Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group
Two important studies have been published this month on chemical exposures that cause obesity in subsequent generations of rodents, long after the exposure ends. Until now, no prior studies on transgenerational obesogen exposures had been published. The results are alarming.
In the first study, pregnant mice (F0 generation) were exposed to low doses of the known obesogen tributyltin (TBT) and bred for 3 generations (up to the F3 generation). Thus, the F0 generation was exposed directly, the F1 generation exposed in the womb, the F2 generationsl could have been primordially exposed as germ cells in the developing fetus, and the F3 generation was not exposed directly (changes in the F3 generation are considered truly transgenerational). The TBT exposure had obesity-promoting effects on fat deposition on the F1 through the F3 generation, including increasing the number of fat cells, fat cell size, fatty tissue weights, and fatty livers (similar to non-alcoholic fatty liver disease (NAFLD) in humans). Interestingly, TBT exposure reprogrammed stem cells to develop into fat cells instead of bone cells.
The study, entitled “Transgenerational inheritance of increased fat depot size, stem cell reprogramming, and hepatic steatosis elicited by prenatal obesogen tributyltin in mice”, was written by Raquel Chamorro-García, Margaret Sahu, Rachelle J. Abbey, Jhyme Laude, Nhieu Pham, and Bruce Blumberg, of the University of California, Irvine.