Exploring recent insights on intermittent fasting in regulating glucocorticoid levels and diet-induced metabolic disorders with focus on MAFLD and hepatic outcomes

📖 Top 20% JournalJan 19, 2026Molecular and cellular endocrinology

Intermittent fasting's effects on stress hormones and diet-related liver problems, focusing on fatty liver disease and liver health

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Intermittent fasting may be a viable strategy for weight reduction and improvement of non-alcoholic fatty liver diseases.

Intermittent fasting regulates liver functions through pathways involving nutrition and hormones.
It aids in maintaining energy balance and enhancing mitochondrial function.
Physiological changes from intermittent fasting include improvements in liver inflammation and metabolic disorders.
Alterations in metabolic processes, such as hepatic metabolism and inflammatory responses, are associated with intermittent fasting.
Glucocorticoids and intermittent fasting interact complexly, with hepatic macrophage glucocorticoid receptors playing a key role.
Intermittent fasting shows promising trends in reducing dyslipidaemia in patients with non-alcoholic fatty liver diseases.

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Consumers' risky eating behaviours aided by the current food environment have led to an increase in diet-related metabolic disorders. Metabolic (dysfunction)-associated fatty liver disease origin represents a major global health burden that is increasing at an alarming rate on an annual basis. Modifying the timing of calorie consumption, dietary composition, or caloric intake offers a promising therapeutic approach for the management of this condition. The aim of this review was to provide a concise analysis of the impact of intermittent fasting on the regulation of glucocorticoid levels and diet-induced metabolic disorders with a focus on non-alcoholic fatty liver diseases. We found that intermittent fasting primarily regulates hepatic autophagy via nutritional and hormonal pathways, aiding in the maintenance of energy equilibrium, enhancement of mitochondrial function, regulation of liver quality, preservation of cellular homeostasis, protection of cells from harmful factors, mitigation of liver metabolic disorders, and improvement of liver inflammation. Also, the physiological changes induced by intermittent fasting and their metabolic consequences arise through multiple mechanisms, including alterations in hepatic metabolism, hepatic autophagy, inflammatory responses, liver functional enzymes, hepatic steatosis, fibroblast growth factor signalling, White adipoe tissue browning, adipokines, circadian rhythms, lipid profiles, body composition, the adipose tissue-gut microbiome axis, skeletal muscle, and the autophagy process. Interestingly, we identified the complex interplay among glucocorticoids, intermittent fasting, and non-alcoholic fatty liver diseases highlighting the hepatic macrophage glucocorticoid receptor as a pivotal mediator of fasting-induced reprogramming of the macrophage secretome, including fasting-suppressed cytokines. In conclusion, existing data indicates that intermittent fasting in patients with non-alcoholic fatty liver diseases is a viable, safe, and successful strategy for weight reduction, demonstrating notable trends in the amelioration of dyslipidaemia and non-alcoholic fatty liver diseases.

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