This study explores the formation of amylose–lipid complexes in green banana flour derived from the Bungulan variety (Musa paradisiaca suaveolens Blanco), enriched with virgin coconut oil (VCO), as a strategy to reduce starch digestibility and lower the glycemic index. The native banana flour was first characterized by its apparent amylose content (AAC), determined to be 19.05 ± 0.82%, confirming its suitability for amylose–lipid complex formation. Two types of VCO—hot-pressed and cold-pressed—were subjected to fatty acid methyl ester (FAME) derivatization and subsequently analyzed via gas chromatography-mass spectrometry (GC-MS). The major FAME components identified included lauric acid (C12:0, 39.16%), myristic acid (C14:0, 20.69%), palmitic acid (C16:0, 12.32%), oleic acid (C18:1, 8.72%), caprylic acid (C8:0, 6.94%), capric acid (C10:0, 6.41%), and stearic acid (C18:0, 4.65%), alongside several minor fatty acids. Hot-pressed and cold-pressed VCO were incorporated into the flour under controlled conditions to optimize complex formation. Fourier-transform infrared (FTIR) spectroscopy confirmed the formation of amylose–lipid complexes through characteristic absorption bands corresponding to O–H stretching (~3450 cm⁻¹), C–H stretching (~2950 cm⁻¹), C=O stretching (~1750 cm⁻¹), and C–O stretching (~1000 cm⁻¹). Differential scanning calorimetry (DSC) further validated complex formation, showing melting transitions at ~24–26 °C, attributed to unbound coconut oil, and distinct endothermic peaks at ~90–105 °C, indicative of thermally stable V-type amylose–lipid complexes. In vitro enzymatic digestion at 37 °C revealed reduced starch hydrolysis in all oil-complexed samples compared to native banana flour. Kinetic modeling based on fitted C∞ values—representing the equilibrium concentration of maltose release per gram of starch—demonstrated a progressive decline in digestibility: the native flour had a C∞ of 36.85 mg/g (3.50% starch hydrolysis). In comparison, cold-pressed and hot-pressed VCO treatments yielded slightly lower values of 35.80 mg/g (3.40%) and 35.30 mg/g (3.35%), respectively. These reductions suggest enhanced resistance to α-amylase digestion due to the formation of amylose–lipid complexes, which act as structural barriers and reduce enzymatic accessibility.