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Review

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

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Pages 333-350 | Received 01 Jun 2016, Accepted 28 Jun 2016, Published online: 25 Jul 2016

Figures & data

Table 1. Transcription factors involved in adipocyte differentiation.

Figure 1. Adipogenic effects of NPY during adipocyte differentiation. When neuropeptide Y (NPY) is included in the differentiation cocktail of preadipocytes and cells from the stromal vascular fraction (mesenchymal stem cells (MSC) and preadipocytes (PreAd)) there is increased cellular proliferation of the precursor cells, a process thought to be mediated primarily via NPY receptor 2 (NPY2R). Throughout differentiation, there is increased expression of peroxisome proliferator activated receptor (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), and decreased expression of uncoupling protein 1 (UCP1), thereby leading to increased lipid accumulation in the terminally differentiated adipocyte. Yellow represents the cell nucleus and red represents the lipid droplet.

Figure 1. Adipogenic effects of NPY during adipocyte differentiation. When neuropeptide Y (NPY) is included in the differentiation cocktail of preadipocytes and cells from the stromal vascular fraction (mesenchymal stem cells (MSC) and preadipocytes (PreAd)) there is increased cellular proliferation of the precursor cells, a process thought to be mediated primarily via NPY receptor 2 (NPY2R). Throughout differentiation, there is increased expression of peroxisome proliferator activated receptor (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), and decreased expression of uncoupling protein 1 (UCP1), thereby leading to increased lipid accumulation in the terminally differentiated adipocyte. Yellow represents the cell nucleus and red represents the lipid droplet.

Table 2. Physiological actions of Neuropeptide Y (NPY) related to energy balance and the receptors (NPYR) involved.

Table 3. Effects of NPY receptor (NPYR) antagonism in preadipocytes and adipocytes.

Figure 2. Actions of α-MSH on the adipocyte. When adipocytes are treated with α-melanocyte stimulating hormone (α-MSH), there is increased expression of nuclear hormone receptor subfamily 4 group A member 1 (NR4A1), and increased lipolysis and inhibition of re-esterification. In animals, this leads to a decrease in fat mass and body weight. These effects are thought to be mediated by melanocortin receptor 5 (MC5R). Yellow represents the cell nucleus and red represents the lipid droplet.

Figure 2. Actions of α-MSH on the adipocyte. When adipocytes are treated with α-melanocyte stimulating hormone (α-MSH), there is increased expression of nuclear hormone receptor subfamily 4 group A member 1 (NR4A1), and increased lipolysis and inhibition of re-esterification. In animals, this leads to a decrease in fat mass and body weight. These effects are thought to be mediated by melanocortin receptor 5 (MC5R). Yellow represents the cell nucleus and red represents the lipid droplet.

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