Fat
Geoffrey P. Webb in Nutrition, 2019
Fatty acids are synthesised by a process that is essentially a reversal of β-oxidation e.g. to synthesise 16-C palmitic acid, 8 units of 2-C acetate (as acetyl coenzyme A) are progressively assembled. Thus fatty acids can be synthesised from carbohydrates via acetyl coenzyme A. Breakdown of fatty acids to acetyl coenzyme A is an oxidative process (hence, β-oxidation), thus the synthesis of fatty acids from acetyl coenzyme A is a reductive process. The reduced form of the phosphorylated derivative of NAD, NADPH2, is used as the source of reducing power in this pathway. NADPH2 is generated in the pentose phosphate pathway and this pathway also generates the pentose sugar, ribose phosphate that is essential for nucleotide (e.g. ATP) biosynthesis and nucleic acid (RNA and DNA) synthesis. The first part of this pathway involves the conversion of glucose phosphate to ribose phosphate and produces reducing power in the form of NADPH2. If the demand for NADPH2 and ribose phosphate is balanced, then these two will represent end products of the pathway. If, however, the demand for NADPH2 for active lipid synthesis exceeds the demand for ribose phosphate, the excess ribose is converted, by a complex series of reactions, to 3-carbon glyceraldehyde phosphate and 6-carbon fructose phosphate. This would also happen if there is an input of ribose from the diet.
Medicinal Plants in Natural Health Care as Phytopharmaceuticals
Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam in 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).
Hereditary Ferrihemoglobinemia
Manfred Kiese in Methemoglobinemia: A Comprehensive Treatise, 2019
The major consequence of G-6-PD deficiency is increased vulnerability of red cells to drug-induced hemolysis,494 which may begin with precipitation of hemoglobin.487 An intact pentose phosphate pathway protects the red cells by several mechanisms against oxidative hemolysis. The most important mechanism is the maintenance of reduced glutathione. This tripeptide is needed for the stability and function of several enzymes in the red cell.495–497 Glutathione either directly reacts with oxidizing agents and prevents them from reaction with proteins or it readily restores the reduced state of oxidized SH-groups of proteins.375,498 It is hard to assess which kind of ferrihemoglobin-forming agents, and to which extent, is inactivated by these mechanisms in red cells. But the quick reduction of glutathione in red cells creates a substantial inactivating capacity. Using the rapid and marked decrease in reduced glutathione content of human red cells produced by methyl phenylazoformate, C6H5N = NCOOCH3, Kosower et al.500 determined that 40% of the original reduced glutathione, about 2 mM, is regenerated in 10 min and 80% in 30 min. G-6-PD-deficient red cells regenerated less than 10% of the reduced glutathione in 30 min. The effect of some ferrihemoglobin-forming agents on reduced glutathione content of red cells is illustrated by results reproduced in Table 11 in the next chapter.
A case of dry beriberi from alcohol use disorder and disordered eating
Published in Substance Abuse, 2022
Kimberly Sycks, Steffen Simerlink, Lucas McKnight, Vincenzo Trovato
Of note in this case report, thiamin, or vitamin B1, is a water-soluble vitamin acquired through diet (e.g., whole grains, legumes, meats) and is utilized in chemical reactions in every organ system in the body. It is absorbed in the duodenum and stored in the liver up to 18 days.3,4 Thiamin is converted to its active form, TPP (thiamin pyrophosphate), in the blood, which requires magnesium. TPP is essential in the production of (a) acetyl-CoA from pyruvate, necessary in the synthesis of NADH, acetylcholine, and ATP via the Krebs cycle; (b) succinyl-CoA for the production of glutamate, aspartate, and GABA (necessary for neuronal inhibition); and (c) NADPH and ribose-5-phosphate via the pentose phosphate pathway, which have roles in the synthesis of steroids, fatty acids, glutathione, amino acids and nucleic acids, and neurotransmitters.4 The inability to absorb and utilize TTP, therefore, leads to further derangements in fatty acids, amino acids, steroids, neurotransmitters, ATP, and more.1,4 Because of thiamin’s important role in metabolism, tissues with high metabolic demand, e.g., neurons, show the first signs of dysfunction in deficiency.4 Common clinical manifestations of low thiamin levels include dry beriberi (peripheral neurologic sequelae), wet beriberi (fluid overload), and Wernicke’s encephalopathy (acute mental status changes and ataxia).4
Gene expression profiling of rat livers after continuous whole-body exposure to low-dose rate of gamma rays
Published in International Journal of Radiation Biology, 2018
The conversion of acetyl-CoA into malonyl-CoA is regulated by acetyl-CoA carboxylase 1 (ACC1) or ACC2. The latter is thought to control mitochondrial fatty acid oxidation by means of the ability of malonyl-CoA to inhibit carnitine palmitoyltransferase I (Cpt1), the rate-limiting step in fatty acid uptake and oxidation by mitochondria (He et al. 2013). Acacb which encoded for ACC2 was down-regulated while Cpt1 was up-regulated significantly. Pentose phosphate pathway is the major source of NADPH, which is required for anabolic reactions such as fatty acid synthesis and the reduction of glutathione (Klepper 2013). In this study, the only two NADPH-generating steps of the pathway, G6PD and PGD, were both transcriptionally down-regulated. Notably, G6PD is also the rate-limiting reaction in the pentose phosphate pathway under physiological conditions.
Prevalence of G6PD deficiency in Thai blood donors, the characteristics of G6PD deficient blood, and the efficacy of fluorescent spot test to screen for G6PD deficiency in a hospital blood bank setting
Published in Hematology, 2022
Phinyada Rojphoung, Thongbai Rungroung, Usanee Siriboonrit, Sasijit Vejbaesya, Parichart Permpikul, Janejira Kittivorapart
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked inherited disorder that is characterized by the insufficiency of an enzyme that is used in the pentose phosphate pathway to generate nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is a crucial oxidation reduction molecule that protects red blood cells (RBC) from reactive oxygen species (ROS). Patients with G6PD deficiency manifest varying degrees of acute hemolysis in response to oxidative stress precipitated by certain medications and foods. Transfusion of red cell products from G6PD enzyme deficient donors could cause a potentially unfavorable outcome, especially in newborns and those with hemoglobinopathies [1–3]. Current screening criteria of blood donors relative to red cell disorders in Thailand relies mostly on history taking and point-of-care hemoglobin (Hb) testing. The screening of G6PD deficiency is not performed in the donors at the moment. According to the World Health Organization (WHO) Blood Donor Selection guidelines, only donors with a previous history of hemolysis are to be permanently deferred [4]. However, countries with a high prevalence of G6PD deficiency should establish their own criteria for screening at-risk donors, and they should establish their own transfusion guidelines [5].
Related Knowledge Centers
- Anabolism
- Glucose
- Metabolic Pathway
- Nicotinamide Adenine Dinucleotide Phosphate
- Nucleotide
- Catabolism
- Glycolysis
- Carbon
- Sugar
- Ribose 5-Phosphate