Lewis Jo E, Brameld John M, Hill Phil, Cocco Cristina, Noli Barbara, Ferri Gian-Luca, Barrett Perry, Ebling Francis J P, Jethwa Preeti H
School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough, United Kingdom.
School of Life Sciences, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom.
PLoS One. 2017 Feb 24;12(2):e0172724. doi: 10.1371/journal.pone.0172724. eCollection 2017.
VGF (non-acronymic) was first highlighted to have a role in energy homeostasis through experiments involving dietary manipulation in mice. Fasting increased VGF mRNA in the Arc and levels were subsequently reduced upon refeeding. This anabolic role for VGF was supported by observations in a VGF null (VGF-/-) mouse and in the diet-induced and gold-thioglucose obese mice. However, this anabolic role for VGF has not been supported by a number of subsequent studies investigating the physiological effects of VGF-derived peptides. Intracerebroventricular (ICV) infusion of TLQP-21 increased resting energy expenditure and rectal temperature in mice and protected against diet-induced obesity. Similarly, ICV infusion of TLQP-21 into Siberian hamsters significantly reduced body weight, but this was due to a decrease in food intake, with no effect on energy expenditure. Subsequently NERP-2 was shown to increase food intake in rats via the orexin system, suggesting opposing roles for these VGF-derived peptides. Thus to further elucidate the role of hypothalamic VGF in the regulation of energy homeostasis we utilised a recombinant adeno-associated viral vector to over-express VGF in adult male Siberian hamsters, thus avoiding any developmental effects or associated functional compensation. Initially, hypothalamic over-expression of VGF in adult Siberian hamsters produced no effect on metabolic parameters, but by 12 weeks post-infusion hamsters had increased oxygen consumption and a tendency to increased carbon dioxide production; this attenuated body weight gain, reduced interscapular white adipose tissue and resulted in a compensatory increase in food intake. These observed changes in energy expenditure and food intake were associated with an increase in the hypothalamic contents of the VGF-derived peptides AQEE, TLQP and NERP-2. The complex phenotype of the VGF-/- mice is a likely consequence of global ablation of the gene and its derived peptides during development, as well as in the adult.
VGF(非首字母缩写词)最初是通过涉及小鼠饮食控制的实验被突显在能量稳态中发挥作用。禁食会增加弓状核中VGF的信使核糖核酸水平,随后再喂食时该水平会降低。VGF的这种合成代谢作用在VGF基因敲除(VGF-/-)小鼠以及饮食诱导和金硫葡萄糖诱导的肥胖小鼠的观察结果中得到了支持。然而,VGF的这种合成代谢作用并未得到一些后续研究的支持,这些研究调查了VGF衍生肽的生理效应。脑室内(ICV)注射TLQP-21可增加小鼠的静息能量消耗和直肠温度,并预防饮食诱导的肥胖。同样,向叙利亚仓鼠脑室内注射TLQP-21可显著降低体重,但这是由于食物摄入量减少,对能量消耗没有影响。随后发现NERP-2通过食欲素系统增加大鼠的食物摄入量,表明这些VGF衍生肽具有相反的作用。因此,为了进一步阐明下丘脑VGF在能量稳态调节中的作用,我们利用重组腺相关病毒载体在成年雄性叙利亚仓鼠中过表达VGF,从而避免任何发育影响或相关的功能补偿。最初,成年叙利亚仓鼠下丘脑过表达VGF对代谢参数没有影响,但在注射后12周,仓鼠的耗氧量增加,二氧化碳产生有增加的趋势;这减弱了体重增加,减少了肩胛间白色脂肪组织,并导致食物摄入量代偿性增加。观察到的能量消耗和食物摄入量的这些变化与下丘脑VGF衍生肽AQEE、TLQP和NERP-2的含量增加有关。VGF-/-小鼠的复杂表型可能是该基因及其衍生肽在发育过程中以及成年期整体缺失的结果。