glucose metabolism

BAY-876 is an orally active, selective inhibitor of glucose transporter 1 (GLUT1, IC50= 2 nM), exhibiting over 130-fold greater selectivity for GLUT1 than GLUT2, GLUT3, and GLUT4. It also inhibits glycolytic metabolism and ovarian cancer growth.

Imeglimin hydrochloride (EMD 387008 hydrochloride) is an oral hypoglycemic agent. Imeglimin improves insulin sensitivity, inhibits the production of reactive oxygen species, increases mitochondrial DNA, and improves mitochondrial function.

Darglitazone (CP-86325) is a potent, selective agonist of PPAR-γ with antidiabetic actions. Darglitazone is effective in controlling blood glucose and lipid metabolism.

D-Galactose (Alpha-D-galactose) is an aldohexose that exists naturally in the D-form in lactose, cerebrosides, gangliosides, and mucoproteins and is converted enzymatically into D-glucose for metabolism or polysaccharides for storage. It accelerates senescence in invertebrates and mammals and has been used as a model for aging.

Trimetazidine dihydrochloride (Vastarel F) can improve myocardial glucose utilization by inhibiting fatty acid metabolism. Trimetazidine is the first cytoprotective anti-ischemic agent, also used as a vasodilator in ischemic heart disease or angina.

Xanthinol Nicotinate (Complamin) is a potent vasodilator that can easily enter the cell and causes an increase in glucose metabolism resulting in an increased energy.

Glabridin (KB-289522) may serve as an anti-inflammatory agent in diabetes-related vascular dysfunction, through regulating the synthesis and activity of iNOS under high-glucose levels; may possess a therapeutic effect on metabolic disorders( such as diabetes and hyperglycemia), by modulating glucose metabolism through AMPK in skeletal muscle cells. Glabridin may have potential as a chemopreventive agent against liver Y metastasis, by inhibiting the invasion of human HCC cells.

Uridine 5′-diphosphoglucose disodium salt (UDP-Glucose sodium salt) is an endogenous nucleotide sugar involved in glycosyltransferase reactions in metabolism. It is an agonist of the P2Y14 receptor (EC50 = 0.35 μM) and can also bind to and activate GPR17, inducing oligodendrocyte differentiation at a maximal concentration of 100 μM.

3-Hydroxybutyric acid (Butanoic acid) (or beta-hydroxybutyrate) is a ketone body. Like the other ketone bodies (acetoacetate and acetone), levels of 3-hydroxybutyrate in blood and urine are raised in ketosis. In humans, 3-hydroxybutyrate is synthesized in the liver from acetyl-CoA and can be used as an energy source by the brain when blood glucose is low. Blood levels of 3-hydroxybutyric acid levels may be monitored in diabetic patients to look for diabetic ketoacidosis. Persistent mild hyperketonemia is a common finding in newborns. Ketone bodies serve as an indispensable source of energy for extrahepatic tissues, especially the brain and lung of developing mammals. Another important function of ketone bodies is to provide acetoacetyl-CoA and acetyl-CoA for the synthesis of cholesterol, fatty acids, and complex lipids. During the early postnatal period, acetoacetate (AcAc) and beta-hydroxybutyrate are preferred over glucose as substrates for synthesis of phospholipids and sphingolipids in accord with requirements for brain growth and myelination. Thus, during the first 2 weeks of postnatal development, when the accumulation of cholesterol and phospholipids accelerates, the proportion of ketone bodies incorporated into these lipids increases. On the other hand, an increased proportion of ketone bodies is utilized for cerebroside synthesis during the period of active myelination. In the lung, AcAc serves better than glucose as a precursor for the synthesis of lung phospholipids. The synthesized lipids, particularly dipalmitoylphosphatidylcholine, are incorporated into surfactant, and thus have a potential role in supplying adequate surfactant lipids to maintain lung function during the early days of life (PMID: 3884391 ). 3-Hydroxybutyric acid is found to be associated with fumarase deficiency and medium-chain acyl-CoA dehydrogenase deficiency, which are inborn errors of metabolism.

Bacterial α-Amylase is an enzyme produced by bacteria that catalyzes the hydrolysis reaction of starch into smaller sugar molecules such as maltose and glucose, and can be used to study starch metabolism and enzymatic mechanisms.

Danthron (Antrapurol) is a natural product, regulates glucose, and lipid metabolism by activating AMPK.

Protoporphyrin IX (PPIX) is a tetrapyrrole that is a metabolic precursor of heme, cytochrome c, and chlorophyll. Protoporphyrin IX has been shown to improve liver function, promote cellular tissue respiration, improve protein and glucose metabolism, and resist complement binding.

PQ-10 (A-844337) is a PDE-10 inhibitor. PQ-10 induces brain glucose metabolism patterns, which may be a potential translational biomarker.

GLP-1(32-36)amide acetate is a pentapeptide and derived from the C terminus of the glucoregulatory hormone GLP-1. GLP-1(32-36)amide acetate could inhibit weight gain and modulate whole body glucose metabolism in diabetic mice.

2,2,14,14-Tetramethyl-8-oxopentadecanedioic acid (compound example II-9) is a ketone used in the research of cardiovascular diseases, dysproteinemias, dyslipidemias, and glucose metabolism disorders.

hydrocotarnine is an inhibitor of Cbl.

AICAR phosphate (Acadesine phosphate) is an AMPK activator and inhibitor of autophagy, YAP, and mitophagy. It serves as an adenosine analog, regulating glucose and lipid metabolism, and inhibiting the production of pro-inflammatory cytokines and iNOS.

AS1949490 activated glucose metabolism via up-regulation of GLUT1 gene in L6 myotubes[1][2]. AS1949490 is a potent and selective SHIP-2 (SH2 domain-containing inositol 5′ phosphatase 2) inhibitor, with an IC50 of 620 nM.

D-Glucose-13C6 (Dextrose-13C6) is an isotopic marker of D-Glucose, which can be used as a metabolic tracer for the study of metabolism-related diseases and metabolic processes of some substances in the body.

ZLY06 is a dual agonist of peroxisome proliferator-activated receptors (PPAR) δ and γ with oral activity (PPAR δ: EC50=341 nM; PPARγ: EC50=237 nM). It mediates the upregulation of CD36 and induces hepatic lipid accumulation by inhibiting the phosphorylation of AKT1. Moreover, ZLY06 significantly improves glucose and lipid metabolism without increasing body weight, primarily by enhancing the β-oxidation of fatty acids and reducing hepatic lipid synthesis, thereby alleviating fatty liver disease.

EB1002 is a selective NK2R agonist that has demonstrated significant enhancements in the expression levels of genes associated with mitochondrial biogenesis (such as PGC-1α) in obese mice. This suggests that EB1002 promotes energy expenditure by enhancing mitochondrial activity. Additionally, EB1002 has improved insulin sensitivity and glucose-lipid metabolism in mice. Therefore, EB1002 holds potential for research into obesity and type 2 diabetes.

PPARγ agonist15 (Compound 7c) functions as an agonist of PPARγ, inhibiting the expression of α-amylase (HPA) and α-glucosidase (HLAG) with IC50 values of 28.35 µM and 26.21 µM, respectively. It enhances glucose uptake in L6 myotubes and improves glucose homeostasis, insulin sensitivity, and lipid metabolism in a rat model of Streptozotocin-induced diabetes.

Pyrithioxin dihydrochloride (Pyrithioxine HCl) has anti-nociceptive and anti-allodynic effects, can promote the metabolism of glucose and amino acids in the brain, improve systemic assimilation, and can be used to study neurological diseases such as atherosclerosis. Pyrithioxin dihydrochloride can induce severe cholestatic hepatitis.

DRB18 is a highly effective pan-class inhibitor of glucose transporter proteins (GLUT). It significantly modulates energy-related metabolism in A549 cells by inducing alterations in the abundance of metabolites associated with glucose-related pathways. DRB18 exerts its effects by promoting G1 S phase arrest, increasing oxidative stress, and prompting necrotic cell death, ultimately displaying notable anti-tumor activity [1].