PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20936253-0	2011	Glucose stimulates human beta cell replication in vivo in islets transplanted into NOD-severe combined immunodeficiency (SCID) mice.	Glucose	0-7	atrophin 1	Homo sapiens	83-86	
7948065-4	1994	When the islets of NOD mice were incubated with the IL-1 (10, 100 U/ml) under condition of high glucose, IAP and endogenous retrovirus type C frequently appeared in the beta-cells.	Glucose	96-103	atrophin 1	Homo sapiens	19-22	
33277775-3	2021	Mitochondrial damage and muscle atrophy are likely the central mechanisms producing SAMS, whereas decreased glucose transport, fatty acid oxidation and insulin secretion are likely involved in the development of NOD.	Glucose	108-115	atrophin 1	Homo sapiens	212-215	
34556496-5	2021	At 12 weeks of age, prior to diabetes conversion, NOD-ibetaSTX4 mice demonstrated superior whole-body glucose tolerance and beta-cell glucose responsiveness than NOD-Ctrl mice.	Glucose	102-109	atrophin 1	Homo sapiens	50-53	
34556496-5	2021	At 12 weeks of age, prior to diabetes conversion, NOD-ibetaSTX4 mice demonstrated superior whole-body glucose tolerance and beta-cell glucose responsiveness than NOD-Ctrl mice.	Glucose	134-141	atrophin 1	Homo sapiens	50-53