Boom to bust? Implications for the continued rapid growth of the eastern Australian humpback whale population despite recovery

Despite heavy overexploitation and near extirpation, some populations of large whales are recovering. Monitoring their recovery has important implications for conservation, management and our understanding of population dynamics and recovery in large mammals. The eastern Australian population of humpback whales was hunted to near-extirpation by the early 1960s. Despite this, the population started to recover, and structured surveys were initiated in the 1980s. These surveys comprise one of the longest and most consistent series of surveys of a population of whales in the world. Collectively, they have demonstrated a rapid recovery of the population with a long-term average rate of increase of 10.9% per annum. Here, we present the results of the last three surveys, conducted in 2007, 2010 and 2015. The 2015 survey shows that the population is essentially recovered, with abundance estimated at 24,545 whales (95% confidence interval 21,631–27,851), and yet continues to grow at a rapid rate. Modeling the rate of growth and abundance suggests that either the whales are heading for a higher than expected abundance of at least 40,000 whales or that an irruption may occur with models suggesting a peak in whale abundance in 2021–2026. Understanding the possible future scenarios of this population is critical to its management. This situation also presents a rare opportunity to study in detail the growth of a well-defined population of large mammal as it recovers from severe depletion.     

A phospholipase D-like mechanism in pancreatic islet cells: stimulation by calcium ionophore, phorbol ester and sodium fluoride

In neonatal rat islet cells prelabelled with [14C-methyl] choline, the phorbol ester 12-O-tetradecanoylphorbol-13-acetate rapidly activated a phospholipase D-like mechanism as suggested by the accumulation in cells and medium of choline (but not of phosphorylcholine or glycerophosphorylcholine, markers for phospholipase C and phospholipase A2 action on phosphatidylcholine). This finding was confirmed by a rise in phosphatidic acid (but not diglyceride or arachidonic acid) in fatty acid-labelled cells. Phospholipase D was also activated by ionomycin or sodium fluoride; however, this was accompanied by parallel increases in diglyceride, monoacylglycerol and arachidonic acid in the absence of phosphorylcholine generation, suggesting that these agents also activated a phospholipase C-diglyceride lipase pathway acting on non-choline-containing phosphoglycerides (presumably phosphoinositides). In conjunction with our recent demonstration of insulinotropic effects of phosphatidic acid (M. Dunlop and R. Larkins, Diabetes, in press), our findings suggest for the first time a possible role for phospholipase D activation in the stimulation of insulin release and may imply a novel site of action for phorbol esters in the regulation of exocytosis.