A new NPY-antagonist strongly stimulates apoptosis and lipolysis on white adipocytes in an obesity model

Margareto, Javier; Aguado, Miriam; Oses-Prieto, Juan; Rivero, Isabel; Monge, Antonio; Aldana, Ignacio; Marti, Amelia; Martínez, J. Alfredo

doi:10.1016/s0024-3205(00)00916-4

Cited by 31 publications

(20 citation statements)

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“…PPAR-γ and C/EBP-α are the two most important transcription factors for promoting adipocyte differentiation. C/EBP-α, which is active early in differentiation, induces and maintains PPAR-γ expression [24], which then up-regulates adipocyte gene expression [25]. Therefore, PPAR-γ and C/EBP-α are considered markers of adipocyte differentiation.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells

Liu

Fang

et al. 2018

Endocr J

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Abstract. Neuropeptide Y (NPY) is an important neurotransmitter in the control of energy metabolism. Several studies have shown that obesity is associated with increased levels of NPY in the hypothalamus. We hypothesized that the release of NPY has coordinated and integrated effects on energy metabolism in different tissues, such as adipocyte tissue, resulting in increased energy storage and decreased energy expenditure. Whether NPY has role in the molecular mechanism of human adipocyte tissue remains unclear. We established the model of human adipose derived stem cells (hADSCs) from human adipose tissue and differentiated it into adipocytes in the presence of NPY at different concentrations (10 -15 -10 -6 mmol/L). We then assessed hADSCs proliferation and differentiation by quantifying lipid accumulation and examining the expression levels of related adipocyte markers after differentiation. Furthermore, the specific markers of white adipocyte tissue (WAT) in hADSCs were also analyzed. The results showed that low doses of NPY stimulated hADSCs proliferation (p < 0.05), while high doses of NPY inhibited hADSCs proliferation (p < 0.05). NPY significantly promoted lipid accumulation and increased the size of lipid droplets during human adipogenic differentiation; the levels of adipocyte markers PPAR-γ and C/EBPα were also increased. At the same time, NPY also increased the levels of WAT markers Cidec and RIP140 after adipocyte differentiation. The results suggested high dose NPY inhibits the proliferation of hADSCs while promotes adipocyte differentiation and increases the expression of WAT markers. This may be the reason why increased levels of NPY can lead to a rise in body weight.Key words: Neuropeptide Y, Human adipose-derived stem cells, Adipocyte differentiation, White adipose tissue NEUROPEPTIDE Y (NPY) is a 36-amino acid neuropeptide, which is widely expressed in the central and peripheral nervous system. In the brain, NPY is found in many brain areas [1], including the hypothalamus, dentate gyrus, lateral thalamus and striatum, with the highest concentrations in the arcuate nucleus of the hypothalamus (Arc). NPY is implicated in the regulation of many physiological processes, including food intake and body energy balance. NPY also regulates cardiovascular, gastrointestinal, reproductive, endocrine and behavioural function [2][3][4]. Recently, studies have revealed that administration of NPY has profound metabolic effects throughout the body. One characteristic of obesity is the This overproduction of fat is associated with increased lipogenesis in different organs, such as liver and white adipose tissue (WAT). Several studies found that obesity is associated with elevated levels of NPY in the hypothalamus [5][6][7][8][9]. Adipose tissue is important for regulation of energy metabolism. A disturbance of metabolic processes, such as thermogenesis, lipogenesis and fatty acid oxidation, may contribute to the pathology of obesity. In order to increase our understanding of how NPY could be involved in the adipoc...

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Section: Discussionmentioning

confidence: 99%

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells

Liu

Fang

et al. 2018

Endocr J

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“…The proliferation of adipocyte precursors and their differentiation into mature adipocytes contribute to the development of obesity in mammals. Apoptosis is another important mechanism regulating adipose tissue mass (19)(20)(21)(22). Therefore, we further investigated the effects of C10orf116 on 3T3-L1 preadipocyte proliferation and apoptosis by establishing a stably transfected 3T3-L1 cell line overexpressing C10orf116 and demonstrated that: i) C10orf116 causes the promotion of cell population growth in 3T3-L1 preadipocytes indicated by results of MTT assay, and cell cycle analysis by flow cytometry showed a significantly increased percentage of cells in the S phase in C10orf116-overexpressing preadipocytes; ii) cell apoptosis analysis by Annexin V-FITC, Hoechst 33342, caspase-3 and -8 activity demonstrated that C10orf116 may prevent apoptosis induced by serum deprivation.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of C10orf116 promotes proliferation, inhibits apoptosis and enhances glucose transport in 3T3-L1 adipocytes

Chen

Zhou

et al. 2013

Molecular Medicine Reports

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Abstract. Data from our previous study demonstrated thatC10orf116 is an adipocyte lineage-specific nuclear factor, which regulates master adipogenesis transcription factors during early differentiation. However, the precise functional properties of this gene have yet to be identified and further investigation is required. In the present study, we report the effects of C10orf116 expression on cell proliferation and apoptosis in vitro and observed that the overexpression of C10orf116 stimulates proliferation and inhibits apoptosis in preadipocytes. Furthermore, we investigated the effects of C10orf116 on glucose uptake and demonstrated that the ectopic expression of C10orf116 significantly increases insulin-stimulated glucose uptake in adipocytes by increasing glucose transporter type 4 (GLUT4) expression levels. Collectively, these data further support the hypothesis that C10orf116 is important in regulating glucose transport in adipocytes as well as the number of preadipocytes. The results of the present study may also provide insights into the complex mechanisms involved in the development of obesity.

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“…Adipose tissue mass reflects the number and average volume of adipocytes, in particular, the balance between cell acquisition and cell loss (10)(11)(12). Therefore, the proliferation of adipocyte precursors and their differentiation into mature adipocytes, combined with the apoptosis of preadipocytes, both contribute to the development of obesity in mammals (13)(14)(15)(16)(17). The 3T3-L1 murine preadipocyte line is one of the established models of adipogenesis and is believed to accurately reflect the in vivo biological features of adipocytes (7,18).…”

Section: Discussionmentioning

confidence: 99%

LYRM1, a novel gene promotes proliferation and inhibits apoptosis of preadipocytes

Qiu¹,

Gao²,

Zhang³

et al. 2009

European Journal of Endocrinology

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Objective: To characterize a novel gene, Homo sapiens LYR motif containing 1 (LYRM1), that is highly expressed in omental adipose tissue of obese subjects. Methods and results: RT-PCR and western blot analysis confirmed that both mRNA and protein levels of LYRM1 were higher in omental adipose tissue of obese subjects than in normal weight subjects. RT-PCR analysis demonstrated that LYRM1 expression is widely distributed, with the highest levels of expression occurring in adipose tissue. A fusion protein of LYRM1 and green fluorescent protein as well as western blot analysis were used to identify the subcellular localization of LYRM1 in the nucleus. Based on Oil red O staining and the expression profile of specific differentiation markers, ectopic LYRM1 expression was not found to significantly affect adipogenesis. MTT assays and cell cycle analysis showed that LYRM1 promotes preadipocyte proliferation, and data from annexin V-FITC and caspase-3 activity assays further determined that LYRM1 can inhibit apoptosis of preadipocytes. Conclusions: By increasing cell proliferation and lowering the rate of apoptosis, LYRM1 has the potential to modulate the size of the preadipocyte pool and influence adipose tissue homeostasis.

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A new NPY-antagonist strongly stimulates apoptosis and lipolysis on white adipocytes in an obesity model

Cited by 31 publications

References 0 publications

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells

Neuropeptide Y promotes adipogenic differentiation in primary cultured human adipose-derived stem cells

Overexpression of C10orf116 promotes proliferation, inhibits apoptosis and enhances glucose transport in 3T3-L1 adipocytes

LYRM1, a novel gene promotes proliferation and inhibits apoptosis of preadipocytes

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