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Postnatal overnutrition programs the thyroid hormone metabolism and function in adulthood.

Patricia C Lisboa1, Ellen P S Conceição2, Elaine de Oliveira2

  • 1Laboratory of Endocrine PhysiologyDepartment of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, Avenida 28 de setembro, 87, Rio de Janeiro, RJ 20551-031, Brazil pclisboa@uerj.br.

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Early overnutrition in pups programs adult thyroid dysfunction, impacting metabolism and obesity risk. This study reveals tissue-specific changes in thyroid hormone (TH) action, offering insights into obesogenesis.

Keywords:
deiodinasehypothyroidismlactationovernutritionprogramming

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Developmental Biology

Background:

  • Early overnutrition (EO) during lactation is linked to adult obesity and leptin resistance.
  • Thyroid hormone (TH) levels are often reduced in adulthood following early overnutrition.
  • The long-term consequences of this thyroid hypofunction on the hypothalamic-pituitary-thyroid (HPT) axis and TH metabolism remain incompletely understood.

Purpose of the Study:

  • To investigate the long-term effects of postnatal early overnutrition (EO) on the hypothalamic-pituitary-thyroid (HPT) axis function.
  • To analyze the impact of EO on thyroid hormone (TH) metabolism and action in adult rats.
  • To elucidate the tissue-specific alterations in TH signaling pathways induced by early life nutritional programming.

Main Methods:

  • Induction of EO by reducing litter size (SL group) versus normal litter size controls.
  • Assessment of TRH (thyrotropin-releasing hormone) and TSH (thyroid-stimulating hormone) levels.
  • Measurement of iodothyronine deiodinase (D1 and D2) activities in various tissues.
  • Evaluation of mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD), uncoupling protein 1 (UCP1), and TH receptor (TRβ1) to assess TH action.

Main Results:

  • The SL group exhibited lower TRH and TSH levels, indicative of HPT axis alterations, despite normal plasma TSH.
  • Hypothyroidism was confirmed by reduced D1 activity and increased D2 activity in specific tissues (thyroid, muscle, adipose tissue, hypothalamus, pituitary).
  • Decreased UCP1 and TRβ1 in brown adipose tissue and white adipose tissue, respectively, suggest a reduced catabolic state. Hepatic TH action was preserved.

Conclusions:

  • Postnatal early overnutrition induces long-lasting, tissue-specific changes in thyroid function and hormone action in adult rats.
  • These alterations in thyroid hormone metabolism and signaling contribute to a lower catabolic status and may play a role in obesogenesis.
  • This study provides a valuable model for understanding the developmental origins of metabolic dysfunction and obesity.