PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2997284-3	1985	Clonidine, N6-phenylisopropyladenosine, prostaglandin E2, and insulin caused a dose-dependent inhibition of glycerol release in the presence of adenosine deaminase.	Dinoprostone	40-56	adenosine deaminase	Homo sapiens	144-163	
3422703-8	1988	If lipolysis was only stimulated by adenosine deaminase, the sensitivity of PGE2 was reduced in obesity (IC50, 1.45 nmol/L v 0.47 nmol/L, P less than .01), but the maximal antilipolytic effect of PGE2 in the two groups was similar, with an inhibitory effect of 95% to 98%.	Dinoprostone	76-80	adenosine deaminase	Homo sapiens	36-55	
3422703-9	1988	If lipolysis was stimulated by both adenosine deaminase and theophylline (2 mmol/L), it was especially the maximal antilipolytic effect of PGE2 that was impaired in adipocytes from obese subjects (lipolysis was maximally inhibited by 61% v 92%, P less than .01).	Dinoprostone	139-143	adenosine deaminase	Homo sapiens	36-55	
3918586-7	1985	In contrast to the relatively minor effect of endogenous prostaglandins, the addition of exogenous prostaglandin E2 significantly stimulated the glucose transport, glucose oxidation and lipogenesis in human adipocytes, especially in the presence of adenosine deaminase.	Dinoprostone	99-115	adenosine deaminase	Homo sapiens	249-268