Communication between the brain and the adipose tissue has been the focus of many studies in recent years, with the "brain-fat axis" identified as a system that orchestrates the assimilation and usage of energy to maintain body mass and adequate fat stores. It is now well-known that appetiteregulating peptides that were studied as neurotransmitters in the central nervous system can act both on the hypothalamus to regulate feeding behavior and also on the adipose tissue to modulate the storage of energy. Energy balance is thus partly controlled by factors that can alter both energy intake and storage/expenditure. Two such factors involved in these processes are neuropeptide Y (NPY) and a-melanocyte stimulating hormone (a-MSH). NPY, an orexigenic factor, is associated with promoting adipogenesis in both mammals and chickens, while a-MSH, an anorexigenic factor, stimulates lipolysis in rodents. There is also evidence of interaction between the 2 peptides. This review aims to summarize recent advances in the study of NPY and a-MSH regarding their role in adipose tissue physiology, with an emphasis on the cellular and molecular mechanisms. A greater understanding of the brain-fat axis and regulation of adiposity by bioactive peptides may provide insights on strategies to prevent or treat obesity and also enhance nutrient utilization efficiency in agriculturally-important species.

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Neuropeptide Y (NPY) promotes adipogenesis in both birds and mammals, although mechanisms in avians remain unclear. The objective of this study was thus to evaluate effects of NPY on chick preadipocyte proliferation and differentiation. Preadipocytes were treated with 0, 1, 10, or 100 nmol/L NPY and gene expression and cellular proliferation were evaluated at 12, 24, and 48 h. At 12 h posttreatment, mRNA abundance of topoisomerase II alpha (TOP2A), and thioredoxin‐dependent peroxidase 2 was upregulated and NPY was downregulated in response to NPY (0 vs. 100 nmol/L) in preadipocytes. Cells were also treated with NPY during differentiation and harvested at 8, 10, and 12 days postinduction of differentiation. At day 8 postinduction of differentiation, there was increased lipid accumulation (0 vs. 10 and 100 nmol/L), expression of CCAAT/enhancer binding protein β and fatty acid binding protein 4 (FABP4) (0 vs. 100 nmol/L), and sterol regulatory element‐binding protein (0 vs. 10 and 100 nmol/L) mRNA in NPY‐treated cells. The number of proliferating cells decreased on day 8 in response to NPY (0 vs. 10 nmol/L). At day 10, FABP4 and Kruppel‐like factor 7 mRNAs were downregulated (0 vs. 10 and 100 nmol/L, and 100 nmol/L, respectively), and at day 12, TOP2A mRNA was down‐regulated (0 vs. 100 nmol/L) in response to NPY treatment. Activity of glycerol‐3‐phosphate dehydrogenase (G3PDH) was increased on days 10 and 12 in NPY‐treated cells (0 vs. 100 nmol/L). Increased gene expression of proliferation markers in preadipocytes, and during differentiation increased expression of transcription factors and a fatty acid transporter, increased lipid accumulation, and increased activity of G3PDH suggest that NPY may enhance preadipocyte activity, adipogenesis, and promotes lipid accumulation throughout chicken adipocyte differentiation.