White adipose tissue is now recognized as the source of a growing list of novel adipocyte-specific factors, or adipokines. These factors regulate energy homeostasis, including the response to food deprivation. We hypothesized that the brain and pituitary gland would also express adipokines and their regulatory factors and subsequently demonstrated that the rodent brain-pituitary system expresses mRNA and protein for leptin and resistin. We now report that the adipokines FIAF and adiponutrin, as well as the nuclear hormone receptor PPAR gamma, are expressed in pituitary, brain and adipose tissue. In pituitary gland, 24 h of food restriction reduced PPAR gamma expression by 54% whereas both adiponutrin and FIAF were increased 1.7 and 2.3 fold, respectively. These changes in expression were similar to those observed in fat, except for adiponutrin, which by contrast is dramatically reduced 95% by fasting. Furthermore, whereas PPAR gamma 2 is the main isoform affected by fasting in adipose tissue, our data suggest that only PPAR gamma 1 is present and downregulated by fasting in pituitary tissue. In contrast to the sensitivity of pituitary tissue to the effects of fasting, no significant change in expression was observed in basal hypothalamus for any of the genes studied. Overall, our data suggest that pituitary-derived adipokines may play an unexpected role in the neuroendocrine regulation of energy homeostasis.
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G Wiesner, BA Morash, E Ur, and M Wilkinson
E. Ur, M. Faria, S. Tsagarakis, J. V. Anderson, G. M. Besser, and A. Grossman
ABSTRACT
Whilst it has been postulated that atrial natriuretic peptide (ANP) may modulate pituitary hormone release, several investigations in non-human species have reported conflicting results when looking for an effect on the hypothalamo-pituitary-adrenal axis. However, in a recent study significant inhibition of corticotrophin-releasing hormone (CRH)-stimulated ACTH in cultured rat anterior pituitary cells occurred only with the complete peptide α-ANP(1–28).
We have therefore investigated whether this form of ANP can inhibit CRH-stimulated ACTH and cortisol release in human subjects. Six healthy male volunteers received human α-ANP or placebo, and human CRH or placebo, on four separate occasions.
ANP was infused at a rate of 0·01 μg/kg per min in order to achieve levels in the high physiological range. CRH was given as a bolus dose of 100 μg 30 min into the ANP infusion. Cortisol and ANP were measured by radioimmunoassay, the latter after extraction. ACTH was measured by immunoradiometric assay. The data were analysed by Student's paired t-test on basal, peak and incremental levels. Basal levels of ANP were within the normal range (2–5 pmol/l). With ANP infusion, mean ± s.e.m. peak ANP levels were 29·6±3·1 pmol/l. There were no significant differences in mean basal cortisol and ACTH levels on each of the 4 study days. Mean peak cortisol and ACTH levels after CRH and ANP did not significantly differ from those achieved with CRH and placebo ANP. We thus conclude that at high physiological doses, circulating ANP does not inhibit CRH-stimulated ACTH or cortisol release.
Journal of Endocrinology (1991) 131, 163–167
