Temperature responses of exercizing dogs to infusion of electrolytes.
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Biomedical subjects
Publications and source records attributed to K Nazar.
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The hypothesis that an increase in ambient temperature modulates neuroendocrine response in clinically used provocative pituitary function tests was verified. Healthy male volunteers were subjected to insulin tolerance tests in two randomized trials. In the first trial hypoglycemia was induced by a bolus injection of insulin (0.1 U per kg of BW, i.v.) at room temperature. In the second trial, the subjects were exposed to increased ambient temperature for 45 min before insulin injection and for 45 min thereafter. The environmental temperature was selected to increase body temperature less than 1C. Under conditions of increased temperature basal hormone levels as measured in antecubital venous blood samples failed to be modified and the hypoglycemia was less severe. Nevertheless, the responses of most (beta-endorphin, ACTH, prolactin, catecholamines), but not all (growth hormone, cortisol), hormones to hypoglycemia were exaggerated. The remarkable increase in ACTH and beta-endorphin release was not accompanied by concomitant increase of plasma cortisol response. The sympathetic-adrenomedullary system was significantly activated, which was manifested particularly by enhanced norepinephrine release. Growth hormone response to hypoglycemia was not modified, while that of prolactin was enhanced. Thus during evaluation of neuroendocrine function under clinical conditions, changes in ambient and body temperature should not be underestimated.
UNLABELLED: Relationships between energy expenditure, body mass index (BMI), blood glucose (BG) responses to glucose ingestion were studied in 35 women aged 22-55 yrs with normal carbohydrate tolerance. In 13 of them plasma insulin (IRI) and catecholamine concentrations were also determined. Thirty seven per cent of patients did not respond to glucose load with an increased energy expenditure. In the remaining women the average thermogenic effect amounted to approx. 10% of their initial metabolic rate. A significant negative correlation (r = -0.415, n = 35, P(0.02) was found between BMI and the overall thermal effect of glucose (sigma TEG) calculated as a sum of the post-glucose energy expenditure measured every 15 min during 2 h minus the baseline value. Neither the fasting nor the post glucose BG concentrations correlated with sigma TEG. Significant correlations were ascertained between sigma TEG and the fasting IRI (r = -0.568), the sigma post-glucose IRI (r = -0.723), the ratio of sigma BG/sigma IRI (r = 0.845) and the post-glucose plasma noradrenaline concentration (r = 0.837). IN CONCLUSION: in women with normal carbohydrate tolerance the thermogenic effect of glucose depends to a large extent on insulin sensitivity and the glucose-induced activation of the sympathetic nervous system.