Brown Adipose Tissue Growth and Development

Symonds, Michael

doi:10.1155/2013/305763

Cited by 111 publications

(112 citation statements)

References 155 publications

(231 reference statements)

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“…NPY is one of the most important adipocyte regulatory factors [13][14][15][16]. Several articles had provided evidence that NPY is produced in subcutaneous and visceral adipose tissue [17,18].…”

Section: Discussionmentioning

confidence: 99%

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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%

“…About 30 g fat tissue was obtained. The technology of isolation and culture of human adipose tissue-derived stem cells was mature [12][13][14]. Briefly, tissue was washed in PBS buffer and digested with 2 mg/mL Collagenase Type I for 1 hour at 37°C with constant shaking.…”

Section: Isolation and Culture Of Human Adscsmentioning

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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“…This could be because, in young sheep, the rate of loss of BAT and its subsequent replacement with white adipose tissue are possibly much more rapid when compared with pigs, due in part to the concomitant growth of wool, widening of the thermoneutral zone (Symonds 2013) and replacement of non-shivering with shivering thermogenesis as the dominant response to acute cold exposure (Symonds et al 1989). It remains to be established whether UCP1 is switched on at birth in piglets, as is the case in both humans and sheep that are also both born with a mature hypothalamic-pituitary axis (Symonds 2013), and/or whether it experiences a period of postnatal maturation as observed in altricial thermoregulators such as rodents (Nedergaard et al 1986). …”

Section: Discussionmentioning

confidence: 99%

“…The onset of non-shivering thermogenesis in BAT at birth is dependent on the rapid appearance of endocrine stimulatory factors, including leptin (Mostyn et al 2001, Symonds 2013. When administered to female postnatal sheep, leptin improves thermoregulation in the newborn and then subsequently promotes the normal loss of UCP1 in the main fat depot (i.e.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, our understanding of BAT has now been transformed as a consequence of the discovery of beige adipocytes that express UCP1 at approximately 10% of the amount observed in classical BAT , Wu et al 2013, but whether comparable depots are be present in young pigs is not known. The onset of non-shivering thermogenesis in BAT at birth is dependent on the rapid appearance of endocrine stimulatory factors, including leptin (Mostyn et al 2001, Symonds 2013. When administered to female postnatal sheep, leptin improves thermoregulation in the newborn and then subsequently promotes the normal loss of UCP1 in the main fat depot (i.e.…”

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UCP1 is present in porcine adipose tissue and is responsive to postnatal leptin

Mostyn¹,

Attig²,

Larcher³

et al. 2014

Journal of Endocrinology

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Intrauterine growth restriction (IUGR) may be accompanied by inadequate thermoregulation, especially in piglets that are not considered to possess any brown adipose tissue (BAT) and are thus entirely dependent on shivering thermogenesis in order to maintain body temperature after birth. Leptin can stimulate heat production by promoting non-shivering thermogenesis in BAT, but whether this response occurs in piglets is unknown. Newborn female piglets that were characterised as showing IUGR (mean birth weight of approximately 0.98 kg) were therefore administered injections of either saline or leptin once a day for the first 5 days of neonatal life. The dose of leptin was 0.5 mg/kg, which is sufficient to increase plasma leptin by approximately tenfold and on the day of birth induced a rapid increase in body temperature to values similar to those of normal-sized 'control' piglets (mean birth weight of w1.47 kg). Perirenal adipose tissue was then sampled from all offspring at 21 days of age and the presence of the BAT-specific uncoupling protein 1 (UCP1) was determined by immunohistochemistry and immunoblotting. UCP1 was clearly detectable in all samples analysed and its abundance was significantly reduced in the IUGR piglets that had received saline compared with controls, but was raised to the same amount as in controls in those IUGR females given leptin. There were no differences in gene expression between primary markers of brown and white adipose tissues between groups. In conclusion, piglets possess BAT that when stimulated exogenously by leptin can promote increased body temperature. IntroductionBrown adipose tissue (BAT) is essential for effective adaptation to cold exposure of the extra-uterine environment in precocial species such as sheep in which there is rapid activation of BAT around the time of birth (Clarke et al. 1997). In pigs, however, it has long been considered that BAT is not present (Trayhurn et al. 1989) and the newborn is Journal of Endocrinology Thematic ResearchA MOSTYN and others UCP1 and leptin in porcine 223:1 M31-M38http://joe.endocrinology-journals.org Ñ 2014 Society for Endocrinology DOI: 10.1530/JOE-14-0155Printed in Great BritainPublished by Bioscientifica Ltd.primarily dependent on shivering thermogenesis in muscle in order to prevent hypothermia at birth (Symonds & Lomax 1992). This due to an open reading frame on the BAT-specific uncoupling protein 1 (UCP1) gene in the porcine species meaning that UCP1 is not expressed (Berg et al. 2006). However, it has more recently been suggested that BAT is present in young piglets because of the different morphological appearances of adipocytes within perirenal adipose tissue in 2-week-old females (Attig et al. 2008). However, this remains to be confirmed by direct measurements of UCP1. Moreover, our understanding of BAT has now been transformed as a consequence of the discovery of beige adipocytes that express UCP1 at approximately 10% of the amount observed in classical BAT , Wu et al. 2013, but whether comparable depots are be pr...

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Modulation of brown adipocyte activity by milk by‐products: Stimulation of brown adipogenesis by buttermilk

Asano

Kida

Muto

et al. 2016

Cell Biochemistry & Function

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Brown adipocytes dissipate chemical energy in the form of heat through the expression of mitochondrial uncoupling protein 1 (Ucp1); Ucp1 expression is further upregulated by the stimulation of β-adrenergic receptors in brown adipocytes. An increase in energy expenditure by activated brown adipocytes potentially contributes to the prevention of or therapeutics for obesity. The present study examined the effects of milk by-products, buttermilk and butter oil, on brown adipogenesis and the function of brown adipocytes. The treatment with buttermilk modulated brown adipogenesis, depending on the product tested; during brown adipogenesis, buttermilk 1 inhibited the differentiation of HB2 brown preadipocytes. In contrast, buttermilk 3 and 5 increased the expression of Ucp1 in the absence of isoproterenol (Iso), a β-adrenergic receptor agonist, suggesting the stimulation of brown adipogenesis. In addition, the Iso-induced expression of Ucp1 was enhanced by buttermilk 2 and 3. The treatment with buttermilk did not affect the basal or induced expression of Ucp1 by Iso in HB2 brown adipocytes, except for buttermilk 5, which increased the basal expression of Ucp1. Conversely, butter oil did not significantly affect the expression of Ucp1, irrespective of the cell phase of HB2 cells, ie, treatment during brown adipogenesis or of brown adipocytes. The results of the present study indicate that buttermilk is a regulator of brown adipogenesis and suggest its usefulness as a potential food material for antiobesity.

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Brown Adipose Tissue Growth and Development

Cited by 111 publications

References 155 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

UCP1 is present in porcine adipose tissue and is responsive to postnatal leptin

Modulation of brown adipocyte activity by milk by‐products: Stimulation of brown adipogenesis by buttermilk

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