In recent times, there has been an increase in the incidence of type-2 diabetes (T2D) particularly in children. T2D is when the body does not produce enough of insulin, or when the body cannot use insulin to its full potential. Understanding the etiology and biology of this disease is important for early detection and treatment. It is thought that, environmental chemical exposure during early years of life might be a significant contributing factor to the increase in the incidence of T2D. This study tests the idea that exposure to environmental contaminants (2-aminonanthracene-2AA) in utero will show effects in the adipose tissue that signify T2D vulnerability. One specific PAH, 2AA has been detected in broiled food and tobacco smoke as well as in a wide range of products including coal, tar, crude oil, cereals, grains, flour, vegetables, and pickled foods. To accomplish the study objective, pregnant dams were fed various amounts of 2AA adulterated diets (0 mg/kg-, 50 mg/kg-, and 100 mg/kg-2AA diet) from gestation through postnatal period. Adipose tissues of pups were analyzed for specific diabetes related gene expression using qRT-PCR; ADIPONECTIN, TNF-α, IL-6, LEPTIN, CD14 and CD68. Specific staining for CD68 positive cells was greater in the low dose group though not significantly different compared with the control. In contrast, CD68 positive cells were significantly reduced in the high dose group relative to control rats. It is interesting to note the over-expression of gene transcripts in the low dose (50 mg/kg-2AA diet) group compared to both control and high dose (100 mg/kg-2AA diet) animals. ADIPONECTIN, IL-6, CD14 and TNFα were up-regulated in the animals that ingested 50 mg/kg-2AA diet. Similarly, ADIPONECTIN was up-regulated in the progeny of dams that ingested to 100 mg/kg-2AA diet. Further study is ongoing to assess the response of offspring to moderate high fat diet.
Available at: http://works.bepress.com/worlanyo_gato/62/