Standardized reporting of the costs of management interventions for biodiversity conservation.

Effective conservation management interventions must combat threats and deliver benefits at costs that can be achieved within limited budgets. Considerable effort has focused on measuring the potential benefits of conservation interventions, but explicit quantification of the financial costs of implementation is rare. Even when costs have been quantified, haphazard and inconsistent reporting means published values are difficult to interpret. This reporting deficiency hinders progress toward a collective understanding of the financial costs of management interventions across projects and thus limits the ability to identify efficient solutions to conservation problems or attract adequate funding. We devised a standardized approach to describing financial costs reported for conservation interventions. The standards call for researchers and practitioners to describe the objective and outcome, context and methods, and scale of costed interventions, and to state which categories of costs are included and the currency and date for reported costs. These standards aim to provide enough contextual information that readers and future users can interpret the cost data appropriately. We suggest these standards be adopted by major conservation organizations, conservation science institutions, and journals so that cost reporting is comparable among studies. This would support shared learning and enhance the ability to identify and perform cost-effective conservation.

Downregulation of plasma insulin levels and hepatic PPARgamma expression during the first week of caloric restriction in mice.

Calorie restriction extends lifespan by decreasing the rate of tumor formation, an effect occurring within 8 weeks of initiating a restricted diet. Our goal was to define how the first weeks of a calorie restricted diet (60% of ad libitum calories) affects putative mediators of the calorie restriction phenotype, focusing on regulators of fatty acid biosynthesis. In C57Bl/6 mice, insulin decreased over 50% (p<0.05) during the first week of calorie restriction whereas IGF-1 was unaffected. In the liver, PPARgamma mRNA fell to 13% of baseline after 1 week of calorie restriction (p<0.05), whereas hepatic SREBP-1c and SIRT1 mRNA levels were unaffected. No changes in abdominal or subcutaneous adipose tissue were observed until after 4 weeks of caloric restriction. We conclude that calorie restriction-induced decreases in insulin and hepatic PPARgamma are rapid enough to support a role for these molecules in triggering the initial phase of the calorie restriction phenotype.

Upregulation of AMPK during cold exposure occurs via distinct mechanisms in brown and white adipose tissue of the mouse.

AMPK (adenosine monophosphate-activated protein kinase), a key regulator of cellular energy metabolism and whole-body energy balance, is present in brown adipose tissue but its role in regulating the acute metabolic state and chronic thermogenic potential of this metabolically unique tissue is unknown. To address this, the AMPK signalling system in brown and white adipose tissue was studied in C57Bl/6 mice under control conditions, during acute and chronic cold exposure, and during chronic adrenergic stimulation. In control mice AMPK activity in brown adipose tissue was higher than in any tissue yet reported (3-fold the level in liver) secondary to a high level of expression of the alpha1 isoform. During the first day of cold, a time of intense non-shivering thermogenesis, AMPK activity remained at basal levels. However, chronic (>7 days) cold caused a progressive increase in brown adipose tissue AMPK activity secondary to increased expression of the alpha1 isoform. To investigate the signalling pathway involved, noradrenaline (norepinephrine) and the beta(3)-adrenergic-specific agonist CL 316, 243 were given for 14 days. This increased uncoupling protein-1 content in brown adipose tissue, but not AMPK activity. In white adipose tissue 15 days of cold increased alpha1 AMPK activity 98 +/- 20%, an effect reproduced by chronic noradrenaline or CL 316 243. We conclude that chronic cold not only increases AMPK activity in brown and white adipose tissue, but that it does so via distinct signalling pathways. Our data are consistent with AMPK acting primarily as a regulator of chronic thermogenic potential in brown adipose tissue, and not in the acute activation of non-shivering thermogenesis.