for this correlation. Effects in different organs Kidneys Renal lipotoxicity occurs when excess long-chain nonesterified fatty acids are stored in the kidney and proximal tubule cells. It is believed that these fatty acids are delivered to the kidneys via serum albumin. This condition leads to tubulointerstitial inflammation and fibrosis in mild cases, and to kidney failure and death in severe cases. The current accepted treatments for lipotoxicity in renal cells are fibrate therapy and intensive insulin therapy. Liver An excess of free fatty acids in liver cells plays a role in Nonalcoholic Fatty Liver Disease (NAFLD). In the liver, it is the type of fatty acid, not the quantity, that determines the extent of the lipotoxic effects. In hepatocytes, the ratio of monounsaturated fatty acids and saturated fatty acids leads to apoptosis and liver damage. There are several potential mechanisms by which the excess fatty acids can cause cell death and damage. They may activate death receptors, stimulate apoptotic pathways, or initiate cellular stress response in the endoplasmic reticulum. These lipotoxic effects have been shown to be prevented by the presence of excess triglycerides within the hepatocytes. Heart Lipotoxicity in cardiac tissue is attributed to excess saturated fatty acids. The apoptosis that follows is believed to be caused by unfolded protein 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. Pancreas Lipotoxicity affects the pancreas when excess free fatty acids are found in beta cells, causing their dysfunction and death. The effects of the lipotoxicity is treated with leptin therapy and insulin sensitizers. Skeletal muscle The skeletal muscle accounts for more than 80 percent of the postprandial whole body glucose uptake and therefore plays an important role in glucose homeostasis. Skeletal muscle lipid levels – intramyocellular lipids (IMCL) – correlate negatively with insulin sensitivity in a sedentary population and hence were considered predictive for insulin resistance and causative in obesity-associated insulin resistance. However, endurance athletes also have high IMCL levels despite being highly insulin sensitive, which indicates that not the level of IMCL accumulation per se, but rather the characteristics of this intramyocellular fat determine whether it negatively affects insulin signaling. Intramyocellular lipids are mainly stored in lipid droplets, the organelles for fat storage. Recent research indicates that creating intramyocellular neutral lipid storage capacity for example by increasing the abundance