Galanin Peptide Signaling in Metabolic Regulation

The neuropeptide galanin is a 29–30 amino acid molecule widely expressed in central and peripheral tissues, where it modulates energy homeostasis, feeding behaviour, glucose metabolism and lipid handling. It acts through three G protein–coupled receptors (GalR1–3), each with distinct tissue distribution and signalling outcomes. In the hypothalamus, galanin influences neurocircuits that govern appetite and satiety, while in peripheral organs such as liver, adipose tissue and pancreas it regulates insulin sensitivity, lipogenesis and inflammatory pathways. Activation of GalR2 in adipocytes promotes lipolysis and thermogenesis, whereas GalR1 engagement in the central nervous system can suppress feeding drive. In hepatic tissue, galanin controls lipid synthesis and fibrogenesis via AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) signalling, and shapes macrophage phenotype to favour anti-inflammatory states. Emerging data also link galanin to the preservation of mitochondrial integrity and biogenesis under metabolic stress, highlighting its role as a versatile regulator of systemic energy balance and a promising target for metabolic disorder interventions.

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Galanin Peptide Signaling in Metabolic Regulation publication trend

The graph below shows the total number of articles in galanin peptide signaling in metabolic regulation across all publications each year (not limited to Nature Index journals).

Technical terms

Acetyl-CoA carboxylase (ACC): Enzyme catalysing the conversion of acetyl-CoA to malonyl-CoA, a key regulatory step in fatty acid synthesis.

AMP-activated protein kinase (AMPK): Cellular energy sensor kinase that promotes catabolic pathways to restore ATP levels and inhibits anabolic processes under energy stress.

Galanin receptors (GalR1–3): Subtypes of G protein–coupled receptors through which galanin exerts tissue-specific effects on metabolism, inflammation and neuronal function.

Macrophage phenotype: Functional states of macrophages classified as pro-inflammatory (M1) or anti-inflammatory (M2), influencing tissue repair and metabolic regulation.

Non-alcoholic steatohepatitis (NASH): Progressive liver disease characterised by fat accumulation, inflammation and fibrosis in the absence of significant alcohol consumption.

Mitochondrial biogenesis: Process by which new mitochondria are formed within a cell, enhancing oxidative capacity and energy production during metabolic adaptation.

References

1. Galanin ameliorates liver inflammation and fibrosis in mice by activating AMPK/ACC signaling and modifying macrophage inflammatory phenotype. Frontiers in Immunology (2023).
2. Effects of celastrol on the heart and liver galaninergic system expression in a mouse model of Western-type diet-induced obesity and metabolic dysfunction-associated steatotic liver disease and steatohepatitis. Frontiers in Pharmacology (2025).