Review Article

Peripheral Pathways in the Food-Intake Control towards the Adipose-Intestinal Missing Link

Table 1

Major peripheral signals involved in food intake regulation.

HormoneSite of secretionMajor receptorsMajor actions

IntestinalAmylinPancreatic cells Inhibits gastric secretion.
Delays gastric emptying.
Decreases blood glucose.
CholecystokininIntestinal IcellsCCK2Gall bladder contraction.
Delays gastric emptying.
Pancreatic enzyme contraction.
Endocannabinoid systemPostsynaptic cellCB1, CB2Modulates appetite besides a variety of physiological processes.
GhrelinGastric fundal A cellsGHS–RIncreases gastric motility.
Growth of hormone release.
GlucagonPancreatic cellsGlucagonGluconeogenesis.
Glycogenolysis.
Glucagon-like peptide-1 (GLP-1)Gastrointestinal L cellsGLP–1Glucose-dependent insulin release.
Delays gastric emptying.
Vagal and CNS effects.
Glucose-dependent insulinotropic polypeptide (GIP)K cells in duodenum and jejunumGIP–RStimulates insulin synthesis and secretion.
OxyntomodulinGastrointestinal L cellsGLP–1Glucose-dependent insulin release.
Delays gastric emptying.
Vagal and CNS effects.
Pancreatic polypeptidePancreatic PP cellsY4Delays gastric emptying.
Peptide YY (PYY)Gastrointestinal L cellsY2Delays gastric emptying.
Vagal and CNS effects.
AdiposeAdiponectinAdipocyte,
skeletal muscle,
endothelial cells, and cardiomyocytes
AdipoR1
AdipoR2
T-cadherin
Adiponectin, via AMPK phosphorylation, increases insulin sensitivity, fatty acid oxidation and reduces the synthesis of glucose in the liver and other tissues.
LeptinAdipocyteLEPRIncreases POMC anorexigenic signals.
Inhibits NPY, stimulating appetite.
Plasminogen activator inhibitor-1 (PAI-1)Endothelium, adipocyteBinds to (tPA)Inhibitor of fibrinolysis.
Tumour necrosis factor alpha (TNF- )AdipocyteTumor necrosis factor receptor (TNFR)Insulin resistance.

AMPK: AMP-activated protein kinase, CNS: central nervous system, NPY: neuropeptide Y, POMC: proopiomelanocortin, and tPA: tissue plasminogen activator.