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There are many old and novel anti-diabetes medications due to our increasing understanding of the pathophysiologic basis of mainly type 2 diabetes mellitus<\/a>. The three core pathophysiologic perturbations were first highlighted by deFronzo in the triumvirate, and this has since evolved into the ominous octet<\/a> (8 defects) and, more recently, egregious eleven <\/a>(11 defects). This represents are significant deviation from a insulin-centric approach to managing diabetes mellitus. There is more to the disease than insulin resistance<\/strong><\/a> or insulin deficiency<\/strong>.\u00a0A simple mnemonic <\/a>for recalling the groups of medications in diabetes pharmacotherapy. You first<\/em> sense<\/em><\/strong> a bowel movement, squeeze<\/strong> to evacuate the bowel, and flush<\/strong>.<\/em><\/p>\n A simple mnemonic for diabetes drugs<\/a>. Sense, Squeeze, and Flush! A complete list of infographics is available at the end of this article.<\/p>\n Metformin,<\/b> Pioglitazone<\/b>, and Dopaminergic agonist<\/b> (bromocriptine)<\/p>\n Metformin by activating the AMP-kinase pathway, reduces hepatic glucose production. It also increases insulin sensitivity(1).<\/p>\n Sulfonylureas <\/b>and Meglitinides<\/b> (directly increase insulin secretion), GLP-1<\/b>, Dual GLP-1<\/a><\/b> and DPP-4 inhibitors<\/b> (incretin pathway<\/a>), and Bile Acid sequestrants<\/b> (increase incretin levels).<\/p>\n Sulfonylureas <\/strong>(glyburide, glipizide and glimepiride) and meglitinides<\/strong> (repaglinide and nateglinide) close potassium-ATP channels on the plasma membrane of beta cells, which induces the secretion of insulin (review the mechanism here).<\/p>\n Incretin mimetics <\/strong>(GLP-1 and dual GIP-GLP1 agonists) activate GLP-1 receptors and produce the following effects<\/a><\/p>\n DPP4 inhibitors<\/strong><\/a> (sitagliptin, alogliptin, linagliptin, saxagliptin) inhibit the activity of dipeptidyl peptidase, thus increasing postprandial concentrations of incretins (GIP and GLP-1). These agents also reduce the release of glucagon.<\/p>\n The proposed mechanism of action of bile acid sequestrants (colesevelam)<\/em><\/p>\n Alpha-glucosidase inhibitors<\/strong> and SGLT-2<\/a> inhibitors<\/strong>.<\/p>\n Flushing of glucose via the urinary system (peeing) or the gastrointestinal system (pooing). Intestinal alpha-glucosidase is required for the breakdown of gastrointestinal carbohydrates. Inhibitors of this enzyme include acarbose <\/strong>and miglitol<\/strong>.<\/p>\n Sodium-Glucose Transporter<\/strong> 2 channels in the proximal nephron<\/strong> are required for glucose<\/a> reabsorption. SGLT-2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) promote glycosuria(2).<\/p>\nSensitizing<\/h2>\n
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<\/p>\nSqueezing<\/h2>\n
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Flushing<\/h2>\n
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