Hepatic steatosis, low-grade chronic inflammation and hormone/growth factor/adipokine imbalance

Abstract

Non-alcoholic fatty liver disease (NAFLD), a further expression of metabolic syndrome, strictly linked to obesity and diabetes mellitus, is characterized by insulin resistance (IR), elevated serum levels of free fatty acids and fatty infiltration of the liver, which is known as hepatic steatosis. Hepatocyte apoptosis is a key feature of this disease and correlates with its severity. Free-fatty-acid-induced toxicity represents one of mechanisms for the pathogenesis of NAFLD and hormones, growth factors and adipokines influence also play a key role. This review highlights the various pathways that contribute to the development of hepatic steatosis. Circulating concentrations of inflammatory cytokines are reckoned to be the most important factor in causing and maintaining IR. Low-grade chronic inflammation is fundamental in the progression of NAFLD toward higher risk cirrhotic states.

Nonalcoholic fatty liver disease in adult hypopituitary patients with GH deficiency and the impact of GH replacement therapy

“…Interestingly, in the non-GH-deficient population, GH, insulin-like growth factor 1 (IGF1), and IGF-binding protein 3 were associated with hepatic fibrosis and steatosis in NAFLD (8), suggesting that the GH-IGF1 axis may play an important role in the liver in the physiological condition. These data strongly suggest an association between GHD and NAFLD/NASH (9), although the precise relationship remains to be elucidated.…”

Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes

“…These two conditions show an increased prevalence and incidence thus becoming a real public health problem due to their strict relationship with diabetes and obesity pandemias. The pathogenesis of NAFLD is not fully clear, but insulin resistance appears to be as the main pathogenetic metabolic event, even if many other predisposing conditions such as obesity, oxidative stress, cytokine/adipokine axis have been reported as plausible coexisting pathogenetic [77] . Insulin resistance represents the clinical expression of the inability of endogenous insulin to enhance glucose uptake and its utilization and it is the physiopathological main factor able to induce the metabolic syndrome.…”

Inflammation as a potential link between nonalcoholic fatty liver disease and insulin resistance

“…NAFLD is estimated to affect at least 30% of the general population (Ratziu et al 2010, Younossi et al 2011. It is histologically characterized by hepatic triglyceride (TG) accumulation of more than 5%, resulting in steatosis and hepatic inflammation (Tarantino et al 2010). NAFLD includes a complex spectrum of disorders ranging from simple fatty liver to nonalcoholic steatohepatitis (NASH) and cirrhosis (Adams et al 2005).…”