Abstract

In order to cope with the physiologic stresses of digesting large meals, the heart of the Burmese python undergoes significant hypertrophy in as little as 24 hours, returning to the fasted state a few days afterwards. This remarkable response has led us to investigate the molecular mechanisms utilized by python ventricular myocytes during the onset and regression of hypertrophy. We have initially focused on using quantitative PCR to examine changes in the transcripts of genes involved in metabolic processes and cardiac function between fasted and post‐fed states in the heart. We have demonstrated that genes involved in glycolysis and lipid import are downregulated during hypertrophy, while the expression of genes that control lipolytic processes are maintained in response to elevated serum lipid concentrations. Moreover, we have shown that the hypertrophic python heart favors the expression of genes that maintain a highly contractile state, and also exhibits a striking pattern of gene markers that would indicate both physiology and pathology in a mammalian system. These results implicate a novel mechanism of molecular regulation utilized by the python in order to facilitate the dynamic changes inherent to cardiac hypertrophy. This research was supported by a grant from Hiberna, Inc.

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