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The pharmaceutical industry specifically designed semaglutide with a long half-life by modifying the molecule to resist breakdown in the body
The therapeutic effect is achieved by reducing FA and cholesterol synthesis through the inhibition of ACLY (143)
Acetyl-CoA is also an allosteric activator of pyruvate carboxylase that catalyzes the gluconeogenesis pathway which is active during catabolic states such as fasting.[6][15][16] In carnitine deficient states, LCFAs cannot be effectively transported to the mitochondria matrix for oxidation and subsequent utilization in Krebs cycle and ketone body production
People who take semaglutide are at an increased risk of medullary thyroid carcinoma (thyroid cancer), acute pancreatitis, gallbladder disease, hypoglycemia (low blood sugar), acute kidney injury, increased heart rate, diabetic retinopathy complications, depression, and suicidal thoughts
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