Metabolic dysfunction-associated steatotic liver disease (MASLD), considered as the hepatic component of the metabolic syndrome, is the leading cause of chronic liver disease around the world(1). The MASLD disease spectrum begins with isolated steatosis. A subset of patients will develop metabolic dysfunction-associated steatohepatitis (MASH) which is characterized by steatosis and inflammation, resulting in hepatocyte injury with or without fibrosis. MASH is regarded as a progressive phenotype, as it can advance to cirrhosis and subsequently to hepatocellular carcinoma(2). Compared with fasting measurements alone, postprandial responses to nutrient challenges offer a greater insight into the phenotypic heterogeneity that occurs across health and disease(3). To better understand the phenotypes that occur across the spectrum of MASLD, we have characterized the postprandial metabolic and inflammatory responses to different dietary challenges in healthy individuals and patients with MASLD and MASH.

10 healthy individuals, 18 patients with MASLD, and 15 with MASH were recruited. Body composition was assessed using bioelectrical impedance analysis (Tanita). Liver fat and stiffness were measured by FibroScan in patients only. All participants completed a high fat mixed meal challenge containing 655kcals, 46g fat, 33g saturated fat, 50g carbohydrates, 45g sugar, and 10g protein. Patients with MASLD and MASH also completed a high-fructose challenge containing 400kcals, 75g fructose and 25g glucose. Fasting and postprandial blood samples were drawn at each challenge at 0, 30, 60, 90, 120, 180, 240 and 360-minutes. Glucose was measured in whole blood using a HemoCue Glucose 201+ analyzer. Serum insulin and plasma IL-6 and CRP will be measured by ELISA. Plasma triglycerides, non-esterified fatty acids (NEFA), and glycerol will be measured by colorimetric assay.

Bodyweight (p = 0.0247), BMI (p = 0.0448), and hip circumference (p = 0.0237) were greater in MASH vs MASLD. Healthy participants had significantly lower bodyweight, BMI, and waist and hip circumferences vs both MASLD and MASH (p<0.0001 for each variable). Liver fat was similar between MASLD and MASH, whereas liver stiffness was greater in MASH (p<0.0001). Alanine transaminase (ALT) was increased in MASH vs MASLD (p = 0.0408), while concentrations of other liver enzymes were similar between groups. Total cholesterol (p = 0.0492) and LDL-cholesterol (p = 0.0197) were also higher in MASH vs MASLD, but there was no difference in triglyceride concentrations or HDL-cholesterol. There was a significant impact of group on glucose response to the HFMM (p = 0.0321), and glucose responses varied between the 3 groups across different time points (p<0.0001).

The HFMM, which is more representative of a typical meal, revealed glucose intolerance in MASLD and MASH which was also greater in MASLD. Analysis of the full cohort will enable greater characterization of the phenotypes that occur across the spectrum of MASLD.

Secondary dispersal is an important stage in the life cycle of tree species, determining the fate of a high proportion of all seeds. For small-seeded species both physical and biological processes may influence the secondary fate of seeds, however the relative importance of these processes is not well known. Seeds of the pioneer tree species Cecropia insignis (seed mass 0.5 mg), Trema micrantha (2.5 mg) and Apeiba aspera (14.2 mg) and five types of artificial seed were sown in understorey, treefall-gap and large-gap sites on Barro Colorado Island, Panama, during the wet season of 2005. Sowing areas were excavated after periods up to 26 d and cores divided into depths of 0–5, 5–10, 10–20 and 20–50 mm to allow high-resolution estimation of the rate and amount of burial and displacement of seeds. Over 26 d, 2.8% of artificial seeds were buried to a mean depth of 10.5 mm below the soil surface and 43.9% of unburied seeds displaced laterally >5 cm. Significantly more (87.9% and 80.9%) seeds of Cecropia insignis and Trema micrantha were displaced than artificial seeds of similar mass, size and density. A generalised linear model suggested that burial mostly occurred within 15 d, while displacement occurred continuously up to 26 d. The dominant cause of displacement and burial was probably rainfall, while seed removal by ants may also have contributed to displacement.

Orthodox, desiccation-tolerant seeds lose desiccation tolerance during germination. Here, we quantify the timing of the loss of desiccation tolerance, and explore the implications of this event for seed mortality and the shape of germination progress curves for pioneer tree species. For the nine species studied, all seeds in a seedlot lost desiccation tolerance after the same fixed proportion of their time to germination, and this proportion was fairly constant across the species (0.63–0.70). The loss of desiccation tolerance after a fixed proportion of the time to germination has the implication that the maximum number of seeds in a seedlot that can be killed by a single drying event during germination (Mmax) increases with an increasing time to 50% germination (t50) and an increasing slope of the germination progress curve. Consequently, to prevent the seed population from becoming highly vulnerable to desiccation-induced mortality, species with a greater t50 would be expected to have a shallower germination progress curve. In conclusion, these data suggest that the loss of desiccation tolerance during germination may constitute a significant, but previously unexplored, source of mortality for seeds in seasonal environments with unpredictable rainfall.