CCAAT/Enhancer Binding Protein β in relation to ER Stress, Inflammation, and Metabolic Disturbances

Table 2

The involvement of C/EBP-β in metabolic processes.

Metabolic process	Involvement of C/EBP-β	C/EBP-β knockout	C/EBP-β overexpression
Adipose tissue development, white and brown	White adipocyte differentiation and maturation (also role for C/EBP-α)	Decreased body fat content
	Brown adipocyte activity and development	Elevated gene expression in brown adipose tissue β-oxidation
Leptin production	Binding possibility on leptin promoter	Decreased leptin production (possibly fat mass related)
Glucose and insulin metabolism	High insulin = low C/EBP-β	Increased insulin production after hepatic knockdown
	Low C/EBP-β = High insulin	Unchanged insulin production after C/EBP-β deletion
	Accumulation of C/EBP-β induces diabetes via; ER stress induction	Increased insulin sensitivity
	Maintenance of plasma glucose levels	Hypoglycemia
	C/EBP binding site in GLUT-4 promoter	Decreased hepatic glucose production
		Decreased cAMP
Triacylglycerol metabolism	Influencing lipogenic enzyme activity	Reduced plasma free fatty acid concentrations
Hepatic steatosis-NASH	Influencing the amount of hepatic TAG	Decreased lipogenic enzyme activity
		Decreased hepatic TAG
		Protected from steatosis, decreased NASH development	Increased steatosis
ER stress	Accumulation of C/EBP-β induces diabetes via ER stress		LIP isoform increased cell death
	C/EBP-β is increased during ER stress		LAP isoform decreased cell death
	High LIP promotes cell death
	LIP lowers prosurvival ATF-4 targets
	In early ER stress response LAP production higher
	In early ER stress response LIP production higher
Inflammation	C/EBP-β activates inflammatory response	Defects in immune response, impaired macrophage activation	Activation of the immune response
	LIP isoform induces inflammation	Decreased high fat induced inflammation
HDL particle production	C/EBP-β has binding place in apoA-I promoter		C/EBP no central role in expression of the apoA-I gene