Sweeney, Gary2015-08-282015-08-282014-12-122015-08-28http://hdl.handle.net/10315/30004Obesity is a key factor contributing to the “metabolic syndrome” which increases the risk for type 2 diabetes, cardiovascular disease and liver complications. In obese conditions, lipotoxicity is a serious concern as the accumulation of lipids and lipid-intermediates in non-adipose tissue such as skeletal muscle, heart, liver and pancreas, leads to cellular dysfunction and activation of stress responses. In this study, I have examined how palmitate-induced lipotoxicity, effects the cellular processes ER stress, autophagy and apoptosis, in L6 rat skeletal muscle cells. I have elucidated cross-talk mechanisms between these processes, and have demonstrated that palmitate induces excessive protein accumulation, thereby stimulating ER stress, activation of the UPR and subsequent apoptosis. Autophagy may be recruited as a compensatory mechanism to help the cell cope with the stress of protein overload through its degradative pathway. Additionally, adiponectin may increase autophagic flux, thereby contributing to cytoprotective effects of reducing ER stress and apoptosis.enAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.BiologyCellular biologyElectronic Thesis or Dissertation2015-08-28ObesityDiabetesMetabolic syndromeLipotoxicityAutophagyEndoplasmic reticulum stressER stressApoptosisSkeletal muscleAdiponectinPalmitateCross-talk