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Food restriction differentially affects mRNAs encoding the major anterior pituitary tropic hormones

E S Han1, D H Lu, J F Nelson

  • 1Department of Physiology, University of Texas Health Science Center, San Antonio, USA. han@uthscsa.edu

Insights

Chronic food restriction (FR) rapidly alters pituitary hormone messenger RNA (mRNA) levels in rats. These neuroendocrine changes suggest a role in the adaptive cellular responses that may slow aging.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Aging Research

Background:

  • Chronic food restriction (FR) induces adaptive cellular changes that can retard aging.
  • These adaptive changes can manifest within weeks of initiating FR.
  • Neuroendocrine mechanisms are hypothesized to mediate these FR-induced effects.

Purpose of the Study:

  • To investigate the impact of FR on the messenger ribonucleic acids (mRNAs) encoding anterior pituitary (AP) tropic hormones.
  • To determine if FR differentially affects the expression of specific pituitary hormone mRNAs.

Main Methods:

  • Measurement of AP tropic hormone mRNA levels in Fischer 344 rats using slot blot and solution hybridization.
  • Comparison of mRNA levels between ad libitum (AL) fed rats and rats subjected to 60% calorie FR since 6 weeks of age.
  • Analysis of mRNA levels at two time points (0500 h and 1500 h) to account for diurnal variations.

Main Results:

  • FR did not alter the overall polyA RNA content per microgram of total RNA.
  • Proopiomelanocortin (POMC) mRNA levels remained unchanged by FR.
  • FR significantly reduced the total AP content of mRNAs for LH beta, FSH beta, TSH beta, GH, and PRL.
  • Specific reductions in GH, FSH beta, TSH beta, and PRL mRNA levels per microgram of RNA were observed at specific time points.

Conclusions:

  • Food restriction differentially impacts pituitary tropic hormone mRNA levels within weeks.
  • These findings support a role for neuroendocrine alterations in initiating adaptive cellular responses to FR.
  • The study highlights the rapid onset of molecular adaptations to caloric restriction.

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