This research aims to investigate the complex interplay between endocrine function and liver health, focusing specifically on how hormonal imbalances contribute to the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD).
Given that the liver plays a dual role as both a metabolic and endocrine organ, disturbances in hormones such as insulin, estrogen, thyroid hormones, and growth hormone may significantly influence hepatic fat accumulation, inflammation, and fibrosis.
Understanding these mechanisms is critical, as MASLD is emerging as the most common chronic liver disease globally, often coexisting with metabolic syndrome and endocrine disorders.
By exploring whether targeted hormonal therapies can modulate disease progression and improve liver function, this research could pave the way for novel prevention and treatment strategies that address both metabolic and endocrine pathways simultaneously.
https://www.researchgate.net/publication/394426243_Hormonal_Health_and_Liver_Health-_A_Bidirectional_Relationship
Targeted correction of hormonal imbalances—particularly in insulin, estrogen, thyroid hormones, and growth hormone—can mitigate metabolic dysfunction, reduce hepatic fat accumulation, and potentially slow or reverse the progression of MASLD.
Alterations in endocrine function play a pivotal role in the onset and progression of metabolic dysfunction–associated steatotic liver disease (MASLD). Hormonal imbalances such as insulin resistance, hyperinsulinemia, and dysregulated adipokine secretion (e.g., decreased adiponectin, increased leptin and resistin) promote hepatic lipid accumulation by enhancing de novo lipogenesis, reducing fatty acid oxidation, and impairing lipid export. Thyroid hormone deficiency can further exacerbate steatosis by lowering basal metabolic rate and mitochondrial activity, while excess glucocorticoids stimulate gluconeogenesis and lipid deposition.
As MASLD advances, altered endocrine signaling amplifies inflammation, oxidative stress, and fibrogenesis in the liver. For example, chronic hyperinsulinemia and hyperandrogenism (notably in polycystic ovary syndrome) worsen hepatic insulin resistance, while growth hormone deficiency or low IGF-1 levels impair hepatocyte regeneration and favor fibrosis. Thus, endocrine dysregulation not only initiates steatosis but also accelerates its progression toward steatohepatitis and advanced liver disease.
Endocrine dyysfunction is a primary driver of the pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) by creating a hormonal environment that promotes hepatic fat accumulation (steatosis), inflammation, and fibrosis. The key hormonal contributors are: Insulin Resistance: This is the central and most dominant factor. Impaired insulin signaling in adipose tissue leads to increased lipolysis, elevating free fatty acid (FFA) delivery to the liver. Simultaneously, hepatic insulin resistance promotes de novo lipogenesis (DNL), creating a dual-hit of lipid overload. Sex Hormone Imbalance: In postmenopausal women, estrogen deficiency is associated with increased visceral fat and hepatic lipid accumulation. In men, low testosterone is linked to increased insulin resistance and higher MASLD prevalence. Thyroid Dysfunction: Hypothyroidism, even at a subclinical level, reduces hepatic lipid metabolism and FFA oxidation while promoting cholesterol synthesis, thereby contributing to steatosis. Growth Hormone (GH) / IGF-1 Axis: GH deficiency or resistance reduces the hormone's lipid-oxidizing effects in the liver, contributing to fat accumulation and potentiaally accelerating the progression from simple steatosis to steatohepatitis (MASH).
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