Bisphenol A and Obesity
Date of Graduation
Master of Science in Biology
Bisphenol A, BPA, obesity, leptin, body composition, TOBEC, metabolic rate, oxygen consumption, food consumption, adiposity, fat
Obesity and excess body fat is generally blamed on low physical activity and pour eating habits. However, there is increasing evidence that environmental chemicals, such as Bisphenol A (BPA), recently linked to altered adipose and glucose metabolism, may be aggravating the problem. Due to chronic human exposure, research is needed to confirm whether or not BPA is able to increase the fat deposition or otherwise alter weight maintenance parameters. To determine a dose/response relationship CF-1 mice were chronically exposed to 0, 0.012, 0.12, and 1.2 æg BPA/ml drinking water from conception to 95 days old in Phase 1 (P1,N=16, 7-9 males/7-9 females per treatment). In phase 2 (P2), 5 groups of mice (N=8-16 per treatment) were exposed to 0.012 æg BPA/ml drinking water (the most active dose in P1) during different developmental periods. Body mass, food consumption, leptin levels, and oxygen consumption rate were measured for both studies, with body composition analysis conducted only in P2. There was no change in food consumption or oxygen consumption for either Phase. Low dose male mice (P1, 0.012 æg treatment) had higher body masses and leptin levels than the other treatment groups, thus indicating more body fat was present in these mice. Chronically exposed males in P2 had lower body masses during other treatment groups, but had a higher percent of body fat. P2 mice (m/f), exposed during lactation only, had higher leptin levels than the control group and the males were larger than the controls. Overall, low dose BPA exposure increased adiposity in chronically exposed males in lactationally exposed male/female mice. It did not have significant effects on the adiposity of females in P1.
© Lara Johnson
Johnson, Lara, "Bisphenol A and Obesity" (2006). MSU Graduate Theses. 1242.