Hypoxia & Glucose Regulation
Wednesday, May 16, 2012, 01:00 PM
Moby B-Wing, Room 213

Garrett Lee Peltonen defends his MS Thesis: Sympathetic Inhibition Attenuates Hypoxia Induced Insulin Resistance.

Audience members welcome, questions encouraged!

Abstract: Acute exposure to hypoxia decreases insulin sensitivity in healthy adult humans; the mechanism is unclear, but increased activation of the sympathetic nervous system may be involved. We have investigated the hypothesis that short-term sympathetic inhibition attenuates hypoxia induced insulin resistance. Insulin sensitivity (via the hyperinsulinemic euglycemic clamp) was determined in 10 healthy men (age 23 ± 1 years, body mass index 24.2 ± 0.8 kg m-2 (mean ± SE)), in a random order, during normoxia (FIO2 = 0.21), hypoxia (FIO2 = 0.11), normoxia and sympathetic inhibition (via 48-hour transdermal administration of the centrally acting alpha-2-adrenergic receptor agonist, clonidine), and hypoxia and sympathetic inhibition. Oxyhaemoglobin saturation (pulse oximetry) was decreased (P<0.001) with hypoxia (63 ± 2%) compared with normoxia (96 ± 0%), and was unaffected by sympathetic inhibition (P>0.25). The area under the noradrenaline curve (relative to the normoxia response) was increased with hypoxia (137 ± 13%; P=0.02); clonidine prevented the hypoxia induced increase (94 ± 14%; P=0.43). The glucose infusion rate (adjusted for fat free mass and circulating insulin concentration) required to maintain blood glucose concentration at 5 mmol L-1 during administration of insulin was decreased in hypoxia compared with normoxia (225 ± 23 vs. 128 ± 30 nmol kg fat free mass-1 pmol L-1 min-1; P=0.03), and unchanged during normoxia and sympathetic inhibition (219 ± 19; P=0.86) and hypoxia and sympathetic inhibition (169 ± 23; P=0.23). We conclude that short-term sympathetic inhibition attenuates hypoxia induced insulin resistance.

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Event Contact: Chris Bell can be reached at (970) 491-7522

Sponsored by the Department of Health and Exercise Science.