In the Short Term, Poor Nutrition Promotes Simple Steatosis without Inflammation in Adolescent Rats

Abstract

The development of hepatic steatosis in adults has been linked to high caloric intake. However, less is known about the physiological consequences of this disease during adolescence. The present study examined the association of high caloric intake and hepatic steatosis in adolescent rats. Six‐week old male Sprague‐Dawley rats were fed one of the following diets: standard rodent chow (18.9% protein, 57.33% carbohydrates), high‐sucrose (HS: 20% protein, 70% carbohydrates (34.5% sucrose), 10% fat) or high‐fat (HF: 20% protein, 20% carbohydrates (6.8% sucrose), 60% fat) for 6 weeks. Following the diet, animals were euthanized (sodium pentobarbital; 200 mg/kg, i.p.) and livers extracted for analyses. An increase in Oil Red O stained areas of liver sections provided evidence for the development of steatosis in the HF fed animals that was confirmed by increased triglyceride concentrations in the liver as compared to animals fed the chow or HS diets (20.73 ± 2.09, 9.75 ± 0.52, and 10.76 ± 0.74 mg triglycerides/g tissue, respectively; p < 0.001). Despite the observed steatosis, western blot analyses showed no significant differences between groups in proteins associated with insulin signaling (p‐PI3K; p85, p=0.711; p55, p=0.740), gluconeogenesis (PEPCK‐C, p=0.333), immune response (XBP1; p=0.613) or inflammation (TLR‐4, p= 0.932; iNOS, p=0.675). The short feeding protocol used in the current study may explain the lack of measurable alterations in protein expression as others typically examine the effects of high caloric diets for 8–12 weeks before measuring changes. Together these findings suggest that short term high fat intake promotes simple steatosis in the absence of changes in insulin signaling or inflammation.Support or Funding InformationThis study was funded in part by new faculty start up funds, and Barrett, The Honors College, Arizona State University.