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Three main hypotheses were proposed to explain how riboflavin deficiency can lead to low parasitaemia: haemolysis, inhibition of reticulocytosis, and oxidative stress

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Clinical research has extended this concept by evaluating cagrilintide-semaglutide treatment in adults with overweight or obesity and type 2 diabetes, providing evidence that combined pathway engagement can improve both weight-related and glycemic outcomes [6]