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, DK-2650 Copenhagen, Denmark. mhr@dadlnet.dk
Juul
Anders
A
Kjems
Lise Lund
LL
Hilsted
Jannik
J
D000328:Adult; D015992:Body Mass Index; D001835:Body Weight; D031204:Caloric Restriction; D002352:Carrier Proteins / Q000097:blood*; D004038:Diet, Reducing; D010450:Endopeptidases / Q000378:metabolism*; D005260:Female; D006023:Glycoproteins / Q000097:blood*; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D007333:Insulin Resistance; D018971:Insulin-Like Growth Factor Binding Protein 2 / Q000097:blood / Q000378:metabolism; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood / Q000378:metabolism; D018974:Insulin-Like Growth Factor Binding Protein 4 / Q000097:blood / Q000378:metabolism; D018969:Insulin-Like Growth Factor Binding Proteins / Q000097:blood* / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood* / Q000178:diet therapy; D011489:Protein Denaturation; D013851:Thinness / Q000097:blood; D013997:Time Factors; D015431:Weight Loss / Q000502:physiology
D002352:Carrier Proteins; D006023:Glycoproteins; D018971:Insulin-Like Growth Factor Binding Protein 2; D018972:Insulin-Like Growth Factor Binding Protein 3; D018974:Insulin-Like Growth Factor Binding Protein 4; D018969:Insulin-Like Growth Factor Binding Proteins; D020738:Leptin; C075944:insulin-like growth factor binding protein, acid labile subunit; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D010450:Endopeptidases; C095329:IGFBP-2 protease; C080473:insulin-like growth factor binding protein-3 protease