PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29444428-4	2018	Crat deletion in AgRP neurons increased peripheral fatty acid substrate utilization and attenuated the switch to glucose utilization after refeeding, indicating altered nutrient partitioning.	Glucose	113-120	carnitine O-acetyltransferase	Homo sapiens	0-4	
24395925-8	2014	These results suggest that lipid-induced antagonism of CrAT might contribute to decreased PDH activity and glucose disposal in the context of obesity and diabetes.	Glucose	107-114	carnitine O-acetyltransferase	Homo sapiens	55-59	
22560225-0	2012	Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility.	Glucose	68-75	carnitine O-acetyltransferase	Homo sapiens	28-55	
22560225-3	2012	Here, we identify an essential role for the mitochondrial matrix enzyme, carnitine acetyltransferase (CrAT), in regulating substrate switching and glucose tolerance.	Glucose	147-154	carnitine O-acetyltransferase	Homo sapiens	73-100	
22560225-3	2012	Here, we identify an essential role for the mitochondrial matrix enzyme, carnitine acetyltransferase (CrAT), in regulating substrate switching and glucose tolerance.	Glucose	147-154	carnitine O-acetyltransferase	Homo sapiens	102-106	
19553674-9	2009	A role for this enzyme in combating glucose intolerance was further supported by the finding that CrAT overexpression in primary human skeletal myocytes increased glucose uptake and attenuated lipid-induced suppression of glucose oxidation.	Glucose	36-43	carnitine O-acetyltransferase	Homo sapiens	98-102	
19553674-9	2009	A role for this enzyme in combating glucose intolerance was further supported by the finding that CrAT overexpression in primary human skeletal myocytes increased glucose uptake and attenuated lipid-induced suppression of glucose oxidation.	Glucose	163-170	carnitine O-acetyltransferase	Homo sapiens	98-102