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Insulin secretion and hepatic insulin clearance as determinants of hyperinsulinaemia in normotolerant grossly obese adolescents.

Published on Jan 2, 2007in Acta Paediatrica2.27
· DOI :10.1111/j.1651-2227.1998.tb01411.x
F. Cerutti23
Estimated H-index: 23
(UNITO: University of Turin),
Sacchetti C10
Estimated H-index: 10
(UNITO: University of Turin)
+ 3 AuthorsGiovanni Pacini52
Estimated H-index: 52
(National Research Council)
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Abstract
Obesity is characterized by variable degrees of hyperinsulinaemia, which has been attributed to either β-cell hypersecretion or reduced hepatic insulin extraction, or both. To investigate this controversial issue, a 4-h frequently sampled i.v. glucose tolerance test (glucose dose 12.8 g m -2 ) was performed in 13 normotolerant, grossly obese adolescents (10 F/3 M; 13 ± 1 y; body mass index 32 ± 0.9; pubertal stage 4-5; obesity duration 7.8 ± 3 y) and in a comparable group of 8 healthy, normal-weight subjects. Glucose, insulin and C-peptide time-course were analysed by the minimal model technique, which estimates β-cell secretion, insulin sensitivity (S i ), glucose effectiveness (S G ) and hepatic insulin extraction (HE). Despite similar fasting and after load glucose patterns (S G similar in the two groups), obese adolescents showed sustained peripheral hyperinsulinaemia (total insulin area under the concentration curve 67.2 ± 10.8 vs 19.1 ± 1.2 pmol I 1 in 240 min; p < 0.002) and a 71% reduction in S i (2.02±0.33 vs 6.95 ± 1.03 x 10 4 min -1 (μU ml -1 ); p < 0.001). Compared with control subjects, the total amounts of prehepatic insulin secretion and posthepatic insulin delivery were also increased significantly in obese adolescents by 30% and 46%, respectively; HE was reduced by 15% during the first 30 min of the test, but recovered within the normal range during the rest of the test. In conclusion, severely obese adolescents are insulin resistant and their hyperinsulinaemia is primarily caused by β-cell hypersecretion, whereas the reduction in insulin hepatic extraction is a transient metabolic phenomenon.
  • References (30)
  • Citations (16)
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References30
Newest
#1L.D. Monti (University of Milan)H-Index: 17
#2Paolo Brambilla (University of Milan)H-Index: 68
Last.Claudio Cobelli (UNIPD: University of Padua)H-Index: 83
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#1P. Cavallo-Perin (UNITO: University of Turin)H-Index: 33
#2Giovanni Pacini (UNITO: University of Turin)H-Index: 2
Last.Gianfranco Pagano (UNITO: University of Turin)H-Index: 44
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#1C. Le Stunff (French Institute of Health and Medical Research)H-Index: 4
#2Pierre-François Bougnères (French Institute of Health and Medical Research)H-Index: 18
Cited By16
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#1Josiane L. Broussard (Cedars-Sinai Medical Center)H-Index: 7
#2Cathryn M. Kolka (Cedars-Sinai Medical Center)H-Index: 15
Last.Richard N. Bergman (Cedars-Sinai Medical Center)H-Index: 103
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#1Yue Zhao (Nanjing University of Science and Technology)H-Index: 6
#2Ying Zhang (Nanjing University of Science and Technology)H-Index: 4
Last.Jianfa Zhang (NU: Nanjing University)H-Index: 2
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#1Mustafa Kanat (University of Texas Health Science Center at San Antonio)H-Index: 7
#2Luke Norton (University of Texas Health Science Center at San Antonio)H-Index: 17
Last.Muhammad A. Abdul-Ghani (University of Texas Health Science Center at San Antonio)H-Index: 41
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#1F. Cerutti (UNITO: University of Turin)H-Index: 23
#2Franco Rabbia (UNITO: University of Turin)H-Index: 27
Last.Giovanni Pacini (National Research Council)H-Index: 52
view all 10 authors...
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