Recent advances in the understanding of how neuropeptide Y andα-melanocyte stimulating hormone function in adipose physiology

Abstract

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.

Nonenzymatic and Trophic Activities of Carboxypeptidase E Regulate Bone Mass and Bioenergetics of Skeletal Stem Cells in Mice

“…(26,27) Moreover, it is also possible that αMSH directly regulates marrow adipocyte. The circulating αMSH increases lipolysis by acting on melanocortin 5 receptors present in adipocytes, (28) including marrow adipocytes (BLC, personal information). Thus, a decrease in αMSH signaling may impair lipolysis and may favor lipid accumulation in marrow adipocytes.…”

The Long-Term Impact of High Levels of Alpha-Melanocyte-Stimulating Hormone in Energy Balance Among Obese Adolescents

“…In a fed state, the leptin levels suppress NPY and AgRP neurons, stimulate a POMC, and consequently α-MSH [1, 2]. Besides the function of energy balance control by anorexigenic/orexigenic axis, both neuropeptides also affect the metabolism profile acting in the physiology of adipose tissue: NPY affects the adipogenesis and α-MSH is responsible for lipolysis [4, 10, 16]. …”

“…The MC4R and MC5R, receptor of α-MSH too, have been related to the stimulation of metabolic pathways by lipid mobilization and increase in the thermogenesis. This mechanism could occur in the sympathetic nervous system by β-adrenergic receptors causing the uncoupling of terminal oxidation and ATP production to white adipose tissue and brown adipose tissue [4, 17-20]. …”

“…These neuropeptides are inhibited by leptin, being antagonists of the α-MSH and modulating appetite stimulation, lipogenesis, and reducing energy expenditure [2, 4, 5]. The deregulation in orexigenic and anorexigenic neuropeptides expression is the basis to understanding the positive energy balance and the determinant factor of the increase in adiposity associated with energy intake and low levels of physical activity.…”

“…When stimulated, POMC releases hypothalamic alpha-melanocyte-stimulating hormone (α-MSH), which is a key catabolic mediator of energy homeostasis. The peptide α-MSH is a part of the melanocortin (MC) system, which is made up of α, β, and γ – MSH, adrenocorticotropic hormone, MC receptors, agouti-related peptide (AgRP), and endogenous MC receptors antagonist [2, 4]. …”