PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22349071-1	2012	AIMS/HYPOTHESIS: We examined the role of protein kinase C-iota (PKC-iota) in mediating alterations in the abundance of enzymes in hepatocytes of type 2 diabetic humans that contribute importantly to the development of lipid and carbohydrate abnormalities in type 2 diabetes.	Carbohydrates	228-240	protein kinase C iota	Homo sapiens	64-72	
22349071-8	2012	CONCLUSIONS/INTERPRETATION: Our findings suggest that a vicious cycle of PKC-iota overactivity and overproduction exists in hepatocytes of humans with type 2 diabetes and contributes importantly to maintaining overactivity of lipogenic, proinflammatory and gluconeogenic pathways, which underlies the lipid and carbohydrate abnormalities in type 2 diabetes.	Carbohydrates	311-323	protein kinase C iota	Homo sapiens	73-81