Effect of Intracerebroventricular Administration of Galanin-Like Peptide on Hepatokines in C57BL/6 J Mice.

J Mol Neurosci

Department of Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Shonan University of Medical Sciences, 16-10, Kamishinano, Totsuka-ku, Yokohama-shi, Kanagawa, 244-0806, Japan.

Published: February 2024

AI Article Synopsis

  • GALP is a neuropeptide linked to anti-obesity effects and was studied for its impact on glucose and lipid metabolism in the liver.
  • Intracerebroventricular administration of GALP in mice led to a decrease in G6Pase gene expression, which is important for gluconeogenesis, without affecting body weight or blood glucose levels.
  • Additionally, GALP administration reduced levels of hepatokines associated with insulin resistance, suggesting it enhances glucose metabolism in the liver.

Article Abstract

Galanin-like peptide (GALP) is a neuropeptide that was first isolated and identified from the porcine hypothalamus. Studies have described an anti-obesity effect of GALP. We previously found that intracerebroventricular administration of GALP in mice resulted in an increase in respiratory exchange rate 12 to 16 h later. GALP may also affect glucose metabolism, but the detailed mechanism has not been elucidated. In this study, we investigated the effects of GALP on glucose and lipid metabolism in the liver. Nine-week-old male C57BL / 6 J mice were administered a single intracerebroventricular dose of saline or GALP and dissected 16 h later. There were no significant between-group differences in body weight and blood glucose levels. With regard to gene and protein expression, G6Pase associated with hepatic gluconeogenesis was significantly reduced in the GALP group. In addition, the hepatokines selenoprotein P and fetuin-A, which induce insulin resistance in the liver, were significantly decreased in the GALP group. These results suggest that intracerebroventricular administration of GALP decreases the expression of key hepatokines, thereby enhancing glucose metabolism.

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Source
http://dx.doi.org/10.1007/s12031-024-02200-yDOI Listing

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