Prenatal microcystin-LR exposure alters pancreatic proteome and impairs insulin secretion in offspring mice.

This study examines the toxic effects of microcystin-LR (MC-LR), a cyanobacterial toxin, on glucose metabolism in the pancreatic β cells of offspring following maternal exposure in mice. Female mice were exposed to varying concentrations of MC-LR for 12 weeks and the period of gestation. While no adverse effects were noted in the mothers, the neonates displayed significantly lower blood glucose levels that persisted into puberty, along with elevated fasting insulin levels. The results indicate a differential expression of pancreatic proteins, particularly those involved in the PPAR signaling pathway, which regulates lipid metabolism and insulin secretion. Key proteins affected include Fabp1, Ivd, Acaa1a, Acad11, Acat1, Hmgcs2, Scarb1, Ehhadh, and Hadh. This altered protein expression appears to be the molecular mechanism underlying the metabolic disturbances observed in the offspring. Additionally, the inhibition of pancreatic cell proliferation by MC-LR may have long-term implications for the metabolic health of the offspring. These findings underscore the potential transgenerational effects of environmental toxicants such as MC-LR, which can disrupt metabolic programming during critical developmental periods. The study highlights the need for further research to understand the broader implications of environmental toxins on metabolic health across generations.