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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Obeticholic acid's effect on HDL function in MASH varies by diabetic status.

Chunki Kim1, Tsung-Heng Tsai2, Rocio Lopez3

  • 1Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, Ohio, USA.

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Obeticholic acid (OCA) improves metabolic dysfunction-associated steatohepatitis (MASH) but affects HDL function differently in diabetic versus nondiabetic patients. This suggests distinct cardiovascular disease risks requiring further study.

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Area of Science:

  • Hepatology
  • Cardiology
  • Endocrinology

Background:

  • Metabolic dysfunction-associated steatohepatitis (MASH) and atherosclerosis share inflammatory and oxidative stress pathways.
  • Obeticholic acid (OCA), a farnesoid X receptor (FXR) agonist, shows promise for MASH but may increase cardiovascular disease (CVD) risk by reducing HDL cholesterol.

Purpose of the Study:

  • To investigate the effects of OCA on HDL cholesterol efflux, antioxidant capacity, and pro-inflammatory index in patients with MASH, comparing diabetic and nondiabetic individuals.
  • To assess potential differences in OCA's impact on cardiovascular risk markers between diabetic and nondiabetic MASH patients.

Main Methods:

  • Assessed HDL cholesterol efflux function, antioxidant (paraoxonase, ceruloplasmin activity), pro-inflammatory index, and particle sizes in MASH patients (10 diabetic, 10 nondiabetic) before and after 18 months of OCA treatment.
  • Excluded patients on lipid-lowering medications.
  • Analyzed baseline ferritin levels and changes in HDL function markers and liver enzymes post-treatment.

Main Results:

  • OCA improved liver histology and enzymes but increased alkaline phosphatase in nondiabetics.
  • OCA did not significantly alter cholesterol efflux or paraoxonase function.
  • In nondiabetics, OCA decreased ceruloplasmin activity and increased HDL's pro-inflammatory index.
  • In diabetics, OCA increased protective pre-β-HDL levels without altering overall HDL functionality.
  • Serum glucose levels negatively correlated with OCA-induced changes in HDL pro-inflammatory function, primarily due to diabetes.

Conclusions:

  • OCA exhibits distinct effects on HDL functionality in diabetic versus nondiabetic MASH patients.
  • The differential impact on HDL may influence CVD risk, particularly in nondiabetic MASH patients.
  • Further large-scale studies are warranted to confirm these preliminary findings and elucidate clinical implications.