title: Minimal changes in environmental temperature result in a significant increase in energy expenditure and changes in the hormonal homeostasis in healthy adults.
abstract: OBJECTIVE
  Resting energy expenditure (EE) is a major contributor to the total EE and thus plays an important role in body weight regulation. Adaptive thermogenesis is a major component of EE in rodents, but little is known on the effects of exposure of humans to mild and sustainable reduction in environmental temperature.
  
  
  METHODS
  To characterize the dynamic changes in continuously measured resting EE, substrate utilization, and hormonal axes simultaneously in response to mild reduction in environmental temperature, we performed a cross-over intervention.
  
  
  METHODS
  Twenty-five volunteers underwent two 12-h recordings of EE in whole room indirect calorimeters at 24 and 19 °C with simultaneous measurement of spontaneous movements and hormonal axes.
  
  
  RESULTS
  Exposure to 19 °C resulted in an increase in plasma and urine norepinephrine levels (P<0.0001), and a 5.96% (P<0.001) increase in EE without significant changes in spontaneous physical activity. Exposure to the lower temperature resulted in a significant increase in free fatty acid levels (P<0.01), fasting insulin levels (P<0.05), and a marginal decrease in postprandial glucose levels. A small but significant (P<0.002) increase in serum free thyroxine and urinary free cortisol (P<0.05) was observed at 19 °C.
  
  
  CONCLUSIONS
  Our observations indicate that exposure to 19 °C, a mild and tolerable cold temperature, results in a predictable increase in EE driven by a sustained rise in catecholamine and the activation of counter-regulatory mechanisms.
authors.affiliation: Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-1613, USA. fc93a@nih.gov
authors.forename: Francesco S
authors.initials: FS
authors.lastname: Celi
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Brychta
authors.forename: Joyce D
authors.initials: JD
authors.lastname: Linderman
authors.forename: Peter W
authors.initials: PW
authors.lastname: Butler
authors.forename: Anna Teresa
authors.initials: AT
authors.lastname: Alberobello
authors.forename: Sheila
authors.initials: S
authors.lastname: Smith
authors.forename: Amber B
authors.initials: AB
authors.lastname: Courville
authors.forename: Edwin W
authors.initials: EW
authors.lastname: Lai
authors.forename: Rene
authors.initials: R
authors.lastname: Costello
authors.forename: Monica C
authors.initials: MC
authors.lastname: Skarulis
authors.forename: Gyorgy
authors.initials: G
authors.lastname: Csako
authors.forename: Alan
authors.initials: A
authors.lastname: Remaley
authors.forename: Karel
authors.initials: K
authors.lastname: Pacak
authors.forename: Kong Y
authors.initials: KY
authors.lastname: Chen
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003080:Cold Temperature; D018592:Cross-Over Studies; D004734:Energy Metabolism / Q000502:physiology*; D004777:Environment; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D009043:Motor Activity; D009638:Norepinephrine / Q000652:urine; D022722:Thermogenesis / Q000502:physiology*; D013974:Thyroxine / Q000097:blood
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D013974:Thyroxine; D006854:Hydrocortisone; D009638:Norepinephrine
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