POTENTIATING EFFECT OF EXCESSIVE FRUCTOSE CONSUMPTION ON THE DEVELOPMENT OF OBESITY IN OFFSPRING OF GESTATIONAL STRESSED MOTHERS

Authors

  • Perets E. V. SI "V. Danilevsky Institute for Endocrine Pathology Problems of the NAMS of Ukraine", Kharkiv
  • Sergiyenko L.Yu. SI "V. Danilevsky Institute for Endocrine Pathology Problems of the NAMS of Ukraine", Kharkiv
  • Seliukova N. Yu. SI "V. Danilevsky Institute for Endocrine Pathology Problems of the NAMS of Ukraine", Kharkiv
  • Cherevko A. N. SI "V. Danilevsky Institute for Endocrine Pathology Problems of the NAMS of Ukraine", Kharkiv
  • Bondarenko T. V. SI "V. Danilevsky Institute for Endocrine Pathology Problems of the NAMS of Ukraine", Kharkiv
  • Sirotenko L. A. SI "V. Danilevsky Institute for Endocrine Pathology Problems of the NAMS of Ukraine", Kharkiv

DOI:

https://doi.org/10.21856/j-PEP.2016.4.11

Keywords:

gestational stress descendants, obesity, fructose, leptin resistance

Abstract

It has been shown that gestational stress of mothers leads to the birth of offspring with decreased body weight and a low level of leptin in the plasma. In adulthood in these offspring with the same amount of consumed food weight and fat mass higher than the corresponding figures in the offspring of mothers intact. The sons of stressed mothers established the presence of leptin resistance hypothalamic structures regulate the body’s energy, which is manifested in the absence of anorectic’s effects at hyperleptinemia. Long-term intake of fructose in the body the children of stressed mothers leads to aggravation due to leptin resistance and gestational already at a young age can contribute to the development of obesity.

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Published

2021-06-24

How to Cite

Perets, E. V., Sergiyenko, L. Y., Seliukova, N. Y., Cherevko, A. N., Bondarenko, T. V., & Sirotenko, L. A. (2021). POTENTIATING EFFECT OF EXCESSIVE FRUCTOSE CONSUMPTION ON THE DEVELOPMENT OF OBESITY IN OFFSPRING OF GESTATIONAL STRESSED MOTHERS. Problems of Endocrine Pathology, 58(4), 82-90. https://doi.org/10.21856/j-PEP.2016.4.11

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