Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

After two months of estivation, the metabolic make-up of spadefoot toad organs had changed considerably. Organ-specific patterns were apparent in the responses of both metabolic enzymes (Tables 1-3) and signal transduction systems (Tables 4-7). In brain, estivation altered the maximal activities of only 25 % of the metabolic enzymes assayed so that, overall, the metabolic scope of brain was relatively unaltered. Estivation affected a larger group of enzymes (38%) in liver whereas skeletal muscle appeared to undergo a profound metabolic reorganization that affected 86% of the metabolic enzymes assayed and impacted on numerous pathways of intermediary metabolism.

Estivation is a complex phenomenon with several influences at work that could differentially affect the metabolic make-up of different organs. Starvation is one element that will change the pattern of use of stored fuels and the activities of the catabolic enzymes involved. In general, the first priority in short term starvation is to maintain glucose supply to those organs that are highly dependent on it (e.g. brain) and this is done be depleting glycogen reserves, switching most organs to a primary dependence on lipid oxidation and increasing gluconeogenesis from glycerol or from amino acids supplied by the breakdown of muscle protein. When starvation is prolonged, however, such protein catabolism could place too much of a drain on skeletal muscle mass so liver begins to synthesize and export ketone bodies (ß-hydroxybutyrate, acetoacetate), products of lipid oxidation, as a alternative fuel to replace glucose. Thus, for estivating toads the general expectations associated with the starved state would be suppression of glycolysis and fatty acid synthesis and increased protein catabolism, gluconeogenesis, ketone body metabolism, and lipid oxidation. In general, these effects were seen in estivating toads.

Another influence on metabolic reorganization during estivation is metabolic arrest. The overall suppression of metabolic rate by about 80 % has been correlated with reversible phosphorylation controls on key enzymes and membrane transporters (1) but may also involve specific changes in the maximal activities of selected enzymes to suppress nonessential metabolic functions during dormancy. Furthermore, defense against dehydration requires increased activities of urea cycle enzymes and enhanced protein catabolism to supply the necessary nitrogen. Reproductive tissues also undergo change (e.g. egg maturation) during estivation so that animals are ready to breed immediately when aroused by summer rainstorms (see poster 150). All of these factors also influenced the metabolic make-up of toad organs to optimize enzymatic pathways to meet the challenges of long term dormancy.

Metabolic suppression during estivation is also facilitated by a suppression of activities of signal transduction enzymes in toad tissues. Results for cAMP-dependent protein kinase were highly consistent in showing a strong reduction in the percentage of enzyme that was present as the active catalytic subunit (PKAc) in all organs (Table 4). Protein kinase C activity was also strongly suppressed in 2 organs with changes in the percent membrane-bound and/or total PKC reducing the amount of active PKC in estivating toads to only 50 % of the control value in brain and just 13 % of control in liver.

In many instances where protein kinase activities are suppressed, protein phosphatase activities respond oppositely by increasing. However, in tissues of estivating toads there were no consistent changes in PP-1 or PP-2 activities. This suggests two things: (1) that control over the responsiveness of signal transduction pathways during estivation probably lies primarily with the modulation of protein kinases, and (2) that suppression of both arms of signal transduction systems (kinases and phosphatases) would facilitate the overall state of metabolic rate depression.

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