Adipokines and proinflammatory cytokines, the key mediators in the pathogenesis of nonalcoholic fatty liver disease

Table 3 Studies and their findings on ghrelin

Study	Finding	Ref.
Human	AG and the AG/DAG ratios positively associated with HOMA-IR in obese children	[128]
	IR obese subjects had elevated AG/DAG ratio compared with non IR obese subjects because of decreased DAG and total ghrelin levels	[129]
	Obese patients with MS had lower total ghrelin and DAG, comparable AG and higher AG/DAG, AG/DAG ratio correlated with IR	[130]
	Ghrelin significantly correlated with HOMA-IR, but was reduced in NAFLD	[131]
	Ghrelin levels were higher in higher stages of fibrosis in morbidly obese patients with NAFLD	[132]
	Higher total ghrelin concentrations in patients with NASH in comparison with steatosis and normal liver	[54]
In vitro	Adipocytes after incubation with AG and DAG significantly increased PPARγ and SREBP-1 mRNA levels and accumulated lipids	[133]
	Ghrelin inhibited AMP-activated protein kinase activity, through which also influenced PPAR-γ in liver and in adipose tissue	[134]
	Administration of ghrelin attenuated NAFLD-induced liver injury, oxidative stress, inflammation, and apoptosis partly through the action of serine/threonine kinase/AMPK and phosphoinositide 3-kinase/protein kinase B pathways in rats	[135]

AG: Acyl-ghrelin; DAG: Des-acyl ghrelin; IR: Insulin resistance; MS: Metabolic syndrome; HOMA-IR: Homeostasis model assessment-estimated insulin resistance; NAFLD: Non-alcoholic fatty liver disease; PPAR-γ: Peroxisome proliferator-activated receptor gamma; SREBP-1: Sterol regulatory element-binding protein 1; AMP: Adenosine monophosphate.