The term lipotoxicity (from English lipotoxicity) was coined to indicate the deleterious effects caused by the body's prolonged exposure to high levels of fatty acids in the blood, a condition typical of obese subjects.
In vitro studies have shown that human pancreatic islets exposed to high concentrations of free fatty acids (FFA) undergo a significant acceleration of apoptosis ( cell death ). Subsequently it was shown that the apoptotic processes of beta-cells are favored above all by the presence of long-chain saturated fatty acids (palmitic in particular), especially when associated with the presence of high glycemic levels (glucotoxicity).
In addition to pancreatic level, lipotoxicity also causes damage to the liver (steatosis and hepatic fibrosis), muscle level (where it reduces insulin sensitivity), cardiac level (where it causes damage to the myocytes) and kidney level (induces phenomena fibrotics that can lead to kidney failure).
The pathogenesis of cellular damage from lipotoxicity is traced to an alteration of the metabolism of fatty acids. These nutrients are normally converted into triglycerides and crammed as a reserve into specific cellular compartments; however, when these reserves are saturated, their metabolism leads to the accumulation of intermediate metabolites such as diacylglycerol, acyl-CoA and ceramides, which negatively impact cellular functions causing the damage listed above.
