Intracerebroventricular injection of apelin-13 reduces food intake in the rat.

Apelin is a peptide recently identified as a ligand for the APJ receptor, a receptor located in tissues such as the small intestine and in the hypothalamus. Apelin has been detected in adipose tissue, gastrointestinal tract, heart and stomach. Recent reports suggest a role for apelin in the regulation of blood pressure and the control of body fluid homeostasis.

The rat arcuate nucleus integrates peripheral signals provided by leptin, insulin, and a ghrelin mimetic.

The hypothalamic circuits controlling food intake and body weight receive and integrate information from circulating satiety signals such as leptin and insulin and also from ghrelin, the only known circulating hormone that stimulates appetite following systemic injection. Activation of arcuate neurons by ghrelin and ghrelin mimetics (the growth hormone secretagogues) is augmented in 48-h-fasted rats compared with fed rats, as reflected by a greater number of cells expressing Fos protein in response to administration of the same maximally effective dose. Here we sought to determine whether this increased responsiveness in fasting might reflect or be influenced by low levels of circulating satiety factors such as leptin or insulin.

Growth hormone (GH) and GH-releasing peptide-6 increase brain insulin-like growth factor-I expression and activate intracellular signaling pathways involved in neuroprotection.

Beneficial effects of GH on memory, mental alertness, and motivation have been documented. Many actions of GH are mediated through IGF-I; hence, we investigated whether systemic administration of GH or GH-releasing peptide (GHRP)-6 modulates the brain IGF system. Treatment of adult male rats with GHRP-6 or GH for 1 wk significantly increased IGF-I mRNA levels in the hypothalamus, cerebellum, and hippocampus, with no effect in cerebral cortex.