Glucocorticoid adiposity with

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

In adipose tissue, the promoter from exon 1.4 is utilized . The same exon is utilized in bone and skin 303, jjj leiomyoma tissue derived from myometrium . This system is regulated with Spl, a glucocorticoid regulatory element, STAT3, and possibly PPAR - . Pre-adipocytes also involve regulation with liver receptor homolog-1 (LRH-1) 30 . 

Rashef and Shapiro (1960) reported that pretreatment of adrenalecto-mizc d rats with either epinephrine or eortisone inereased the depressed rate of free fatty acid release by their mesenteric adipose tissue in vitro however, maximal effects were, obtained only when both were given. It was further pointed out that epinephrine alone was highly effective in restorii the depressed rate of free fatty acid release by tissue from adrenal demedul-lated rats. Reshef and Shapiro (1960) also observed that pretreatment of starved intact rats with cortisone had little effect on the release of free fatty acid by mesenteric adipose tissue. Such treatment, however, inereased and prolonged the response of tissue removed from rats injected with epinephrine (sec Section VI, A). These results may reflect in part the effects of glucocorticoid administration on the adipose tissue stores of the intact animal, but the interesting relation between the effects of epinephrine and adrenocortical steroids on the release of free fatty acids deserves further study. 

Thyroid hormones stimulate the rate of triacylglycerol biosynthesis in liver but have the opposite effect in adipose tissue. This may be due to an increased rate of general metabolic turnover rather than a specific effect on PAP. Recent research indicates that the hormones most immediately implicated in the control of PAP activity are the glucocorticoids. High serum cortisol concentrations are associated with most of the conditions described above that lead to an increased activity of PAP and an elevated rate of... 

---