Liver, NAFLD and COVID-19.

Coronavirus disease 2019 (COVID-19) is characterized by a wide clinical spectrum that includes abnormalities in liver function indicative of liver damage. Conversely, people with liver diseases are at higher risk of severe COVID-19. In the current review, we summarize first the epidemiologic evidence describing the bidirectional relationship between COVID-19 and liver function/liver diseases. Additionally, we present the most frequent histologic findings as well as the most important direct and indirect mechanisms supporting a COVID-19 mediated liver injury. Furthermore, we focus on the most frequent liver disease in the general population, non-alcoholic or metabolic-associated fatty liver disease (NAFLD/MAFLD), and describe how COVID-19 may affect NAFLD/MAFLD development and progression and conversely how NAFLD/MAFLD may further aggravate a COVID-19 infection. Finally, we present the long-term consequences of the pandemic on the development and management of NAFLD.

Circulating levels of gastrointestinal hormones in prediabetes reversing to normoglycemia or progressing to diabetes in a year-A cross-sectional and prospective analysis.

AIMS: We aimed to compare the concentrations of GLP-1, glucagon and GIP (established regulators of glucose homeostasis) and glicentin (emerging new metabolic marker)during an OGTT in patients with normal glucose tolerance (NGT), prediabetes and diabetes at onset, and one-year before, when all had prediabetes. METHODS: GLP-1, glucagon, GIP and glicentin concentrations were measured and compared with markers of body composition, insulin sensitivity and ß-cell function at a 5-timepoint OGTT in 125 subjects (30 diabetes, 65 prediabetes, 30 NGT) and in 106 of them one-year before, when all had prediabetes. RESULTS: At baseline, when all subjects were in prediabetic state, hormonal levels did not differ between groups. One year later, patients progressing to diabetes had lower postprandial increases of glicentin and GLP-1, lower postprandial decrease of glucagon, and higher levels of fasting GIP compared to patients regressing to NGT. Changes in glicentin and GLP-1 AUC within this year correlated negatively with changes in Glucose AUC of OGTT and with changes in markers of beta cell function. CONCLUSION: Incretins, glucagon and glicentin profiles in prediabetic state cannot predict future glycemic traits, but prediabetes progressing to diabetes is accompanied by deterioration of postprandial increases of GLP-1 and glicentin.