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aP2 (adipocyte Protein 2) [5] is a carrier protein for fatty acids that is primarily expressed in adipocytes and macrophages. aP2 is also called fatty acid binding protein 4 (FABP4). Blocking this protein either through genetic engineering or drugs [6] has the possibility of treating heart disease and the metabolic syndrome. [7]
Out of 25 anti-obesity medications withdrawn from the market between 1964 and 2009, 23 acted by altering the functions of chemical neurotransmitters in the brain. The most common side effects of these drugs that led to withdrawals were mental disturbances, cardiac side effects, and drug abuse or drug dependence.
Sotagliflozin (Inpefa) is a dual SGLT1/SGLT2 inhibitor approved by the US Food and Drug Administration (FDA) in May 2023, to reduce the risk of cardiovascular death, hospitalization for heart failure, and urgent heart failure visit in adults with heart failure or type 2 diabetes, chronic kidney disease, and other cardiovascular risk factors.
All proton pump inhibitors except for rabeprazole and pantoprazole are metabolized by the hepatic CYP450 enzyme and therefore, may interact with the metabolism of clopidogrel. Omeprazole is considered to have higher potential for drug-drug interaction than other protein pump inhibitors because it is a CYP2C19 inhibitor. [17]
Thiazolidinedione ligand dependent transactivation is responsible for the majority of anti-diabetic effects. The activated PPAR/RXR heterodimer binds to peroxisome proliferator hormone response elements upstream of target genes in complex with a number of coactivators such as nuclear receptor coactivator 1 and CREB binding protein, this causes upregulation of genes (for a full list see PPARγ):
Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation. [10] [11] [12] Adiponectin is secreted from adipose tissue (and also from the placenta in pregnancy [13]) into the bloodstream and is very abundant in plasma relative to many hormones.
Administration can prevent common side-effects, such as nausea and vomiting, as a result of interaction with D 2 receptors in the vomiting center (or cheomoreceptor trigger zone) located outside the blood–brain barrier. [2] Examples of extracerebral decarboxylase inhibitors include carbidopa and benserazide.
Specifically, it is an inhibitor of Rho-associated coiled-coil kinase 2 (ROCK2; ROCK-II). [7] ROCK2-mediated signaling pathways are major players in pro- and anti-inflammatory immune cell responses. A study in cultured human cells demonstrated that the drug also has effects on oxidative phosphorylation, WNT signaling, angiogenesis, and KRAS ...