OBJECTIVE: To assess whether the phase of the menstrual cycle influences the counter-regulatory response to hypoglycemia. DESIGN: Prospective randomized euglycemia-hypoglycemia clamp studies in the follicular and luteal phases of the menstrual cycle in the same woman. SETTINGS: Clinical Research Center, Yale University School of Medicine. PATIENTS: Eight regularly menstruating nonobese women. MAIN OUTCOME MEASURES: 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). CONCLUSION: 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.
RCT Entities:
OBJECTIVE: To assess whether the phase of the menstrual cycle influences the counter-regulatory response to hypoglycemia. DESIGN: Prospective randomized euglycemia-hypoglycemia clamp studies in the follicular and luteal phases of the menstrual cycle in the same woman. SETTINGS: Clinical Research Center, Yale University School of Medicine. PATIENTS: Eight regularly menstruating nonobese women. MAIN OUTCOME MEASURES: 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). CONCLUSION: 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: Erica A Wehrwein; Rita Basu; Ananda Basu; Timothy B Curry; Robert A Rizza; Michael J Joyner Journal: J Physiol Date: 2010-10-04 Impact factor: 5.182
Authors: Marcia R Batista; Marta S Smith; Wanda L Snead; Cynthia C Connolly; D Brooks Lacy; Mary Courtney Moore Journal: Am J Physiol Regul Integr Comp Physiol Date: 2005-06-16 Impact factor: 3.619