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首页> 外文期刊>Endocrinology, Diabetes & Metabolism >Circadian‐timed dopamine agonist treatment reverses high‐fat diet‐induced diabetogenic shift in ventromedial hypothalamic glucose sensing
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Circadian‐timed dopamine agonist treatment reverses high‐fat diet‐induced diabetogenic shift in ventromedial hypothalamic glucose sensing

机译：昼夜定期的多巴胺激动剂治疗逆转高脂饮食诱导的腹侧下丘脑葡萄糖感测的糖苷转变

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Introduction Within the ventromedial hypothalamus (VMH), glucose inhibitory (GI) neurons sense hypoglycaemia while glucose excitatory (GE) neurons sense hyperglycaemia to initiate counter control mechanisms under normal conditions. However, potential electrophysiological alterations of these two neuronal types in vivo in insulin‐resistant states have never been simultaneously fully documented. Further, the anti‐diabetic effect of dopamine agonism on this VMH system under insulin resistance has not been studied. Methods This study examined the impact of a high‐fat diet (HFD) on in vivo electrophysiological recordings from VMH GE and GI neurons and the ability of circadian‐timed dopamine agonist therapy to reverse any adverse effect of the HFD on such VMH activities and peripheral glucose metabolism. Results HFD significantly inhibited VMH GE neuronal electrophysiological response to local hyperglycaemia (36.3%) and augmented GI neuronal excitation response to local hypoglycaemia (47.0%). Bromocriptine (dopamine agonist) administration at onset of daily activity (but not during the daily sleep phase) completely reversed both VMH GE and GI neuronal aberrations induced by HFD. Such timed treatment also normalized glucose intolerance and insulin resistance. These VMH and peripheral glucose metabolism effects of circadian‐timed bromocriptine may involve its known effect to reduce elevated VMH noradrenergic activity in insulin‐resistant states as local VMH administration of norepinephrine was observed to significantly inhibit VMH GE neuronal sensing of local hyperglycaemia in insulin‐sensitive animals on regular chow diet (52.4%). Conclusions HFD alters VMH glucose sensing in a manner that potentiates hyperglycaemia and this effect on the VMH can be reversed by appropriately circadian‐timed dopamine agonist administration.
机译：腹侧下丘脑（VMH）内引入，葡萄糖抑制（GI）神经元感测低血糖，而葡萄糖兴奋剂（GE）神经元感测高血糖在正常条件下启动计数器控制机制。然而，在胰岛素抗性状态体内体内两种神经元类型的潜在电生理改变从未被同时记录过。此外，尚未研究在胰岛素抗性下该VMH系统对该VMH系统的抗糖尿病效应。方法本研究检测了高脂饮食（HFD）对来自VMHGE和GI神经元的体内电生理记录的影响以及昼夜定时的多巴胺激动剂治疗逆转HFD对这些VMH活动和外围的任何不利影响的能力葡萄糖新陈代谢。结果HFD显着抑制局部高血糖（36.3％）和增强GI神经元激发反应对局部低血糖（47.0％）的VMH GE神经元电生理反应。溴隐亭（多巴胺激动剂）在日常活性开始（但在日常睡眠期期间）的施用完全逆转了HFD诱导的VMHGe和Gi神经元像差。这种定时处理还标准化葡萄糖不耐受和胰岛素抵抗力。昼夜时序溴杉木的这些VMH和外周葡萄糖代谢作用可能涉及其已知的效果，以减少胰岛素抗性状态的升高的VMH丙肾上腺素能活性，因为局部VMH施用去甲肾上腺素，以显着抑制胰岛素敏感的局部高血糖血症的VMH GE神经元传感常规味道饮食（52.4％）的动物。结论HFD以增强高血糖血症的方式改变VMH葡萄糖感测，并且通过适当的昼夜定时的多巴胺激动剂给药可以逆转对VMH的这种影响。

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