Okumura T, Saito K
Department of Medical Chemistry, Kansai Medical School, Osaka, Japan.
Biochim Biophys Acta. 1990 Mar 9;1051(3):300-5. doi: 10.1016/0167-4889(90)90138-4.
E series prostaglandins and their biologically active analogue, 16,16-dimethylprostaglandin E2 (dimethylprostaglandin E2), have inhibited hormone-stimulated glycogenolysis in hepatocytes cultured from male rats (Okumura, T., Sago, T. and Saito, K. (1988) Biochim. Biophys. Acta 958, 179-187). However, in the case of female rat hepatocytes, it is evident that dimethylprostaglandin E2 did not inhibit the glycogenolysis stimulated by glucagon, isoproterenol (beta-adrenergic response) or epinephrine (with propranolol, alpha 1-adrenergic response) in cultures on day 1. Dimethylprostaglandin E2 inhibited such hormone-stimulated glycogenolysis in cultures on day 2 and 3, but to a lesser extent than in the male-derived cells. The concentration for 50% inhibition was approx. 10(-8) M; inhibition was completely blocked by a pertussis toxin. Prostaglandin E2 had the same effect as dimethylprostaglandin E2; prostaglandins D2 and F2 alpha had no effect. Additions of sex hormones, 17 beta-estradiol and testosterone, and palmitic acid (diminishing the prostaglandin catabolism) to the culture medium did not change the effect of dimethylprostaglandin E2. These data indicate that a sex difference exists in the inhibition of hepatic glycogenolysis by prostaglandin E2 and its analogue in rat cultured hepatocytes, although the factor causing such a difference is a present unknown.
