Endocrine Abstracts

Obesity is a multi-factorial condition generally attributed to diet and lack of exercise. More recent evidence suggests that maternal malnutrition during pregnancy and lactation can contribute to the development of obesity in offspring. We have developed an animal model to examine the specific influence of a maternal ‘junk food’ diet rich in fat, sugar and salt and have shown that offspring exposed to this junk food diet during their fetal and suckling lives overate and developed a greater preference for junk food by the end of adolescence. Offspring from junk food fed mothers also developed exacerbated adiposity with raised circulating glucose, insulin, triglyceride and/or cholesterol which would put the offspring at greater risk of developing cardiovascular diseases and diabetes. The increased adiposity was more pronounced in female offspring and was accompanied by increased mRNA expression for factors which regulate adipocyte proliferation and differentiation (IGF-1, IRS-1, VEGF-A and PPARγ), factors which regulate glucose and fatty acid uptake into adipocytes (Glut1, Glut3 and LPL) and factors which regulate appetite and peripheral insulin sensitivity (leptin, adiponectin). Changes in gene expression were not as pronounced in male offspring with only IRS-1, VEGF-A, Glut4 and LPL being up-regulated which highlighted sex differences in the molecular metabolic adaptation to diet-induced obesity. Exercise is key in combating obesity and so we examined the influence of the maternal junk food diet on the offspring’s muscle development and force production. Results showed that weanling pups from junk food fed mothers exhibited muscle atrophy with fewer fibres and nuclei. At the end of adolescence offspring from junk food fed mothers exhibited reduced muscle specific twitch and tetanic tension. Therefore, a maternal junk food diet can impair muscle development and function in the offspring and further work needs to be done to examine how this may affect their ability to exercise.