We evaluated the relationship between hypoglycemic symptoms, glucose nadir levels, and hormone changes in patients with impaired glucose tolerance (IGT) after an oral glucose tolerance test (OGTT). The peak counterregulatory hormone response was determined at the glucose nadir identified by continuous glucose monitoring. Eight patients with IGT who had symptoms and signs typical of hypoglycemia at the glucose nadir were compared with completely asymptomatic subjects (5 IGT patients and 13 patients who had normal glucose tolerance [NGT]). The mean glucose nadir of symptomatic IGT patients was 3.50 +/- 0.46 mM, which was not statistically different from the mean of asymptomatic NGT patients (4.10 +/- 0.56 mM) but was significantly lower than that for asymptomatic IGT patients (5.10 +/- 0.81 mM, P less than 0.001). Seven of 8 symptomatic IGT patients had glucose levels that never fell below the range of glucose nadirs for asymptomatic NGT patients. However, the symptomatic IGT group had significantly higher levels of growth hormone, cortisol, epinephrine, and norepinephrine than the asymptomatic groups in response to the nadir. We conclude that patients with IGT are capable of experiencing signs and symptoms of hypoglycemia at physiological glucose levels during OGTT with reflex stimulation of counterregulatory hormone release. This may indicate that symptomatic IGT patients have a higher glucose threshold for eliciting characteristic hypoglycemic symptom episodes than individuals with NGT.

Adult↗

PubMed1989

Developmental and hormonal factors in the sexually dimorphic, asymmetrical response to focal cortical lesions.

The developmental and hormonal determinants of the lateralized response to focal cortical suction lesions were examined in a series of experiments. In an initial study, Sprague-Dawley male rats 25, 30, 55 or 90 days of age, received right unilateral focal frontocortical suction lesions. Only 90-day-old rats developed hyperactivity, suggesting a specific role for maturational factors in the production of this response. Prepubertally castrated adult male rats receiving right frontocortical suction lesions at 90 days also failed to develop hyperactivity, suggesting that sexual maturational factors and/or the presence of testosterone are necessary for the expression of this response. Testosterone implants, producing physiological relevant levels of circulating testosterone reinstated the hyperactivity response to adult cortical lesions in prepubertally castrated male rats. Similar lesions in the left hemisphere, however, did not produce hyperactivity in castrated male rats with testosterone replacement. Finally, in ovariectomized adult female rats, testosterone did not allow the expression of a hyperactivity response to right frontocortical suction lesions. Together, these results demonstrate both an organizational and permissive role for sex steroids in the sexually dimorphic asymmetrical response to cortical injury.

Aging↗

PubMed1988

Estrogen-secreting adrenal tumor responsive to ACTH: localization by adrenal venous sampling.

In a 48-year-old man with gynecomastia but no other signs of feminization, routine evaluation revealed only minimally elevated serum estrogens. The diagnosis of an estrogen-secreting adrenal tumor was suggested by CT and confirmed by adrenal venous sampling. This tumor was found to be ACTH-responsive. Results in this patient are compared with those in normal volunteers, in whom adrenal venous sampling failed to localize estrogen secretion and in whom ACTH did not increase estrogens.

Adrenal Cortex Neoplasms↗

PubMed1987

Inhibition of captopril-induced renin release by angiotensin II.

The angiotensin-converting enzyme inhibitor (CEI) captopril has been shown to elevate plasma renin activity (PRA) and prostaglandin E2 levels, and to lower blood pressure and angiotensin II (AII) levels. Renin is secreted in both active and inactive forms; however, the interrelationship of these forms and responses to captopril are unclear. We proposed to determine if PRA rise induced by captopril is due primarily to release from AII inhibition, and if inactive renin is converted to active renin when PRA increases. Seven normal volunteers were given captopril, 50 mg orally, while on a moderately sodium-restricted diet (35 mEq/day). Changes in PRA and total and inactive renin, as well as prostaglandin E2, were measured. Then, on two different occasions, the captopril dose was preceded or followed by infusion of AII, to negate changes in AII induced by CEI. The dose of AII was obtained by dose-response infusion until a minimal increase in blood pressure occurred. Active renin increased with captopril alone, from 8.2 to 48.3 ng/ml/h by 90 min (p less than 0.01). AII completely blocked the rise in PRA induced by captopril, whether given before or after captopril. Inactive renin did not decline as active renin increased over the 90-min study. Therefore, the PRA rise induced by captopril is mediated through a fall in AII levels and loss of feedback on renin-secreting cells. The rise in PRA comes from secretion of active renin rather than conversion from inactive renin.

Adult↗