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.
10.3803/EnM.2017.32.4.475
- Author:
Manita SHAKYA
1
;
Karen P BRISKI
Author Information
1. Department of Basic Pharmaceutical Sciences, School of Pharmacy, College of Health and Pharmaceutical Sciences, The University of Louisiana Monroe, Monroe, LA, USA. briski@ulm.edu
- Publication Type:Original Article
- Keywords:
Refeeding;
Food deprivation;
AMP-activated protein kinases;
Compound C;
Estradiol;
Insulin
- MeSH:
AMP-Activated Protein Kinases;
Animals;
Appetite;
Body Weight;
Capsules;
Eating*;
Estradiol*;
Estrous Cycle*;
Female;
Food Deprivation;
Glucose;
Humans;
Hyperglycemia;
Hyperphagia;
Insulin;
Insulin Resistance;
Leptin;
Plasma;
Protein Kinases;
Rats;
Rhombencephalon
- From:Endocrinology and Metabolism
2017;32(4):475-484
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
