Background: Fatty liver, a major health problem worldwide, is the earliest pathological change in the progression of alcohol-associated (AFL) and non-alcoholic fatty liver disease (NAFL). Though the causes of AFL and NAFL differ, both share similar histological and some common pathophysiological characteristics. In this study, we sought to examine mechanisms responsible for lipid dynamics in liver and adipose tissue in the setting of AFL and NAFL in response to 48 h of fasting.Methods: Male rats were fed Lieber-DeCarli liquid control or alcohol-containing diet (AFL model), chow or high-fat pellet diet (NAFL model). After 6–8 weeks of feeding, half of the rats from each group were fasted for 48 h while the other half remained on their respective diets. Following sacrifice, blood, adipose, and the liver were collected for analysis.Results: Though rats fed AFL and NAFL diets both showed fatty liver, the physiological mechanisms involved in the development of each was different. Here, we show that increased hepatic de novo fatty acid synthesis, increased uptake of adipose-derived free fatty acids, and impaired triglyceride breakdown contribute to the development of AFL. In the case of NAFL, however, increased dietary fatty acid uptake is the major contributor to hepatic steatosis. Likewise, the response to starvation in the two fatty liver disease models also varied. While there was a decrease in hepatic steatosis after fasting in ethanol-fed rats, the control, chow and high-fat diet-fed rats showed higher levels of hepatic steatosis than pair-fed counterparts. This diverse response was a result of increased adipose lipolysis in all experimental groups except fasted ethanol-fed rats.Conclusion: Even though AFL and NAFL are nearly histologically indistinguishable, the physiological mechanisms that cause hepatic fat accumulation are different as are their responses to starvation.

An undergraduate gross anatomy dissection was performed at Westminster College as part of a human anatomy class, with one objective being to determine the cause of death in the cadaver. The cadaver was procured from Washington University. The dissection proceeded according to the details outlined in Grant's Dissector. During dissection several significant anatomical abnormalities were noted. A polytetrafluoroethylene (PTFE) vein graft was present in the left forearm joining the radial artery and cephalic vein, indicating dialysis. The kidneys were irregularly shaped and had various‐sized cysts (0.1–5.0 cm) and dense, black nodules on their surfaces, as well as internal abnormalities. These factors combined with other abnormalities (left ventricular hypertrophy [2.0 cm thick myocardium compared to a normal range of 0.6–1.1 cm], calcium deposits, and plaque in the abdominal aorta and renal arteries), support our preliminary findings of renal failure as the cause of death. Histopathological analysis of several samples will be conducted to support these findings.