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Phytotherapeutic Potential For the Treatment of Alzheimer’s Disease
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
Muhammad Akram, Atanu Bhattacharjee, Naveed Munir, Naheed Akhter, Fozia Anjum, Abida Parveen, Samreen Gul Khan, Muhammad Daniyal, Muhammad Riaz, Fahad Said Khan, Rumaisa Ansari, Umme Laila
Caprylic acid, which is a triglyceride and an important component of Axona, which is obtained from the oil of coconut, has important features for the treatment of AD. As the disease progresses, the AD brain does not properly use glucose, resulting in the appearance of neurological signs and symptoms that slowly lead to AD. Glucose transporter-1 (GLUT-1) is the carrier that transports glucose across the blood–brain barrier and cell membrane. AD progresses when GLUT-1 function is reduced (Winkler, Nishida et al. 2015). Using caprylic acid, the brain damage can be prevented because caprylic acid has the ability to be converted into keto bodies, which act as an alternative energy source (Geun Kim and Sook Oh 2012).
Glycogenosis type I – von Gierke disease
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The glucose-6-phosphatase system also depends on the transport of glucose. A number of glucose transport proteins has been identified and they have been designated GLUT 1–6. Deficiency of GLUT 2 causes the syndrome of hepatic glycogenosis in the Fanconi-Bickel syndrome [81].
A “C Odyssey”
Published in Qi Chen, Margreet C.M. Vissers, Vitamin C, 2020
Mark Levine, Pierre-Christian Violet, Ifechukwude C. Ebenuwa, Hongbin Tu, Yaohui Wang
Dehydroascorbic acid in its hydrated form has a structure similar to that of glucose (Figure 1.6). Dehydroascorbic acid was predicted and found to be transported by GLUTs [98,107]. Of the 14 identified GLUTs [108], many transport dehydroascorbic acid [109]. GLUT1, expressed in many cell types, has an affinity for dehydroascorbic acid that can be estimated to be approximately three orders of magnitude more than glucose [107]. Multiple mechanisms have been proposed to explain GLUT transport activity [110]. These mechanisms are based on using glucose or glucose analogs as substrates. A confirmation model is believed to be the best explanation of the mechanism of GLUT1 transport [110], but it is unclear whether dehydroascorbic acid transport fits any of the molecular mechanistic transport models for GLUTs.
Advancement in transporter-oriented nanoplatforms for cancer therapy
Published in Journal of Drug Targeting, 2023
Yunchun Zhao, Shuya Ye, Yao Zhu, Yue Chen, Shan Yang, Fengmei Wang, Rong Wang, Dongxu Qin, Dongli Sun, Caihong Zheng
GLUT-1 possesses a high affinity for glucose. In malignant tumours, the over-expression of GLUT-1 can lead to the transportation of more glucose to support the high metabolic rate and rapid growth of malignant cells, promote the enhanced absorption and utilisation of glucose, accelerate glycolysis, improve the survival ability of tumour cells, and promote tumour growth [38,39]. Some studies found that the elevated GLUT-1 expression in head and neck cancer, and other malignant tumours, is associated with the development, metastasis and poor prognosis of tumours, as well as with the resistance of malignant cells to radiation. In oral, rectal, cervical, and other forms of malignant tumours, studies have shown that the expression of GLUT-1 is significantly increased after radiation therapy and that an increase in GLUT-1 expression is significantly and positively correlated with radiation resistance [40–42]. The high expression levels of GLUT-1 in tumour sites are considered as a potential target for diagnostic and therapeutic action.
Emerging therapeutic targets for epilepsy: preclinical insights
Published in Expert Opinion on Therapeutic Targets, 2022
Krzysztof Łukawski, Stanisław J. Czuczwar
Non-pharmacological approaches include epilepsy surgery, neurostimulation, dietary therapies and lifestyle changes [2,27]. Epilepsy surgery is an option only for patients with resectable single lesions causing epilepsy, such as hippocampal sclerosis [5]. Also, the age of a patient and medical comorbidities that increase the dangers of surgery must be considered within this treatment strategy of DRE [8]. Neuromodulation, an alternative treatment to epilepsy surgery, includes vagus nerve stimulation, deep brain stimulation and responsive neurostimulation [2]. Data on these modalities are limited and they tend to be palliative, rarely causing seizure freedom [8]. Different dietary therapies have been used in the treatment of DRE such as ketogenic diet, Modified Atkins Diet, Medium Chain Triglyceride diet, and low glycemic diet [8]. The ketogenic diet, a restrictive high-fat, low protein and very low carbohydrate diet, is a well-established treatment for children with DRE, particularly in those with glucose type-1 transporter (GLUT1) deficiency syndrome (GLUT1DS) [28]. However, the ketogenic diet constitutes a treatment with serious potential adverse effects, and often with difficulties in implementing and adhering to it [29]. Minimizing seizure triggers originated from lifestyle (alcohol, nicotine, caffeine, drugs of abuse, mental stress, emotional tension, strobe light, video games, etc) can help control seizures [27].
The Expression and Survival Significance of Glucose Transporter-1 in Pancreatic Cancer: Meta-Analysis, Bioinformatics Analysis and Retrospective Study
Published in Cancer Investigation, 2021
Jiali Du, Jichun Gu, Junyuan Deng, Lei Kong, Yujie Guo, Chen Jin, Yun Bao, Deliang Fu, Ji Li
In our study, the meta-analysis with a total of 713 cases of nine studies demonstrated that overexpression of GLUT-1 could be an effective predictor for poor prognosis, consistent with the conclusion in a meta-analysis containing eight studies with a total of 538 cases (40). But the heterogeneity was quite high, thus, we performed subgroup analysis via different treatment method, cohort origin, volume of center, and quality of study. It was shown that the heterogeneity was mainly associated with the treatment method, cohort origin, volume of center, and quality of studies. A sensitivity analysis showed that the stability of the results was mainly affected by the study of Olca et al, which reported the smallest HR of GLUT-1. In addition, there was a priority in studies with positive results. Taken together, given the strict and standard inclusion and exclusion criteria in our meta-analysis, we speculated that the role of GLUT-1 might be overclaimed by published studies. Thus, we examined the survival significance of GLUT-1 in our own cohort.