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Body Composition and Metabolic Caging Analysis in High Fat Fed Mice

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Published on: May 24, 2018

Mice with chronically increased circulating ghrelin develop age-related glucose intolerance.

Jacquelyn A Reed¹, Stephen C Benoit, Paul T Pfluger

¹Department of Psychiatry, Genome Research Institute, University of Cincinnati, Cincinnati, OH 45237, USA.

American Journal of Physiology. Endocrinology and Metabolism

|February 14, 2008

Summary

Overexpressing ghrelin in neurons did not affect body weight or fat mass but impaired glucose tolerance in older mice, suggesting ghrelin’s role in age-related metabolic changes.

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Area of Science:

Neuroendocrinology
Metabolic Research
Genetics

Background:

Ghrelin, a gut peptide, is known to stimulate food intake and increase body fat.
Its role in long-term metabolic regulation, particularly concerning aging, requires further investigation.

Purpose of the Study:

To investigate the effects of neuronal ghrelin overexpression on body weight, composition, energy expenditure, and glucose homeostasis.
To determine if elevated ghrelin levels in the brain impact metabolic parameters over time.

Main Methods:

Neuronal ghrelin overexpression was achieved using neuron-specific enolase (NSE) promoter and mouse ghrelin cDNA (NSE-Ghr).
Body weight, composition, food intake, energy expenditure, locomotor activity, and glucose tolerance were assessed in NSE-Ghr mice (two lines: L43 with high circulating ghrelin, L73 with normal levels) compared to wild-type controls.
Ghrelin expression levels were measured in brain, liver, stomach, and duodenum.

Main Results:

NSE-Ghr mice exhibited increased ghrelin expression in brain tissues and slightly in the liver, but not in the stomach or duodenum.
No significant differences in body weight, food intake, or fat mass were observed between NSE-Ghr mice and wild-type controls.
While locomotor activity was increased, energy expenditure remained unchanged. Young NSE-Ghr mice showed normal glucose tolerance, but L43 mice developed glucose intolerance by 32 weeks of age, without changes in insulin levels.

Conclusions:

Neuronal ghrelin overexpression does not lead to obesity or increased food intake.
Elevated circulating bioactive ghrelin in NSE-Ghr mice is associated with age-dependent glucose intolerance.
These findings suggest a potential role for ghrelin in the age-associated decline of glucose homeostasis.