The diminished export results in hepatic lipid overload and subsequent intracellular lipid accumulation, leading to steatosis, lipotoxicity, and liver damage, and promoting disease progression and fibrosis
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The increased risk may relate to rapid weight loss, changes in gallbladder motility, or alterations in bile acid composition
129 Glucosidase (intestinal) converted disaccharides into glucose
Persistent inflammatory responses contribute to interstitial fibrosis, further accelerating kidney damage and systemic complications [145, 147]