Branch Audrey, Zhang Yiwen, Shen Ping
Department of Cellular Biology and Biomedical and Health Sciences Institute, University of Georgia, 500 D. W. Brooks Drive, Athens, GA, 30602, USA.
Sci Rep. 2017 Dec 15;7(1):17642. doi: 10.1038/s41598-017-17760-w.
Regular overconsumption of sugar is associated with obesity and type-2 diabetes, but how genetic factors contribute to variable sugar preferences and intake levels remains mostly unclear. Here we provide evidence for the usefulness of a Drosophila larva model to investigate genetic influence on vulnerability to sugar overconsumption. Using genetic and RNA interference approaches, we show that the activity of the Oamb gene, which encodes a receptor for octopamine (OA, the invertebrate homologue of norepinephrine), plays a major role in controlled sugar consumption. Furthermore, Oamb appears to suppress sugar food intake in fed larvae in an acute manner, and neurons expressing this Oamb receptor do not overlap with neurons expressing Octβ3R, another OA receptor previously implicated in hunger-driven exuberant sugar intake. Together, these results suggest that two separate sub-circuits, defined by Oamb and Octβ3R respectively, co-regulate sugar consumption according to changes in energy needs. We propose that the noradrenergic-like system defines an ancient regulatory mechanism for prevention of sugar overload.
经常过量摄入糖与肥胖和2型糖尿病有关，但基因因素如何导致不同的糖偏好和摄入水平仍大多不清楚。在这里，我们提供证据表明果蝇幼虫模型对于研究基因对糖过量摄入易感性的影响是有用的。使用基因和RNA干扰方法，我们表明Oamb基因的活性在控制糖消耗中起主要作用，该基因编码章鱼胺（OA，去甲肾上腺素的无脊椎动物同源物）的受体。此外，Oamb似乎以急性方式抑制进食幼虫的糖摄入量，并且表达该Oamb受体的神经元与表达Octβ3R的神经元不重叠，Octβ3R是先前涉及饥饿驱动的过量糖摄入的另一种OA受体。总之，这些结果表明，分别由Oamb和Octβ3R定义的两个独立子回路根据能量需求的变化共同调节糖消耗。我们提出，去甲肾上腺素能样系统定义了一种古老的预防糖过载的调节机制。
