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Also, nonylphenol was shown to promote NAFLD in the context of this dietary manipulation with associated lipid accumulation and inflammatory changes 121.
Chronic exposure to TCDD in the context of a high fat diet promoted weight gain with sexually dimorphic effects on fat distribution and hepatic steatosis with females exhibiting increases in liver lipid content 122.
In a transgenerational study tributyltin TBT exposure in the F 0 generation increased the sensitivity of mice in the F 4 generation to a high fat diet 32. These mice exhibited normal weight gain until exposure to the high fat diet, which triggered accelerated weight gain and impaired weight loss upon switching back to a low fat diet.
Finally, rats exposed gestationally and lactationally to BPA exhibited increased liver lipid accumulation and inflammation on a high fat diet after weaning 123. A critical issue is how diets enriched in fat augment absorption of lipophilic MDCs when diet and exposures are both manipulated.
In contrast, when dietary manipulation is dissociated from developmental exposure, data suggest a priming of metabolic dysfunction induced by developmental exposure to MDCs that is induced later in life.
These findings broadly support standard clinical interventions to address metabolic dysfunction by restricting caloric consumption and limiting consumption of excess fats and sugars.
On a standard rodent chow, exposure to the phenylsulfamide fungicide tolylfluanid promoted weight gain, increased fat mass, glucose intolerance, insulin resistance, and a disruption in circadian rhythms of feeding behavior 124. The same exposure in the context of a high fat plus high sucrose diet vs.
In the context of a high fat plus high sucrose diet, tolylfluanid did not appreciably affect weight gain, reduced adipose content modestly, but markedly exacerbated glucose intolerance with no effect on insulin sensitivity 125.
In contrast, when incorporated into a high sucrose diet alone, tolylfluanid reduced weight gain while augmenting fat accumulation without any appreciable change in glucose tolerance or insulin sensitivity 125. Moreover, these data indicate that dietary sugars are modulators of MDC effects.
This is important because many studies focus on high fat diets alone, even though increased sugar and refined carbohydrate intake tightly correlate with the onset of the metabolic disease pandemic in the last half century 126.