Dataset for "Hepatic glycogen participates in the regulation of hypothalamic pAkt/Akt ratio in high-sugar/high-fat diet-induced obesity."

This data was used in the production of the article entitled "Hepatic glycogen participates in the regulation of hypothalamic pAkt/Akt ratio in high-sugar/high-fat diet-induced obesity." published in 2022 at Metabolic Brain Disease (ISSN: 0885-7490) (DOI : 10.1007/s11011-022-00944-3) Abstract (DOI : 10.1007/s11011-022-00944-3) The hypothalamus is a major integrating centre that controls energy homeostasis and plays a major role in hepatic glycogen (HGlyc) turnover. Not only do hypothalamic and hepatic Akt levels influence glucose homeostasis and glycogen synthesis, but exposure to high-sugar/high-fat diets (HSHF) can also lead to hypothalamic inflammation and HGlyc accumulation. HSHF withdrawal overall restores energy and glucose homeostasis, but the actual relationship between hypothalamic inflammation and HGlyc after short-term HSHF withdrawal has not yet been fully elucidated. Here we investigated the short-term effects of HSHF withdrawal preceded by a 30-day HSHF intake on the liver-hypothalamus crosstalk and glucose homeostasis. Sixty-day old male Wistar rats were fed for 30 days a control chow (n=10) (Ct), or an HSHF diet (n=20). On the 30th day of dietary intervention, a random HSHF subset (n=10) had their diets switched to control chow for 48 h (Hw) whilst the remaining HSHF rats remained in the HSHF diet (n=10) (Hd). All rats were anaesthetized and euthanized at the end of the protocol. We quantified HGlyc, Akt phosphorylation, inflammation and glucose homeostasis biomarkers. We also assessed the effect of propensity to obesity on those biomarkers, as detailed previously. Hd rats showed impaired glucose homeostasis, higher HGlyc and hypothalamic inflammation, and lower pAkt/Akt. Increased HGlyc was significantly associated with HSHF intake on pAkt/Akt lowered levels. We also found that HGlyc breakdown may have prevented a further pAkt/Akt drop after HSHF withdrawal. Propensity to obesity showed no apparent effect on hypothalamic inflammation or glucose homeostasis. Our findings suggest a comprehensive role of HGlyc as a structural and functional modulator of energy metabolism, and such roles may come into play relatively rapidly. It contains the .csv file with the data used in the publication. Researcher in charge: Debora Estadella Researcher in charge of data collection: Breno Picin Casagrande Date of data collection: 01/04/2018 - 1/12/2019 Financial support: CAPES - Brazil, FAPESP (2017/25420-3), CNPq

本数据集用于支撑2022年发表于《代谢性脑疾病》（Metabolic Brain Disease，ISSN: 0885-7490，DOI: 10.1007/s11011-022-00944-3）、题为《肝糖原参与高糖高脂饮食诱导肥胖时下丘脑pAkt/Akt比值的调控》的研究论文的相关工作。
该论文摘要如下：
下丘脑是调控能量稳态的核心整合中枢，同时在肝糖原（hepatic glycogen）周转过程中发挥关键作用。下丘脑与肝脏的Akt蛋白水平不仅影响葡萄糖稳态与糖原合成，高糖高脂饮食（high-sugar/high-fat diets, HSHF）暴露还可诱发下丘脑炎症与肝糖原蓄积。尽管撤除高糖高脂饮食可整体恢复能量与葡萄糖稳态，但短期撤除该饮食后，下丘脑炎症与肝糖原之间的具体关联尚未完全阐明。
本研究探究了先经30天高糖高脂饮食喂养后，短期撤除该饮食对肝-下丘脑信号串扰及葡萄糖稳态的短期影响。实验选用60日龄雄性Wistar大鼠，随机分为两组：普通饲料喂养对照组（n=10，Ct组）与高糖高脂饮食喂养组（n=20）。造模第30天时，随机选取10只高糖高脂饮食组大鼠更换为普通饲料喂养48小时（饮食撤除组，Hw组），剩余10只高糖高脂饮食组大鼠继续维持原饮食（持续饮食组，Hd组）。实验结束时对所有大鼠进行麻醉并处死，我们定量检测了肝糖原、Akt磷酸化水平、炎症标志物及葡萄糖稳态相关生物标志物，并如前文所述评估了肥胖易感性对上述生物标志物的影响。
实验结果显示：持续高糖高脂饮食组大鼠出现葡萄糖稳态受损、肝糖原水平升高及下丘脑炎症加重，同时pAkt/Akt比值降低；肝糖原水平升高与高糖高脂饮食导致的pAkt/Akt比值降低显著相关。本研究还发现，肝糖原分解可能阻止了撤除高糖高脂饮食后pAkt/Akt比值的进一步下降。肥胖易感性对下丘脑炎症或葡萄糖稳态无明显影响。
本研究结果提示，肝糖原在能量代谢的结构与功能调控中发挥全面作用，且该作用可相对快速地显现。
本数据集包含本研究使用的.csv格式数据。
负责研究者：Debora Estadella
负责数据收集的研究者：Breno Picin Casagrande
数据收集时间：2018年4月1日 — 2019年12月1日
资助来源：巴西高等教育人员发展协调局（CAPES）、圣保罗研究基金会（FAPESP，项目编号2017/25420-3）及巴西国家科学技术发展委员会（CNPq）