Circulating glucose levels inversely correlate with Drosophila larval feeding through insulin signaling and SLC5A11.

Circulating glucose levels inversely correlate with Drosophila larval feeding through insulin signaling and SLC5A11.
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DOI:
10.1038/s42003-018-0109-4
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发表时间:
2018
影响因子:
5.9
通讯作者:
Graff JM
Graff JM
中科院分区:
生物学2区
文献类型:
--
作者:
Ugrankar R;Theodoropoulos P;Akdemir F;Henne WM;Graff JM

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在哺乳动物中,血糖水平可能在食欲调节中发挥作用,但这种现象背后的机制仍然不透明。机制通常可以从果蝇遗传学方法中探索。为了确定循环糖是否可能参与果蝇的进食行为,我们对血淋巴葡萄糖和海藻糖以及接受各种饮食、基因突变或RNA干扰的幼虫的食物摄入进行了评分。我们发现,幼虫与葡萄糖升高,高血糖症,有一个厌恶进食,但海藻糖水平不跟踪与摄食行为。我们进一步发现胰岛素和SLC 5A 11可能参与葡萄糖调节摄食。为了了解食物厌恶是否可能是高血糖候选人的适当筛选方法,我们开发了食物厌恶筛选来对葡萄糖异常摄食的幼虫进行评分。我们发现,许多喂养缺陷的幼虫有葡萄糖升高。这些发现突出了葡萄糖在苍蝇生物学中作为食欲的潜在线索和调节剂的有趣作用。Rupali Ugrankar等人的研究表明,具有高水平循环葡萄糖但不含海藻糖的果蝇幼虫吃得不多。这项研究表明,循环葡萄糖与胰岛素信号和钠/溶质协同转运蛋白SLC 5A 11在大脑中沟通,以抑制幼虫的食欲。
In mammals, blood glucose levels likely play a role in appetite regulation yet the mechanisms underlying this phenomenon remain opaque. Mechanisms can often be explored from Drosophila genetic approaches. To determine if circulating sugars might be involved in Drosophila feeding behaviors, we scored hemolymph glucose and trehalose, and food ingestion in larvae subjected to various diets, genetic mutations, or RNAi. We found that larvae with glucose elevations, hyperglycemia, have an aversion to feeding; however, trehalose levels do not track with feeding behavior. We further discovered that insulins and SLC5A11 may participate in glucose-regulated feeding. To see if food aversion might be an appropriate screening method for hyperglycemia candidates, we developed a food aversion screen to score larvae with abnormal feeding for glucose. We found that many feeding defective larvae have glucose elevations. These findings highlight intriguing roles for glucose in fly biology as a potential cue and regulator of appetite. Rupali Ugrankar et al. show that Drosophila larvae with high levels of circulating glucose, but not trehalose, don’t eat much. This study suggests that circulating glucose communicates with insulin signaling and the sodium/solute co-transporter SLC5A11 in the brain to suppress larval appetite.
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