Enhanced neuroendocrine response to insulin tolerance test performed under increased ambient temperature

Abstract

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.

Passive heating and glycaemic control in non-diabetic and diabetic individuals: A systematic review and meta-analysis

“…In four studies, both male and female individuals were examined [63,64,67,71], while ten studies examined males only [30,61,62,65,66,68–70,72,73]. The mean age of the participants varied between 19 years [73] and 56 years [63].…”

“…A glucose load and insulin were given before PH and control trials in three studies using diabetic individuals [61,72,73]. No glucose or insulin was given before PH and control in four experiments [30,66,68,70]. Three experiments included data where a glucose load was given immediately [30], 120 minutes [30] or 24-hours post-heating [64].…”

“…If an increase in iHSP is necessary for improvements in glucose homeostasis in diabetic individuals, then a sufficient heating stimulus is required. Exposure to 43 °C– 53 °C air for 60 minutes increased body temperature by ≤0.5 °C [65,70], while immersion in 39 °C water for the same time increased temperature to ~38.5 °C (~1.6 °C difference versus control) [64]. A deep body temperature rise of >0.8 °C has been shown to increase eHSP concentrations [84–86], but it is unknown whether this modest rise in deep body temperature is a great enough stimulus to increase iHSP concentrations.…”

Enhancement of stress-induced pituitary hormone release and cardiovascular activation by antidepressant treatment in healthy men

“…As a stress stimulus, insulin-induced hypoglycaemia was selected because hypoglycaemia induces the release of a wide spectrum of hormones (Ježová et al, 1998) and the insulin tolerance test is a clinically useful tool to assess pituitary function (Mahajan and Lightman, 2000) Subjects and methods…”

“…In experimental animals, long-term treatment with amitriptyline, moclobemide or tianeptine reduced HPA axis activation in response to stress stimuli (Delbende et al, 1994;Reul et al, 1994). However, other treatments were found to be ineffective (Duncan et al, 1998) and two studies described a stimulatory action of fluoxetine on stress-induced rise in plasma corticosterone (Ježová et al, 1984;Durand et al, 1999). Surprisingly, no information is available on the effects of antidepressants on hormone release during stress exposure in humans.…”