Hormonal, subjective, and neurocognitive responses to brief hypoglycemia in postmenopausal women and age-matched men with type 2 diabetes mellitus.
Sexual dimorphisms in hypoglycemic counterregulation are well documented in young healthy and type 1 diabetic subjects. Here, we questioned whether sex differences in counterregulation are present also in type 2 diabetic patients who are in a postmenopausal state. In an attempt to answer this question, we examined hormonal responses to a single-step hypoglycemic clamp (50 mg/dL) in 15 postmenopausal women and 15 age-matched men. Patients were also matched for body mass index, HbA(1c), diabetes duration, and diabetes therapy. In addition to hormonal counterregulation, perception of symptoms as well as aspects of neurocognitive function (short-term memory of words and reaction time on an auditory vigilance task) was assessed at baseline and during the hypoglycemic clamp. Hypoglycemia induced a profound rise in almost all counterregulatory hormones, that is, epinephrine, norepinephrine, corticotropin, cortisol, and growth hormone (all P < .007), except for glucagon, which slightly decreased (P = .014). However, none of the responses differed between sexes (all P > .256). In addition, perceived symptoms (P < .001) as well as reaction time on the vigilance task (P < .001) increased, and short-term memory performance tended to deteriorate (P = .091) during hypoglycemia. Again these changes did not differ between the sexes (all P > .370). In sum, data suggest that, in contrast to previous observations in young, healthy, and type 1 diabetic subjects, sex does not represent an important determinant of hormonal, subjective, and neurocognitive responses to hypoglycemia in postmenopausal type 2 diabetic patients. However, the women in our study were all postmenopausal and not receiving hormone replacement therapy. Therefore, our results cannot be generalized to female patients with type 2 diabetes who are premenopausal or on hormone replacement therapy, that is, conditions characterized by increased blood estrogen levels.
Bremer
Jan Phillip
JP
Department of Internal Medicine I, University of Luebeck, D-23538 Luebeck, Germany.
Baron
Maria
M
Peters
Horst
H
Oltmanns
Kerstin M
KM
Kern
Werner
W
Fehm
Horst L
HL
Born
Jan
J
Schultes
Bernd
B
D000324:Adrenocorticotropic Hormone / Q000097:blood; D003071:Cognition; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000503:physiopathology; D004837:Epinephrine / Q000097:blood; D005260:Female; D015309:Glucose Clamp Technique; D006728:Hormones / Q000097:blood*; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000097:blood / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D017698:Postmenopause / Q000097:blood*; D012737:Sex Factors
D006728:Hormones; D019382:Human Growth Hormone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine