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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

Department of Endocrinology, Hvidovre Hospital, University of Copenhagen, DK-2650 Copenhagen, Denmark and ¹ Department of Growth and Reproduction, Rigshospitalet, University of Copenhagen, DK-2200 Copenhagen, Denmark

(Correspondence should be addressed to M H Rasmussen who is now at Langs Hegnet 52 B, Kongens Lyngby DK-2800, Denmark; Email: mhr{at}dadlnet.dk)

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).

Design: 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.

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