Abstract
The gastrointestinal tract secretes gut hormones in response to food consumption, and some of these stimulate insulin secretion. Glucagon-like peptide-1 (GLP-1) is an incretin peptide hormone released from the lower digestive tract that stimulates insulin secretion, suppresses glucagon secretion, and decreases hunger. GLP-1 receptor agonist (GLP-1RA) mimics the action of endogenous GLP-1, consequently reversing hyperglycemia and causing weight reduction, demonstrating its efficacy as an antidiabetic and antiobesity agent. Previously restricted to injection only, the invention of the absorption enhancer sodium N-(8-[2-hydroxybenzoyl]amino) caprylate resulted in the development of oral semaglutide, the first ingestible GLP-1RA. Oral semaglutide demonstrated its efficacy in glycemic management and body weight loss with a low risk of hypoglycemia as a monotherapy and in combination with other hypoglycemic medications in its clinical trial programs named Peptide Innovation for Early Diabetes Treatment. Consistent with other injectable GLP-1RAs, gastrointestinal side effects were often reported. Additionally, cardiovascular safety was established by demonstrating that oral semaglutide was not inferior to a placebo in terms of cardiovascular outcomes. Thus, oral semaglutide represents a novel treatment option that is particularly well-suited for patients with type 2 diabetes and/or obesity.
Highlights
This review focuses oral semaglutide and levothyroxine since the pharmacokinetics of levothyroxine are inmostly on the treatment policy estimand
Oral semaglutide was found to be more efficacious than placebo as a monotherapy in patients with Type 2 diabetes (T2D) in the PIONEER 1 study, and the side effects were similar to those seen with other injectable GLP-1 receptor agonist (GLP-1RA) [43]
In patients with T2D who were uncontrolled on metformin alone, oral semaglutide significantly improved HbA1c versus empagliflozin, while fasting glucose reductions were similar in both groups, implying that changes in glycemic control are mostly due to the greater reduction of postprandial glucose with oral semaglutide
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. New antidiabetic drugs have been introduced, expanding T2D therapy choices while increasing treatment complexity [1,2]. Obesity is a modifiable risk factor, correcting the etiology of obesity and insulin resistance may help prevent and treat T2D [5]. Sulfonylureas, meglitinides, thiazolidinediones, alphaglucosidase inhibitors, and insulin are examples of traditional agents [1]. While these medications can effectively lower blood glucose levels, many have limitations due to weight gain and hypoglycemia [1]. Only metformin and thiazolidinediones are used to improve insulin sensitivity and affect the pathophysiology of T2D [1].
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