Permissive Effects of Hormones on Lipolysis1

Hypophysectomy severely reduced glycerol and free fatty acid (FFA) production by segments of epididymal fat. Preincubation of adipose tissue from either hypophysectomized or normal rats with dexamethasone (.016 μg/ml) increased glycerol and FFA production in response to low concentrations of epinephrine (.01–0.05 μg/ml). This effect of dexamethasone had a lag period in excess of 2 hr, and was blocked by actinomycin d. Glucose was not required. Even greater potentiation was seen when growth hormone was also present. It is suggested that acute effects of dexamethasone on lipolysis may result from some modification in the metabolism of cyclic adenosine monophosphate, secondary to the induction of synthesis of some new species of protein. Pretreatment of hypophysectomized rats with triiodothyronine (T3, 5 μg/rat) also markedly potentiated the lipolytic response of segments of adipose tissue to epinephrine and theophylline when tested in vitro 16 hr later. This effect of T3 was not inhibited by actinomycin d. At 3, 6 and 12 hr after injection, T3 increased lipolysis in response to epinephrine but not to theophylline. Exposure of adipose tissue to T8 in vitro at a concentration of 10−6M for 3 or 6 hr failed to increase the lipolytic response to epinephrine in the subsequent hour. Addition of T3in vitro along with growth hormone and dexamethasone produced no greater increase in the lipolytic response to epinephrine than did growth hormone and dexamethasone alone. Lipolysis in response to epinephrine was not enhanced by dexamethasone or dexamethasone and growth hormone when tested in tissues of hypophysectomized rats which received T3 16 hr earlier. It is suggested that T2 causes multiple, temporally separable modifications of the lipolytic apparatus. (Endocrinology86: 1064, 1970)