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This may include ongoing pharmacotherapy at lower doses, structured dietary counseling, exercise programming, or combination protocols with other medications to sustain long-term results

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Collectively, these findings establish a mechanistic pathway whereby LEO restores dysregulated SCFA production in diabetic mice, highlighting dose-responsive butyrate accumulation as the dominant effector mediating enhanced GLP-1 secretion in functionally compromised enteroendocrine cells

Maximum results often occur between 6-12 months, though individual responses vary based on starting weight, adherence to lifestyle changes, and medication tolerance

These mechanisms contribute to the therapeutic benefits of GLP-1 based therapies in mitigating hepatic steatosis and improving overall lipid homeostasis [27, 29]