Insulin resistance and Metabolic dysfunction-associated steatotic liver disease (MASLD): Pathways of action of hypoglycemic agents.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by overweight/obesity, and the presence of type 2 diabetes mellitus is the most important criterion. We propose an independent disease perspective without exclusion criteria and with less heterogeneity and greater impact because, according to the National Health and Nutrition Survey (ENSANUT), in Mexico, 25 % of adults over 60 years of age suffer from diabetes, and 96 % of those over 50 years of age have abdominal obesity. Due to the impact of insulin resistance in the pathophysiology of MASLD, which results in damage to hepatocytes, this work aims to provide an overview of the action pathways of hypoglycemic agents such as glucagon-like-1 receptor agonist and peroxisome proliferator-activated receptor-gamma agonists, whose importance lies in the fact that they are currently undergoing phase 2 studies, as well as dipeptidyl peptidase 4 inhibitors and sodium-glucose co-transporter type 2 inhibitors, which are undergoing phase 1 study trials.

Hunger & satiety signals: another key mechanism involved in the NAFLD pathway.

Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent metabolic disease, although prevalence could change according to region, nowadays is considered a public health problem whose real impact on the health system is unknown. NAFLD has a multifactorial and complex pathophysiology, due to this, developing a unique and effective pharmacological treatment has not been successful in reverting or avoiding the progression of this liver disease. Even though NAFLD pathophysiology is known, all actual treatments are focused on modifying or regulating the metabolic pathways, some of which interplay with obesity. It has been known that impairments in hunger and satiety signals are associated with obesity, however, abnormalities in these signals in patients with NAFLD and obesity are not fully elucidated. To describe these mechanisms opens an additional option as a therapeutic target sharing metabolic pathways with NAFLD, therefore, this review aims to describe the hormones and peptides implicated in both hunger-satiety in NAFLD. It has been established that NAFLD pharmacological treatment cannot be focused on a single purpose; hence, identifying interplays that lead to adding or modifying current treatment options could also have an impact on another related outcome such as hunger or satiety signals.