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Abstract 455: The Burmese Python as a Model of Metabolic Protection

Abstract only Introduction: The postprandial Burmese python displays a remarkable level of cardiac adaptation to high levels of circulating triglycerides and an increased metabolic rate without any evidence of cardiac pathology. To challenge the level of cardioprotection, we designed an experiment t...

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Bibliographic Details
Published in:Circulation research 2017-07, Vol.121 (suppl_1)
Main Authors: Peter, Angela K, Ozeroff, Christopher D, Leinwand, Leslie A
Format: Article
Language:English
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Summary:Abstract only Introduction: The postprandial Burmese python displays a remarkable level of cardiac adaptation to high levels of circulating triglycerides and an increased metabolic rate without any evidence of cardiac pathology. To challenge the level of cardioprotection, we designed an experiment to attempt to induce metabolic syndrome in the Burmese python. Metabolic syndrome is typically defined as obesity concomitant with other metabolic abnormalities which contribute to an increased risk for cardiovascular disease. Methods and Results: Unlike mice or rats who readily undergo hypertrophy in response to pressure-overload or β-adrenergic receptor stimulation, inducing pathological hypertrophy in the Burmese python is challenging. In the current study, we attempted to induce metabolic syndrome through overfeeding. We offered Burmese pythons a meal equivalent to 25% of the python’s body mass every 4 days for a period of 2 months. Two similar groups of pythons were maintained on our standard python feeding schedule (one meal equivalent to 25% of their body weight every 28 days) over the same time course. At the end of 2 months, the weight of the overfed pythons (6197g ± 180g) dramatically increased when compared to fasted (2352g ± 23g) or normal fed pythons (3044g ± 62g). In addition to an overall increase in body weight, the ventricle weight/brain weight ratio increased significantly in the overfed pythons (19.5 ± 1.1) compared to fasted (7.5 ± 0.2) or normal fed pythons (8.8 ± 0.2) indicating considerable hypertrophy. However, despite developing hypertrophy, there was no evidence of aberrant gene expression or impaired glucose tolerance when compared to normal fed pythons. Conclusions: Despite repeatedly consuming a large meal, nearly tripling in body weight, and developing significant hypertrophy, the Burmese python is protected from developing metabolic abnormalities such as impaired glucose tolerance. Fetal gene expression markers of pathological cardiac hypertrophy were not induced in overfed pythons. Thus, studying the mechanisms of cardiac adaptation in the Burmese python may potentially provide insights into therapeutic targets for combating metabolic syndrome in patients.
ISSN:0009-7330
1524-4571
DOI:10.1161/res.121.suppl_1.455