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Excess intake of fat and sugar potentiates epinephrine-induced hyperglycemia in male rats
Abstract Aims Over the past five decades, per capita caloric intake has increased significantly, and diet- and stress-related diseases are more prevalent. The stress hormone epinephrine stimulates hepatic glucose release during a stress response. The present experiment tested the hypothesis that exc...
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Published in: | Journal of diabetes and its complications 2015-04, Vol.29 (3), p.329-337 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract Aims Over the past five decades, per capita caloric intake has increased significantly, and diet- and stress-related diseases are more prevalent. The stress hormone epinephrine stimulates hepatic glucose release during a stress response. The present experiment tested the hypothesis that excess caloric intake alters this ability of epinephrine to increase blood glucose. Methods Sprague–Dawley rats were fed a high-energy cafeteria-style diet (HED). Weight gain during the first 5 days on the diet was used to divide the rats into an HED-lean group and HED-obese group. After 9 weeks, the rats were injected with epinephrine, and blood glucose was measured. Results HED-obese rats gained body and fat mass, and developed insulin resistance (IR) and hepatic steatosis. HED-lean and control rats did not differ. Epinephrine produced larger increases in blood glucose in the HED-obese rats than in the HED-lean and control rats. Removing the high-energy components of the diet for 4 weeks reversed the potentiated effects of epinephrine on glucose and corrected the IR but not the steatosis or obesity. Conclusions Consumption of a high-energy cafeteria diet potentiates epinephrine-induced hyperglycemia. This effect is associated with insulin resistance but not adiposity or steatosis and is reversed by 4 weeks of standard chow. |
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ISSN: | 1056-8727 1873-460X |
DOI: | 10.1016/j.jdiacomp.2014.12.017 |