Abstract of “Oral Semaglutide: A Potential Solution for Obesity in Mice – A Glimpse into Human Treatment?”
In a recent research breakthrough featured in the journal Nutrients, scientists embarked on a mission to unravel the metabolic impact of oral semaglutide in diet-induced obese (DIO) mice, potentially opening new doors for combating obesity in humans.
Understanding the Background
Semaglutide, an oral version of the glucagon-like peptide-1 receptor agonist (GLP-1RA), stands as a groundbreaking type 2 diabetes (T2D) medication with an unexpected twist—it could hold the key to tackling obesity. This revelation led to the approval of three doses of semaglutide (3 mg, 7 mg, and 14 mg) for clinical use in humans.
The PIONEER 1 study was a pivotal moment, showcasing that semaglutide at 7 mg and 14 mg significantly reduced both hemoglobin A1C (HbA1C) levels and body weight (BW) over 26 and 52 weeks of treatment in T2D patients. Moreover, it effectively curbed body fat mass and energy intake within just 12 weeks and bolstered feelings of satiety, especially after high-calorie breakfasts. Remarkably, oral semaglutide even outperformed two other GLP-1RAs, dulaglutide and liraglutide, in reducing body weight.
However, there was an intriguing twist. Because humans and laboratory animals possess different gastrointestinal (GI) tracts, the absorption of oral semaglutide might vary. This discrepancy necessitated the need for an appropriate experimental model to fathom the mechanics of oral semaglutide in humans.
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Unveiling the Study
In this groundbreaking study, researchers handpicked DIO mice as their experimental model to scrutinize the metabolic consequences of orally administered semaglutide. They assessed various parameters, including food intake (FI), BW, and blood glucose (BG) levels. The study encompassed oral semaglutide doses equivalent to those administered to humans: 0.05 mg/kg, 0.12 mg/kg, 0.23 mg/kg, and 0.7 mg/kg.
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The Experimental Landscape
The researchers meticulously categorized DIO mice, factoring in factors like Blood Glucose Levels, age, and daily FI, to fine-tune their experiments. They conducted injections of oral semaglutide and distilled water (DW) for control groups. Multiple measurements and observations were made at various time points to ascertain the drug’s effects.
Key Study Outcomes
The study unfolded critical findings, indicating that oral semaglutide, administered in 0.1 mL DW, effectively lowered glycemia, FI, and BW in DIO mice. However, when administered in a larger volume of 0.5 mL DW, its effect on FI was negated. This suggests that successful absorption of oral semaglutide in mice’s stomachs requires a smaller water volume.
Moreover, oral semaglutide consistently reduced daily FI and progressively curbed BW gain in DIO mice. A three-day treatment regimen further decreased FI and BW gain, showcasing a dose-dependent response. The implications are significant, considering ongoing trials evaluating higher semaglutide doses for treating obesity in humans.
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Conclusions
Oral semaglutide, administered at a dose of 0.23 mg/kg following fasting and water deprivation, triggered rapid reductions in BG levels and total FI in DIO mice, with significant effects observed four hours after injection-refed time.
A key highlight of this research lies in the successful replication of oral semaglutide’s metabolic effects in humans using the DIO murine model. This model’s potential to mirror human responses positions it as a valuable asset for exploring the mechanisms of action behind oral semaglutide in forthcoming studies focused on treating obesity and T2D.
