Counterregulatory Hormone Responses To Hypoglycemia In Women

There is a large sexual dimorphism in counterregulatory responses to hypoglycemia. It has been clearly demonstrated that both healthy young men and women with T1DM have reduced neuroendocrine, ANS, and EGP as compared to age and body mass indexed matched men (39-43). Davis et al. (2000) (43) illustrated that healthy and T1DM women have lower catecholamine, glucagon, cortisol, growth hormone, EGP, and lactate responses compared to age and BMI matched men. On the other hand, women have increased lipolytic responses to hypoglycemia. This sexual dimorphism also occurs during exercise and is not due to differences in glycemic thresholds for activation of counterregulatory responses (43) (Fig. 5).

In a series of separate glucose clamp studies at glycemic targets of 90, 70, and 50 mg/dL, Davis et al. (2000) (41) demonstrated that reduced central nervous system drive is responsible for the sexual dimorphic responses to hypoglycemia occurring in women. In a subsequent study, Sandoval et al. (2003) (42) determined that estrogen is the mechanism responsible for this sexual dimorphism in counterregulatory responses to hypoglycemia. Despite this, the prevalence of hypoglycemic episodes in T1DM for men and women are similar (4). This apparent paradox may be explained by the fact that women are more resistant to the blunting effects of antecedent hypoglycemia on the ANS as compared to men (43). Thus, two episodes of antecedent hypoglycemia in men will cause a twofold greater blunting of counterregulatory responses to subsequent hypoglycemia as compared to women. The result was that the usual sexual dimorphic response to hypoglycemia is abolished.

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