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[English Abstract] This monograph formulates a rigorous biophysical and thermodynamic model governing the phase transitions of biliary micro-calculi (cholesterol-phospholipid-bile salt ternary systems) and establishes a deterministic lipid routing protocol via cholecystokinin (CCK) receptor modulation. Conventional hepatobiliary frameworks treat biliary sludge and micro-calculi nucleation as stochastic physiological events, frequently resulting in acute cholecystitis, sphincter of Oddi spasms, or secondary pancreatitis triggered by erratic high-fat bolus ingestion. In contrast, this paper models the ternary phase diagram of bile as a deterministic free-energy landscape where cholesterol monohydrate crystal nucleation is governed by supersaturation indices, vesicular aggregation kinetics, and hydrodynamic shear stress within the cystic and common bile ducts. We introduce a precision nutritional-kinetic control architecture utilizing specific unsaturated fatty acid profiles—specifically eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) (Omega-3 polyunsaturated fatty acids), and oleic acid (Omega-9 monounsaturated fatty acid)—to modulate I-cell mediated CCK secretion curves. By calibrating the chain length, degree of unsaturation, and dosage cadence of dietary lipids, the proposed model achieves: (1) homeostatic, low-amplitude gallbladder contractility that prevents hyper-contractile biliary colic while flushing mucin-gel micro-precipitates; (2) thermodynamic shifts of the biliary lipid composition from the metastable two-phase/three-phase nucleation zone back into the stable micellar liquid-crystalline single-phase region via hepatic phospholipid-cholesterol coupling; and (3) suppression of pro-inflammatory eicosanoid cascades in the gallbladder mucosa. This deterministic lipid routing framework bridges molecular thermodynamics with actionable physiological infrastructure control.
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Yoko(洋子) Hasebe(長谷部) (2026) studied this question.
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