最近研究指出長期不良的飲食習慣可能導致下視丘發炎和神經膠質增生，在其他大腦區域也可能受到影響。脂肪細胞通常在體內扮演儲存脂質的角色，可以很好地處理多餘的脂質。然而，過量的脂質累積將使這些脂肪細胞過載，並導致脂質累積到非脂肪細胞中，這時就會產生脂毒性。脂毒性是一種代謝綜合症，是由脂質累積到非脂肪組織而產生，這樣會導致細胞功能出現障礙和死亡。通常受影響的組織包括腎臟，肝臟，心臟和骨骼肌。游離脂肪酸的過載導致胰腺β細胞凋亡和功能障礙。 第II型糖尿病是全球最普遍的代謝綜合徵，脂肪酸的全身水平升高現被認為是該綜合徵進展的重要因素，脂毒性被認為與肥胖和糖尿病有關。棕櫚酸（PA）是飲食和血清中存在的最豐富的游離脂肪酸，棕櫚酸的積累會誘發脂毒性，也會引起內質網壓力和線粒體功能障礙。已知用PA處理的INS-1細胞會損害葡萄糖刺激的胰島素分泌。注射PA的慢性小鼠由於ATP敏感性鉀通道（KATP）通道的缺陷運輸而表現出第II型糖尿病特徵，因為胰腺β細胞- KATP通道對於胰島素分泌至關重要。神經變性疾病的共同特徵是神經炎症反應的發生，其中涉及神經膠質細胞死亡的膠質細胞（主要是小膠質細胞和星形膠質細胞）的細胞過程被激活。而興奮性中毒是突觸的谷氨酸和鈣平衡的改變導致神經元和神經膠質谷氨酸的受體過度活化，最終導致神經元死亡和神經迴路功能障礙。微膠細胞是最不易受興奮性毒性影響的神經膠質細胞類型，因為它們在反應時主要表達谷氨酸受體。如果暴露於興奮性毒性的時間或強度受到限制，這種炎症的益處可能會很大，有助於避免進一步的神經元損傷。否則，小膠質細胞的作用將通過長期的ROS形成和細胞因子分泌而有害，並直接與神經退行性過程有關。實際上，積累的證據表明衰老的小膠質細胞在退行性中樞神經系統疾病中具有直接的致病作用。通過控制小膠質細胞線粒體活性來調節小膠質細胞活性構成了一種創新的方法來干擾神經變性過程。腺核甘三磷酸敏感鉀離子通道（KATP）是包含4個SUR1和4個Kir6.2亞基的八聚體複合物，由細胞[ATP]和[ADP]門閥控制。藉由KATP通道是控制小膠質細胞活性避免其毒性表型並促進疾病。在大腦中，已經在黑質，新皮層，海馬和下丘腦中描述了KATP的神經元表達。在小膠質細胞中也已經提出了KATP通道的表達。先前的研究表明，在腦部疾病例如中風和阿爾茨海默氏病（AD）發生後，反應性小膠質細胞會增加其KATP通道成SUR1的表達。

Prolonged poor dietary habits can result in hypothalamic inflammation and gliosis with more recent studies suggest that other brain areas may also be affected. Adipocytes usually play the role of storing lipids in the body and can handle excess lipids well. However, excessive lipid accumulation will overload these adipocytes and lead to accumulation of lipids in non-adipocytes, which can lead to lipotoxicity. Lipotoxicity is a metabolic syndrome that is caused by the accumulation of lipids in non-fat tissues, which can lead to cell dysfunction and death. Commonly affected tissues include the kidneys, liver, heart, and skeletal muscles. The overload of free fatty acids leads to apoptosis and dysfunction of pancreatic β-cells. Type II diabetes is the most common metabolic syndrome in the world. It is now believed that elevated levels of fatty acids in the body are an important factor in the development of this syndrome, and lipotoxicity is believed to be related to obesity and diabetes. Palmitic acid (PA) is the most abundant free fatty acids present in the diet and serum, and accumulation of palmitic acid induces lipotoxicity, causes ER stress and mitochondrial dysfunction. It is known that INS-1 cells treated with PA impair glucose-stimulated insulin secretion. Chronic mice injected with PA exhibited the characteristics of type II diabetes due to defective transport of ATP-sensitive potassium channel (KATP) channels, because the pancreatic β-cell KATP channels are essential for insulin secretion. The common feature of neurodegenerative diseases is the occurrence of neuroinflammatory response, in which the cellular processes of glial cells (mainly microglia and astrocytes) involved in the death of glial cells are activated. Excitatory poisoning is the alteration of synaptic glutamate and calcium balance that leads to excessive activation of neurons and glial glutamate receptors, which ultimately leads to neuronal death and neural circuit dysfunction. Microglia are the type of glial cells least susceptible to excitotoxicity because they mainly express glutamate receptors in response. If the time or intensity of exposure to excitotoxicity is limited, the benefits of this inflammation may be great, helping to avoid further neuronal damage. Otherwise, the effects of microglia will be harmful through long-term ROS formation and cytokine secretion, and are directly related to the neurodegenerative process. In fact, accumulated evidence indicates that aging of microglia has a direct pathogenic role in degenerative central nervous system diseases. Regulating the activity of microglia by controlling the mitochondrial activity of microglia constitutes an innovative method to interfere with the neurodegenerative process.
ATP sensitive potassium channel (KATP), the octamer complex containing 4 SUR1 and 4 Kir6.2 subunits, is gated by the cellular [ATP] and [ADP]. KATP channels are used to control the activity of microglia to avoid their toxic phenotype and promote disease. In the brain, the neuronal expression of KATP has been described in the substantia nigra, neocortex, hippocampus, and hypothalamus. The expression of KATP channels has also been proposed in microglia. Previous studies have shown that after brain diseases such as stroke and Alzheimer's disease (AD), reactive microglia increase the expression of their KATP channel into SUR1.

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