Lipotoxicity

Lipotoxicity is a metabolic syndrome that results from the accumulation of lipid intermediates in non-adipose tissue, leading to cellular dysfunction and death.

Lipotoxicity is believed to have a role in heart failure, obesity, and diabetes, and is estimated to affect approximately 25% of the adult American population.

Triacylglycerol consists of three fatty acids bound to a glycerol molecule and is considered the most neutral and harmless type of intracellular lipid storage.

[3] A theory has been put forward by Cambridge researchers relating the development of lipotoxicity to the perturbation of membrane glycerophospholipid/sphingolipid homeostasis and their associated signalling events.

Some researchers claim that obesity has protective effects against lipotoxicity as it results in extra adipose tissue in which excess lipids can be stored.

[5] Renal lipotoxicity occurs when excess long-chain nonesterified fatty acids are stored in the kidney and proximal tubule cells.

They may activate death receptors, stimulate apoptotic pathways, or initiate cellular stress response in the endoplasmic reticulum.

Researchers are working on treatments that will increase the oxidation of these fatty acids within the heart in order to prevent the lipotoxic effects.

[8] Lipotoxicity affects the pancreas when excess free fatty acids are found in beta cells, causing their dysfunction and death.

This is accomplished with thiazolidinediones, a group of medications that activate nuclear receptor proteins responsible for lipid metabolism.

[3] Lipoexpediency refers to the beneficial effects of lipids in a cell or a tissue, primarily lipid-mediated signal transmission events, that may occur even in the setting of excess fatty acids.