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Sympathetic inhibition attenuates hypoxia induced insulin resistance
Author(s) -
Peltonen Garrett Lee,
Scalzo Rebecca L,
Schweder Melani M,
Szallar Steve E,
Binns Scott E,
Wood Lacey M,
Klochak Anna L,
Schroeder Thies,
Irwin David C,
Hamilton Karyn L,
Bell Christopher
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1150.5
Subject(s) - endocrinology , medicine , hypoxia (environmental) , insulin resistance , insulin , chemistry , oxygen , organic chemistry
Acute exposure to hypoxia decreases insulin sensitivity in healthy humans. The mechanism is unclear but increased activation of the sympathetic nervous system (SNS) may be involved. We hypothesized that SNS inhibition would attenuate hypoxia induced insulin resistance. Insulin sensitivity (hyperinsulinemic euglycemic clamp) was determined in 10 men (23±1 years, body mass index 24.2±0.8 kg/m 2 (mean±SE)) during normoxia (FIO 2 =0.21), hypoxia (FIO 2 =0.11), normoxia and SNS inhibition (48‐hour transdermal clonidine), and hypoxia and SNS inhibition. Oxyhemoglobin saturation was decreased ( P <0.01) in hypoxia (63±2%) compared with normoxia (96±0%), and was unaffected by SNS inhibition ( P >0.25). The area under the norepinephrine curve (relative to the normoxia response) was increased in hypoxia (137±13%; P =0.02); clonidine prevented the hypoxia induced increase under the norepinephrine curve (94±14%; P =0.43). Compared with normoxia (225±23 nmol/kg fat free mass/pmol/L/min) the glucose infusion rate (adjusted for fat free mass and circulating insulin), required to maintain blood glucose at 5 mmol/Lduring administration of insulin, was decreased in hypoxia (128±30; P =0.03), and unchanged during normoxia and SNS inhibition (219±19; P =0.86), and hypoxia and SNS inhibition (169±23; P =0.23). We conclude that short‐term SNS inhibition attenuates hypoxia induced insulin resistance. Support: DARPA N66001 ‐10‐c‐2134

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