forskolin/トウモロコシ

Specific [3H]-forskolin binding was linear as a function of the membrane protein concentration and reached steady-state by 30-40 min of incubation at 37 degrees C. Such binding was saturable and the bound radioligand could be readily dissociated by an excess of unlabelled forskolin. There was only

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes cardiovascular toxicity in laboratory animals, including alteration in several processes in which beta-adrenergic receptor (beta-AR) signaling plays important roles. Thus, our laboratory investigated the effects of TCDD on beta-AR expression and

Three groups of male weanling Sprague-Dawley rats were fed diets containing 20% corn oil, 20% partially hydrogenated soybean oil (PHSBO) or 18% PHSBO + 2% corn oil. PHSBO contained about 48% of its total fatty acids as trans-octadecenoate. Rats were killed after 16-18 weeks of feeding the various

Glucagon-stimulated adenylyl cyclase activity has been shown to change in liver membranes manipulated to alter either their fatty acid composition or fluidity. We examined whether membrane alterations induced by dietary manipulation affected receptor function. Glucagon- and

We have examined the effect on rat liver glucagon receptors and adenylate cyclase activity of a high saturated fat diet (butter fat), a high n-6 polyunsaturated fat diet (corn oil), and a high n-3 polyunsaturated fat diet (menhaden fish oil) with or without additional cholesterol. The number and

We have previously shown the incorporation of dietary omega-3 and omega-6 fatty acids from menhaden oil and corn oil, respectively, into membrane phospholipids of submandibular salivary gland (SMSG) of rat [Alam S. Q. and Alam B. S. (1988) Arch. Oral Biol. 33, 295-299]. We now demonstrate the

Melatonin provides a circadian signal that regulates linoleic acid (LA)-dependent tumor growth. In rodent and human cancer xenografts of epithelial origin in vivo, melatonin suppresses the growth-stimulatory effects of linoleic acid (LA) by blocking its uptake and metabolism to the mitogenic agent,