TY - JOUR
T1 - Acute altitude-induced hypoxia suppresses plasma glucose and leptin in healthy humans
AU - Kelly, Karen R.
AU - Williamson, David L.
AU - Fealy, Ciarán E.
AU - Kriz, David A.
AU - Krishnan, Raj K.
AU - Huang, Hazel
AU - Ahn, Janice
AU - Loomis, Joseph L.
AU - Kirwan, John P.
N1 - Funding Information:
The authors wish to acknowledge the excellent technical support provided by the Nursing and Dietary Staff of the General Clinical Research Center and the Technical/Engineering Staff of the Noll Physiological Research Center. We thank Dr Thomas Solomon and Dr Jacob Haus for their thoughtful comments on the manuscript. This research was supported by National Institutes of Health grant AG12834 to JPK and General Clinical Research Center grant MO1 RR10732.
PY - 2010/2
Y1 - 2010/2
N2 - To examine the effects of acute altitude-induced hypoxia on the hormonal and metabolic response to ingested glucose, 8 young, healthy subjects (5 men and 3 women; age, 26 ± 2 years; body mass index, 23.1 ± 1.0 kg/m2) performed 2 randomized trials in a hypobaric chamber where a 75-g glucose solution was ingested under simulated altitude (ALT, 4300 m) or ambient (AMB, 362 m) conditions. Plasma glucose, insulin, C-peptide, epinephrine, leptin, and lactate concentrations were measured at baseline and 30, 60, 90, and 120 minutes after glucose ingestion during both trials. Compared with AMB, the plasma glucose response to glucose ingestion was reduced during the ALT trial (P = .04). There were no differences in the insulin and C-peptide responses between trials or in insulin sensitivity based on the homeostasis model assessment of insulin resistance. Epinephrine and lactate were both elevated during the ALT trial (P < .05), whereas the plasma leptin response was reduced compared with AMB (P < .05). The data suggest that the plasma glucose response is suppressed at ALT, but this is not due to insulin per se because insulin and C-peptide levels were similar for both trials. Elevated plasma epinephrine and lactate during ALT are indicative of increased glycogenolysis, which may have masked the magnitude of the reduced glucose response. We conclude that, during acute altitude exposure, there is a rapid metabolic response that is accompanied by a shift in the hormonal milieu that appears to favor increased glucose utilization.
AB - To examine the effects of acute altitude-induced hypoxia on the hormonal and metabolic response to ingested glucose, 8 young, healthy subjects (5 men and 3 women; age, 26 ± 2 years; body mass index, 23.1 ± 1.0 kg/m2) performed 2 randomized trials in a hypobaric chamber where a 75-g glucose solution was ingested under simulated altitude (ALT, 4300 m) or ambient (AMB, 362 m) conditions. Plasma glucose, insulin, C-peptide, epinephrine, leptin, and lactate concentrations were measured at baseline and 30, 60, 90, and 120 minutes after glucose ingestion during both trials. Compared with AMB, the plasma glucose response to glucose ingestion was reduced during the ALT trial (P = .04). There were no differences in the insulin and C-peptide responses between trials or in insulin sensitivity based on the homeostasis model assessment of insulin resistance. Epinephrine and lactate were both elevated during the ALT trial (P < .05), whereas the plasma leptin response was reduced compared with AMB (P < .05). The data suggest that the plasma glucose response is suppressed at ALT, but this is not due to insulin per se because insulin and C-peptide levels were similar for both trials. Elevated plasma epinephrine and lactate during ALT are indicative of increased glycogenolysis, which may have masked the magnitude of the reduced glucose response. We conclude that, during acute altitude exposure, there is a rapid metabolic response that is accompanied by a shift in the hormonal milieu that appears to favor increased glucose utilization.
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U2 - 10.1016/j.metabol.2009.07.014
DO - 10.1016/j.metabol.2009.07.014
M3 - Article
C2 - 19765784
AN - SCOPUS:74049142850
SN - 0026-0495
VL - 59
SP - 200
EP - 205
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 2
ER -