Skip Navigation
Skip to contents

Endocrinol Metab : Endocrinology and Metabolism

clarivate
OPEN ACCESS
SEARCH
Search

Author index

Page Path
HOME > BROWSE ARTICLES > Author index
Search
Karen P. Briski  (Briski KP) 1 Article
Endocrine Research
Rebound Feeding in the Wake of Short-Term Suspension of Food Intake Differs in the Presence of Estrous Cycle Peak versus Nadir Levels of Estradiol
Manita Shakya, Karen P. Briski
Endocrinol Metab. 2017;32(4):475-484.   Published online December 14, 2017
DOI: https://doi.org/10.3803/EnM.2017.32.4.475
  • 3,615 View
  • 25 Download
  • 2 Web of Science
  • 2 Crossref
AbstractAbstract PDFPubReader   
Background

Short-term interruption of feeding is ordinary in modern life but negatively impacts appetite control and body weight. Estradiol (E) imposes long-term inhibitory tonus on food consumption; however, E influence on energy repletion secondary to food deprivation (FD) is unclear. This study investigated the hypothesis that E signal strength regulates hyperphagic responses to FD of varying duration.

Methods

Ovariectomized female rats were implanted with E-containing silastic capsules (30 [E-30] or 300 µg [E-300]/mL) to replicate plasma concentrations at cycle nadir versus peak levels.

Results

Data show that food intake was increased equally in E-30 and E-300 rats after 12 hours of food deprivation (FD-12); yet, FD of 18 hours (FD-18) amplified refeeding by E-300 versus E-30. Caudal fourth ventricular administration of the 5′-monophosphate-activated protein kinase (AMPK) inhibitor compound C (Cc) did not modify FD-induced hyperphagia in E-30 (regardless of FD interval) or E-300 animals exposed to FD-12, but diminished refeeding after FD-18 in E-300 rats. Cc-reversible hyperglycemia occurred in refed FD-18 groups. Serum insulin was resistant to FD-12 plus refeeding, but was elevated by AMPK-dependent mechanisms in refed E-300 FD-18 rats; equivalent Cc-insensitive decrements in circulating leptin occurred in all FD groups.

Conclusion

Current results show that estrous cycle peak, but not baseline, E levels engage hindbrain AMPK signaling to intensify hyperphagia in response to prolongation of FD. Observations of hindbrain AMPK-dependent hyperglycemia, alongside elevated insulin secretion, in refed rats exposed to FD-18 implicate this sensor in insulin resistance mechanisms of glucose partitioning in response to this metabolic imbalance.

Citations

Citations to this article as recorded by  
  • A Framework for Developing Translationally Relevant Animal Models of Stress-Induced Changes in Eating Behavior
    Marie François, Olaya Fernández-Gayol, Lori M. Zeltser
    Biological Psychiatry.2022; 91(10): 888.     CrossRef
  • Assessing the effects of stress on feeding behaviors in laboratory mice
    Marie Francois, Isabella Canal Delgado, Nikolay Shargorodsky, Cheng-Shiun Leu, Lori Zeltser
    eLife.2022;[Epub]     CrossRef
Close layer

Endocrinol Metab : Endocrinology and Metabolism