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Aims: Roux‐en‐Y gastric bypass (RYGB) surgery alters postprandial glucose profiles, causing post‐bariatric hypoglycaemia (PBH) in some individuals. Due to the liver's central role in glucose homeostasis, hepatic glucose handling might differ in RYGB‐operated patients with PBH compared to non‐operated healthy controls (HC). Materials and Methods: We enrolled RYGB‐operated adults with PBH and HCs (n = 10 each). Participants ingested 60 g of [6,6′‐2H2]‐glucose (d‐glucose) after an overnight fast. Deuterium metabolic imaging (DMI) with interleaved 13C magnetic resonance spectroscopy was performed before and until 150 min post‐d‐glucose intake, with frequent blood sampling to quantify glucose enrichment and gluco‐regulatory hormones until 180 min. Glucose fluxes were assessed by mathematical modelling. Outcome trajectories were described using generalized additive models. Results: In RYGB subjects, the hepatic d‐glucose signal increased early, followed by a decrease, whereas HCs exhibited a gradual increase and consecutive stabilization. Postprandial hepatic glycogen accumulation and the suppression of endogenous glucose production were lower in RYGB patients than in HCs, despite higher insulin exposure, indicating lower hepatic insulin sensitivity. The systemic rate of ingested d‐glucose was faster in RYGB, leading to a higher, earlier plasma glucose peak and increased insulin secretion. Postprandial glucose disposal increased in RYGB patients, without between‐group differences in peripheral insulin sensitivity. Conclusions: Exploiting DMI with stable isotope flux analysis, we observed distinct postprandial hepatic glucose trajectories and parameters of glucose–insulin homeostasis in RYGB patients with PBH versus HCs. Despite altered postprandial glucose kinetics and higher insulin exposure, there was no evidence of impaired hepatic glucose uptake or output predisposing to PBH in RYGB patients. [ABSTRACT FROM AUTHOR]

In many countries worldwide, the burden of hepatocellular carcinoma (HCC) associated with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is increasing. Preventive strategies are needed to counteract this trend. In this review, we provide an overview of the evidence on preventive strategies in NAFLD-associated HCC. We consider the impact of lifestyle factors such as weight loss, physical activity, smoking, dietary patterns and food items, including coffee and alcohol, on both HCC and NAFLD/NASH. Furthermore, evidence on chemopreventive treatments, including aspirin, antidiabetic treatments and statins is summarised. The role of adjuvant therapies for tertiary prevention of HCC is briefly reviewed. [ABSTRACT FROM AUTHOR]

Background: In patients with non‐alcoholic fatty liver disease (NAFLD), the impact of the severity of steatosis and inflammatory activity on the accuracy of liver stiffness measurement (LSM) by transient elastography (TE) and by two‐dimensional shear wave elastography (2D‐SWE) in staging liver fibrosis is still debated and scarce. We aimed to focus on this aspect. Methods: We prospectively studied 104 patients requiring biopsy for the assessment of NAFLD. We used ordinary least squares regression to test for differences in the association between fibrosis and LSM by TE and 2D‐SWE when other factors (steatosis and inflammatory activity) are considered. Results: Among 104 patients, 102 had reliable LSM by TE, and 88 had valid LSM by 2D‐SWE. The association between fibrosis based on histology and LSM was significantly stronger when 2D‐SWE assessed LSM compared to TE (Spearman's correlation coefficient of.71; P <.001 vs.51, P <.001; Z = 2.21, P =.027). Inflammatory activity was an independent predictor of LSM by TE but not of LSM by 2D‐SWE. After controlling for fibrosis, age, sex and body mass index, the inflammatory activity and the interaction between inflammatory activity and fibrosis independently explained 11% and 13% of variance in LSM by TE respectively. Steatosis did not affect the association of fibrosis and LSM by either method. Conclusion: Inflammatory activity on histology significantly affects LSM by TE, but not LSM by 2D‐SWE in NAFLD. LSM by 2D‐SWE reflects liver fibrosis more accurately than LSM by TE. Furthermore, the severity of steatosis on histology did not influence the association of LSM and fibrosis by either elastography method. [ABSTRACT FROM AUTHOR]