TOPLINE:

Individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) had a higher rate of appearance of oral glucose — particularly during the first hour after a glucose load — and higher 1-hour plasma glucose levels than those without MASLD.

METHODOLOGY:

• Patients with MASLD often have increased expression of duodenal glucose transporters, which may facilitate intestinal glucose absorption and increase glucose delivery to the liver; however, the role of oral glucose absorption in the pathogenesis of MASLD remains unclear.
• Researchers in Italy conducted a study with 32 volunteers without diabetes and with or without MASLD (mean age, 47.8 years; 50% women; mean BMI, 27.5) who underwent an oral glucose tolerance test using two stable glucose isotopes — one given orally and the other given intravenously.
• They then measured the rate of appearance of oral glucose, endogenous glucose production, glucose clearance, and rate of insulin secretion in the study participants.

TAKEAWAY:

• A total of 16 individuals had MASLD; they had higher BMI +4.1 (P = .019), fasting plasma insulin levels +24 pmol/L (P = .015), insulin resistance +1.2 (P = .008), low-density lipoprotein cholesterol levels +22 mg/dL (P = .046), and triglyceride levels +46 mg/dL (P = .0002) than those without MASLD.
• Individuals with MASLD had a higher rate of appearance of oral glucose — especially in the first hour after glucose load — than those without MASLD (difference in area under the curve, +555 µmol/kg; P = .032), as well as higher 1-hour plasma glucose levels (difference, +23 mg/dL; P = .041).
• The elevated rate of appearance of oral glucose in the first hour after glucose load in individuals with MASLD remained significant after adjusting for multiple factors, including BMI, age, and sex (P = .011).
• Endogenous glucose production and glucose clearance did not differ between individuals with MASLD and those without the condition.

IN PRACTICE:

“Intestinal glucose absorption is augmented in individuals with liver steatosis. This metabolic alteration, leading to postprandial glucose overload to the liver, may be a critical driver of MASLD pathogenesis. Therapeutic strategies modulating intestinal glucose transport may complement existing treatments targeting MASLD,” the authors of the study concluded.

SOURCE:

This study was led by Domenico Tricò, University of Pisa in Pisa, Italy. It was presented at the European Association for the Study of Diabetes (EASD) 2025 Annual Meeting in Vienna, Austria, on September 18.

LIMITATIONS:

This abstract reported no specific limitations.

DISCLOSURES:

This study reported receiving support from the European Foundation for the Study of Diabetes (EFSD) Future Leaders Mentorship Programme for Clinical Diabetologists, supported by AstraZeneca, and the EFSD Rising Star Fellowship Programme, supported by Novo Nordisk. The authors did not declare any conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.