|
|
||||||||
Departments of Pediatrics and Internal Medicine, and the Yale Children's General Clinical Research Center, Yale University School of Medicine, New Haven, Connecticut 06520; and the Department of Vascular Surgery, Huddinge University Hospital, Karolinska Institute, S-105 21 Stockholm, Sweden
Impaired stimulation of glucose metabolism and
reduced suppression of lipolytic activity have both been suggested as
important defects related to the insulin resistance of adolescent
obesity. To further explore the relationship between these
abnormalities, we studied seven obese [body mass index (BMI) 35 ± 2 kg/m2] and seven
lean (BMI 21 ± 1 kg/m2)
adolescents aged 13-15 yr and compared them with nine lean adults (aged 21-27 yr, BMI 23 ± 1 kg/m2) during a two-step
euglycemic-hyperinsulinemic clamp in combination with
1) a constant
[2H5]glycerol
(1.2 mg · m
2 · min
1)
infusion to quantify glycerol turnover and
2) indirect calorimetry to estimate
glucose and net lipid oxidation rates. In absolute terms, basal
glycerol turnover was increased and suppression by insulin was impaired
in obese adolescents compared with both groups of lean subjects
(P < 0.01). However, when the rates
of glycerol turnover were adjusted for differences in body fat mass,
the rates were similar in all three groups. Basal plasma free fatty
acid (FFA) concentrations were significantly elevated, and the
suppression by physiological increments in plasma insulin was impaired
in obese adolescents compared with lean adults
(P < 0.05). In parallel with the
high circulating FFA levels, net lipid oxidation in the basal state and
during the clamp was also elevated in the obese group compared with
lean adults. Net lipid oxidation was inversely correlated with glucose
oxidation (r =
0.50,
P < 0.01). In conclusion, these data
suggest that lipolysis is increased in obese adolescents (vs. lean
adolescents and adults) as a consequence of an enlarged adipose mass
rather than altered sensitivity of adipocytes to the suppressing action
of insulin.
glycerol turnover; lipid oxidation; glucose metabolism
This article has been cited by other articles:
![]() |
V. Ferchaud-Roucher, E. Pouteau, H. Piloquet, Y. Zair, and M. Krempf Colonic fermentation from lactulose inhibits lipolysis in overweight subjects Am J Physiol Endocrinol Metab, October 1, 2005; 289(4): E716 - E720. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Kalderon, N. Mayorek, L. Ben-Yaacov, and J. Bar-Tana Adipose tissue sensitization to insulin induced by troglitazone and MEDICA 16 in obese Zucker rats in vivo Am J Physiol Endocrinol Metab, April 1, 2003; 284(4): E795 - E803. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. E. Shangraw and F. Jahoor Lipolysis and lipid oxidation in cirrhosis and after liver transplantation Am J Physiol Gastrointest Liver Physiol, June 1, 2000; 278(6): G967 - G973. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. S. Zawalich, G. J. Tesz, and K. C. Zawalich Are 5-Hydroxytryptamine-preloaded beta -Cells an Appropriate Physiologic Model System for Establishing That Insulin Stimulates Insulin Secretion? J. Biol. Chem., September 28, 2001; 276(40): 37120 - 37123. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |