The analysis has been performed for the contribution of hormones to the pathogenetic mechanisms of metabolic‑associated steatotic liver disease (MASLD). The role of adipose tissue hormones in the development of metabolic disorders and systemic inflammatory reactions is well investigated and proved. With progression of metabolic‑associated steatohepatitis (MASH), the leptin levels increase, and adiponectin and omentin levels decrease, associating with the proinflammatory and profibrotic state of the liver and impaired glucose metabolism. The liver also produces hormone‑like proteins, hepatokines, which actively affect the extrahepatic regulation of metabolism, namely, contribute to the development of insulin resistance and dyslipidemia. Medications, affecting the endocrinological component of MASLD/MASH pathogenesis, are considered one the of the most promising approaches for the treatment of these diseases. It should be noted that only pioglitazone and glucagon‑like peptide (GLP)‑1 receptor agonists are the two antihyperglycemic drugs with proven efficacy and safety at MASH. Thus, the use of GLP‑1 agonists results in the reduction of food intake, body weight, improvement of glucose control in patients with MASH, they reduce steatosis and insulin resistance, and the level of inflammation in the liver. The data are available indicating the prospect of using dual agonists of GLP‑1/glucagon and GLP‑1 and glucose‑dependent insulinotropic peptide for the treatment of MASLD/MASH. According to preliminary data, such combinations resulted in the decrease in steatosis and improvement in liver fibrosis indicators, though additional proof is required to confirm changes in the histological liver characteristics. Another group of hormones with significant importance in MASLD pathogenesis, are hormones of the adrenal glands (aldosterone, cortisol and androgens), as they take an active part in the regulation of the response to stress and lipolysis. In this aspect, androgens attract special attention, because firstly, both their deficiency and excess will contribute to the development of hepatic steatosis, obesity, insulin resistance and other signs of metabolic syndrome, and secondly, their deficiency will contribute to the development of sarcopenia, which is very important in the aspect of MASLD. A lack of estrogen in women will also contribute to liver steatosis, insulin resistance, dyslipidemia, and obesity. One of the factors affecting the development of liver steatosis can be growth hormone, decrease in its level will contribute to the intrahepatic accumulation of fat, which will increase the risk of MASHP. Thyroid hormones can also play a role in the development of MASLD, the severity of hypothyroidism has a direct correlation with the severity of MASLD, and the levels of thyroid‑stimulating hormone and free thyroxine have an association with liver fibrosis.