An analogue of the Prolactin Releasing Peptide reduces obesity and promotes adult neurogenesis.

Hypothalamic Adult Neurogenesis (hAN) has been implicated in regulating energy homeostasis. Adult-generated neurons and adult Neural Stem Cells (aNSCs) in the hypothalamus control food intake and body weight. Conversely, diet-induced obesity (DIO) by high fat diets (HFD) exerts adverse influence on hAN. However, the effects of anti-obesity compounds on hAN are not known. To address this, we administered a lipidized analogue of an anti-obesity neuropeptide, Prolactin Releasing Peptide (PrRP), so-called LiPR, to mice. In the HFD context, LiPR rescued the survival of adult-born hypothalamic neurons and increased the number of aNSCs by reducing their activation. LiPR also rescued the reduction of immature hippocampal neurons and modulated calcium dynamics in iPSC-derived human neurons. In addition, some of these neurogenic effects were exerted by another anti-obesity compound, Liraglutide. These results show for the first time that anti-obesity neuropeptides influence adult neurogenesis and suggest that the neurogenic process can serve as a target of anti-obesity pharmacotherapy.

A randomized controlled crossover trial of the effect of ginseng consumption on the immune response to moderate exercise in healthy sedentary men.

Ginseng is a popular herbal remedy that is reputed to increase resistance to stress and improve immune function. Regular exercise results in acute physiologic stress that affects the immune response. This study was conducted to investigate the effects of daily consumption of a standardized ginsenoside-containing North American ginseng (Panax quinquefolius) extract on immune function before, during, and after a moderate-exercise protocol in healthy sedentary men. Ten healthy males were randomized to receive either ginseng (1125 mg.d-1) or placebo for 35 days. After a 3 month washout period, subjects received the opposite treatment for another 35 days. An exercise test and blood collection were performed at the end of each treatment period. Immune parameters and blood hormone levels were measured before, during, and after the exercise stress protocol. Ginseng treatment reduced the peripheral blood concentration of CD8+ T cells and increased mitogen-stimulated T cell production of interleukin-2 ex vivo. Ginseng had no effect on total white blood cell counts; on concentrations of neutrophils, monocytes, or lymphocytes (CD3+, CD4+, CD16+, CD20+); on lymphocyte proliferation; or on neutrophil oxidative burst. Ginseng did not significantly affect exercise-induced changes in plasma concentrations of lactate, insulin, cortisol, or growth hormone. The consumption of ginseng for 5 weeks had a limited effect on the immune response to an acute exercise protocol.