title: Counter-regulatory response to hypoglycemia in the follicular and luteal phases of the menstrual cycle.
abstract: OBJECTIVE
  To assess whether the phase of the menstrual cycle influences the counter-regulatory response to hypoglycemia.
  
  
  METHODS
  Prospective randomized euglycemia-hypoglycemia clamp studies in the follicular and luteal phases of the menstrual cycle in the same woman.
  
  
  METHODS
  Clinical Research Center, Yale University School of Medicine.
  
  
  METHODS
  Eight regularly menstruating nonobese women.
  
  
  METHODS
  Counter-regulatory hormonal response to hypoglycemia-epinephrine, norepinephrine, glucagon, cortisol, GH, and PRL; glucose homeostasis: rates of whole-body glucose appearance and utilization, and the rate of hepatic glucose production.
  
  
  RESULTS
  In the follicular and luteal phases of the cycle fasting glucose levels (88 +/- 1 and 85 +/- 2 mg/dL, mean +/- SEM, respectively; conversion factor to SI units, 0.05551), basal glucose turnover (2.37 +/- 0.20 and 2.63 +/- 0.13 mg/kg per minute), basal insulin levels (10 +/- 1 and 9 +/- 1 microU/mL; conversion factor to SI units, 6.0), and insulin levels during the clamp study (53 +/- 3 and 45 +/- 4 microU/mL) were not significantly different. During the euglycemic phase of both studies, glucose utilization rose twofold (to 4.73 +/- 0.31 and 4.39 +/- 0.31 mg/kg per minute): hepatic glucose production was suppressed; and counter-regulatory hormones remained unchanged. Induction of hypoglycemia produced increases in the concentrations of counter-regulatory hormones that were indistinguishable in both phases of the cycle. Similarly, the increase in hepatic glucose production provoked during hypoglycemia was similar in each phase of the cycle (1.20 +/- 0.24 and 1.28 +/- 0.36 mg/kg per minute).
  
  
  CONCLUSIONS
  The counter-regulatory hormonal response to hypoglycemia, as well as the metabolic sequelae of these hormonal changes, are similar in the follicular and luteal phases of the menstrual cycle.
authors.affiliation: Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut.
authors.forename: M P
authors.initials: MP
authors.lastname: Diamond
authors.forename: D A
authors.initials: DA
authors.lastname: Grainger
authors.forename: G
authors.initials: G
authors.lastname: Rossi
authors.forename: M
authors.initials: M
authors.lastname: Connolly-Diamond
authors.forename: R S
authors.initials: RS
authors.lastname: Sherwin
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D004837:Epinephrine / Q000097:blood; D004958:Estradiol / Q000097:blood; D005260:Female; D005498:Follicular Phase / Q000502:physiology*; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000096:biosynthesis; D015309:Glucose Clamp Technique; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D008099:Liver / Q000378:metabolism; D008183:Luteal Phase / Q000502:physiology*; D009638:Norepinephrine / Q000097:blood; D011374:Progesterone / Q000097:blood; D011388:Prolactin / Q000097:blood; D011446:Prospective Studies; D011897:Random Allocation
chemical_list: D001786:Blood Glucose; D007328:Insulin; D011374:Progesterone; D004958:Estradiol; D011388:Prolactin; D013006:Growth Hormone; D005934:Glucagon; D005947:Glucose; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine