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Metabolic syndrome and selenium in fetal programming: gender differences.

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Selenium (Se) distribution and tissue deposits in offspring of dams fed a fructose-rich diet are altered by sex, impacting glutathione peroxidase (GPx) activity and potentially disrupting insulin signaling, especially in females.

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Area of Science:

  • Biochemistry
  • Nutritional Science
  • Reproductive Biology

Background:

  • Selenium (Se) is a component of glutathione peroxidase (GPx), an enzyme with a complex role in Metabolic Syndrome (MS).
  • Understanding Se's role in MS transmission to offspring is crucial for preventative strategies.

Purpose of the Study:

  • To evaluate the implication of Selenium (Se) in the transmission of Metabolic Syndrome (MS) to progeny.
  • To investigate sex-specific effects of maternal fructose-rich diet on Se homeostasis and metabolic parameters in offspring.

Main Methods:

  • Offspring from dams fed a fructose-rich diet (65%) with normal Se content (0.01 ppm) were analyzed.
  • Measurements included Se body distribution, glucose, lipids, insulin, metabolic hormones, growth factors, RANK-L, osteopontin, and hepatic oxidative balance, analyzed by sex.

Main Results:

  • Fructose-fed pups exhibited altered body weight and growth indicators, with sex-specific differences.
  • Se homeostasis was disrupted, with tissue-specific depletion or repletion of Se, notably in the heart and liver.
  • Female pups showed altered GPx activity and hepatic oxidation, potentially linked to insulin signaling disruption.

Conclusions:

  • Maternal fructose exposure alters Se balance and tissue distribution in offspring in a sex-dependent manner.
  • Hepatic Se deposits and GPx activity are affected, potentially influencing insulin signaling, particularly in female offspring.
  • Se depletion in the heart of fructose-exposed pups is a significant finding, given Se's importance for cardiac function.