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Updated: Feb 23, 2026

Assessment of the Metabolic Effects of Isocaloric 2:1 Intermittent Fasting in Mice
Published on: November 27, 2019
Refeeding after caloric restriction reverses altered liver glucose release
Rosângela F Garcia1, Isabela R Mariano2, Isabela C Stolarz3
1a Department of Physiological Sciences , State University of Maringá , Maringá , Brazil.
Caloric restriction boosts liver glucose release (LGR), but refeeding reverses this effect. Enhanced LGR is tied to current nutrition, not early feeding, in rats.
Area of Science:
- Metabolism and Endocrinology
- Nutritional Physiology
- Hepatic Glucose Production
Background:
- Caloric restriction (CR) is known to increase liver glucose release (LGR).
- The long-term or permanent nature of CR-induced LGR alterations was previously unknown.
- Understanding nutritional impacts on hepatic function is crucial for metabolic health.
Purpose of the Study:
- To determine if refeeding can reverse the elevated LGR caused by caloric restriction.
- To investigate the dynamic relationship between nutritional status and liver glucose production.
- To clarify whether CR-induced LGR changes are permanent or reversible.
Main Methods:
- Rats were studied under three conditions: control (GC), caloric restriction (GR), and caloric restriction followed by refeeding (GRL).
- Caloric restriction involved 50% reduction from 21 to 80 days of age.
- Liver perfusion studies were conducted at 80 days of age to measure LGR under basal and stimulated conditions.
Main Results:
- Caloric restriction significantly increased LGR in rats, both under basal and adrenaline-stimulated states.
- Refeeding (GRL group) effectively reduced LGR to levels comparable to control rats (GC).
- These findings indicate that elevated LGR due to CR is reversible.
Conclusions:
- The elevated liver glucose release associated with caloric restriction is reversible through refeeding.
- Nutritional status, rather than early-life feeding patterns, dictates the observed changes in LGR.
- Hypothalamic neuropeptides may play a role in mediating these nutritional effects on hepatic glucose production.
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