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Inborn Errors of Metabolism
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Surekha Pendyal, Areeg Hassan El-Gharbawy
Glucose 6-phosphatase (G6Pase) is required for the final step of glycogenolysis and gluconeogenesis to cleave glucose from glucose 6-phosphate (Figure 23.5). Glucose 6-phosphate is formed from the breakdown of glycogen and from fructose and galactose. In the absence of G6Pase, hypoglycemia is the primary consequence of GSD I with secondary consequences of lactic acidosis, hyperlipidemia, and hyperuricemia. GSD I has two sub-types: GSD Ia results from deficiency of G6Pase and GSD Ib results from deficiency of the enzyme translocase that transports G6Pase across the endoplasmic reticulum.
Medicinal Plants in Natural Health Care as Phytopharmaceuticals
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
Studies have demonstrated the hypoglycaemic action and effects of coriander on carbohydrate metabolism. The effect of coriander seeds on carbohydrate metabolism was studied in rats that were fed with a fat-rich cholesterol diet. The spice exhibited noteworthy hypoglycemic action. There was an increase in the concentration of hepatic glycogen as was evident from the increased activity of glycogen synthase. Activities of glycogen phosphorylase and gluconeogenic enzymes revealed decreased rates of glycogenolysis and gluconeogenesis. The increased activities of glucose-6-phosphate dehydrogenase and glycolytic enzymes suggest the utilization of glucose by the pentose phosphate pathway and glycolysis. These observations clearly indicated that coriander seeds demonstrate good hypoglycemic activity through enhanced glycogenesis, glycolysis and decreased glycogenolysis and gluconeogenesis (Aissaoui et al., 2011).
Functions of the Liver
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Glycogen formation from glucose-6-phosphate proceeds via glucose-1-phosphate. Glycogen synthase uses energy from uridine triphosphate to phosphorylate glucose-1-phosphate to build up glycogen polymers. With feeding, insulin is secreted in response to an increase in portal blood sugar, and this enhances glucose phosphorylation, activates glycogen synthetase, increases glycolysis, stimulates pyruvate dehydrogenase activity with increased acetyl coenzyme A (CoA) formation and inhibits glycogenolysis and gluconeogenesis. In humans, glycogen arises mainly from lactate and, to a lesser extent, from pyruvate, glycerol and gluconeogenic amino acids. Glycogen may also arise from fructose, via triose phosphates. Overall, about 10% of dietary glucose is converted to glycogen.
Advances in oxidative stress in pathogenesis of diabetic kidney disease and efficacy of TCM intervention
Published in Renal Failure, 2023
Xiaoju Ma, Jingru Ma, Tian Leng, Zhongzhu Yuan, Tingting Hu, Qiuyan Liu, Tao Shen
In the glycolysis pathway, approximately 2–5% glucose-6-phosphate (G6P) is converted to fructose-6-phosphate (F6P) and then enters the hexosamine pathway [13]. At states of sustained hyperglycemia, excessive F6P is converted to glucosamine-6-phosphate (GlcN6P) under the catalysis of glutamine fructose-6-phosphate aminotransferase (GFAT), followed by generation of uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) with the action of related enzymes. The UDP-GlcNAc is then used as substrate for O-linked N-acetylglucosamine (O-GlcNAc) glycosylation under the catalysis of O-GlcNAc transferase. It was reported that hexosamine can induce endoplasmic reticulum (ER) stress in endothelial cells and macrophages, leading to increased oxidative stress responses. Another study revealed that overexpression of GFAT increases NF-κB promoter activity and TNF-α expression in mesangial cells and stimulates the production of TGF-β1 and PAI-1, inducing inflammatory response, extracellular matrix (ECM) accumulation and diabetic glomerulosclerosis [14].
Immune metabolism: a bridge of dendritic cells function
Published in International Reviews of Immunology, 2022
Yuting Sun, Liyu Zhou, Weikai Chen, Linhui Zhang, Hongbo Zeng, Yunxia Sun, Jun Long, Dongping Yuan
There are two glycolytic branches during the conversion of glucose (Figure 2). First, glucose-derived G6P can produce ribose-5-phosphate which promotes nucleotide and ribosome biosynthesis through the pentose phosphate pathway (PPP). This pathway also allows conversion of nicotinamide adenine dinucleotide phosphate (NADP) to reduced nicotinamide adenine dinucleotide phosphate (NADPH), which is significant for fatty acid synthesis that promotes the expansion of endoplasmic reticulum (ER) and Golgi required for TLR-driven DCs activation [22]. Second, under anaerobic conditions, pyruvate derived from G6P is reduced by NADH to lactate in the presence of lactate dehydrogenase (LDH) accompanying the production of nicotinamide adenine dinucleotide (NAD+). Then NAD+ can be further used for glycolysis and promotes ATP production. Interestingly, the energy produced by OXPHOS and glycolysis is derived from glucose, but the efficiency is significantly different. OXPHOS generates up to 36 molecules of ATP per molecule of glucose, anaerobic glycolysis produces only 2 molecules of ATP, and aerobic glycolysis produces 4 molecules of ATP because a small portion of glucose is converted to pyruvate, thereby participating in the TCA in the presence of oxygen [21, 30, 32, 35, 36].
Tafenoquine for the treatment of Plasmodium vivax malaria
Published in Expert Opinion on Pharmacotherapy, 2022
Alejandro Llanos-Cuentas, Paulo Manrrique, Angel Rosas-Aguirre, Sonia Herrera, Michelle S. Hsiang
There are two major challenges associated with PQ administration. First, the total dose is administered over a long 7 to 14 day, or even 8 week period, resulting in poor adherence. Non-adherence to PQ treatment varies from 2 to 40% [20,23]. Other factors contributing to non-adherence include: lack of immediate benefit, limited understanding of long-term benefits for the individual and community, and mis-perception of vivax malaria as a benign disease. Providers and patients are concerned about potential adverse effects, and especially the risk of severe hemolysis in people with underlying glucose 6-phosphate dehydrogenase (G6PD) deficiency. To address the challenge of adherence to PQ, the 8-aminoquinoline, tafenoquine (TFQ), was co-developed by GlaxoSmithKline and Medicines for Malaria Venture as a single-dose therapy for radical cure of P. vivax malaria. At a dose of 300 mg, the drug was approved for radical cure for adults 16 years of age and older by the United States Food and Drug Administration (FDA) [24] and the Australian Therapeutic Goods Administration (TGA) in 2018 [25]. These approvals came after TFQ was shown to have similar efficacy to PQ in preventing recurrences [26–28]. Although there are concerns regarding the safety of TFQ in people with G6PD deficiency, the recent availability of point-of-care tests to quantitatively measure the activity of the G6PD enzyme [29,30] provides an opportunity national malaria programs to incorporate these tools into their control and elimination strategies.