Table 2.

Main enterohormones involved in the hunger–satiety pathway, and findings from in vivo and in vitro studies evaluating metabolic effects of naringenin (NAR) treatments.

Hormone/Physiological Effect	Entero-Endocrine Cell Type	Localization by Highest Density	Main Receptor in Hunger–Satiety Pathway	Levels in Normal Weight	Levels in Obesity	Reported Effects of NAR
Ghrelin Orexigenic	P	Stomach	GHSR1A	Increase before meals, decrease after meals.	Low before meals and shorter duration of suppression after meals [83]	Ghrelin receptor is activated by NAR in vitro [84]
CCK Anorexigenic	I	Duodenum and proximal jejunum	CCK1	Increase after meals, max. concentration 15 min.	Low after meals or failure to decrease after meals [85,86]	NAR stimulates CCK secretion in vitro [87]
GLP-1 Anorexigenic	L	Duodenum and colon	GLP-1	Low before meals, high after meals.	Low before and after meals [88]	NR
PYY (3–36) Anorexigenic	L	Colon	Y2	Increase after meals, max concentration 60–90 min	Variable. Some report low after meals [89]	NR
Insulin Anorexigenic	Pancreatic β-cells	Pancreas	IR	Low (compared with obese state)	High (in the insulin resistant state)	NAR enhances glucose-stimulated insulin secretion and glucose sensitivity in vitro [58] NAR improves insulin sensitivity, improves glucose and insulin tolerance in vivo through AMPK GLUT4 translocation [16]
Leptin Anorexigenic	Adipocyte	Adipose tissue	LepRb	Low (compared with obese state)	High [90]	NAR decreases serum leptin [19] and it′s expression in vivo [15]
Adiponectin Anorexigenic	Adipocyte	Adipose tissue	AdipoR1 and adipoR2	High (compared with obese state)	Low (inversely proportional to adipose tissue mass) [91]	NAR increases serum adiponectin levels despite an HFD in vivo [19]. NAR enhances adiponectin mRNA expression in vivo [92]

NAR = naringenin; CCK = cholecystokinin; GLP-1 = glucagon-like peptide 1; PYY = peptide YY; mRNA = messenger RNA; NR = not reported.