Scale-dependence in species-area relationships

Species-area relationships (SARs) are among the most studied phenomena in ecology, and are important both to our basic understanding of biodiversity and to improving our ability to conserve it. But despite many advances to date, our knowledge of how various factors contribute to SARs is limited, searches for single causal factors are often inconclusive, and true predictive power remains elusive. We believe that progress in these areas has been impeded by 1) an emphasis on single-factor approaches and thinking of factors underlying SARs as mutually exclusive hypotheses rather than potentially interacting processes, and 2) failure to place SAR-generating factors in a scale-dependent framework. We here review mathematical, ecological, and evolutionary factors contributing to species-area relationships, synthesizing major hypotheses from the literature in a scale-dependent context. We then highlight new research directions and unanswered questions raised by this scale-dependent synthesis.     

The importance of samples and isolates for species–area relationships

Species–area relationships (SARs) are a key tool for understanding patterns of species diversity. A framework for the interpretation of SARs and their prediction under different landscape configurations remains elusive, however. This article addresses one of these configurations: how species' minimum-area requirements affect the shape of island or other isolate Species–area curves. We distinguish between two classes of SARs: sample-area curves, compiled entirely within larger contiguous areas, and isolate curves, compiled between isolated areas. We develop this conceptual and graphic model in order to illuminate landscape-scale diversity patterns, to discuss how various landscape and species characteristics affect outcomes, and to investigate the dynamics of local extinction under conditions of habitat fragmentation. Minimum-area effects on actual islands and other isolates predictably cause Species–area curves either to be sigmoid in arithmetic space or to be lowered for smaller areas. In order to illustrate the inherent shape of isolate curves, this study fits convex and sigmoid regression models to empirical isolate (island) data sets that cover the small scales expected to include inflection points.     

Growth hormone and cortisol treatment stimulate seawater tolerance in both anadromous and landlocked Arctic charr

In a comparative experiment the effect of cortisol and growth hormone (GH) on the hypo-osmoregulatory ability of a landlocked and an anadromous strain of Arctic charr (Salvelinus alpinus) was investigated. Cortisol and GH were implanted either alone or in combination, and the fish were exposed to a 24 h seawater challenge test (SWT) on days 14 and 28 after implantation. Hypo-osmoregulatory ability, measured as plasma osmolality and chloride concentration after the SWTs, was better in the anadromous than in the landlocked strain, irrespective of treatment. However, cortisol provided a strong stimulation of hypo-osmoregualtory ability in both strains, and this stimulation seemed to be potentiated by GH in an additive manner. Improved hypo-osmoregulatory ability in GH + cortisol treated anadromous Arctic charr was accompanied by increased gill Na⁺, K⁺-ATPase activity and Na⁺–K⁺–2Cl⁻ cotransporter protein abundance, but no changes in gill Na⁺,K⁺-ATPase α1a and α1b mRNA levels. For landlocked charr the improved hypo-osmoregulatory ability in GH +cortisol treated fish was accompanied only with an increase in gill Na⁺–K⁺–2Cl⁻ cotransporter protein abundance. Hormone treatment caused an improvement of hypo-osmoregulatory ability that was of approximately the same magnitude in the landlocked as in the anadromous Arctic charr. This suggests that the lack of spontaneous development of hypo-osmoregulatory ability often seen in landlocked populations of Arctic charr may depend, at least partly, on a lack of the hormonal activation seen in anadromous populations.     

Melatonin implantation during spring and summer does not affect the seasonal rhythm of feeding in anadromous Arctic charr (Salvelinus alpinus)

Plasma melatonin levels in the high-latitude teleost Arctic charr (Salvelinus alpinus) are constantly low during summer when feeding activity is high, and high during the dark winter when they eat little and loose weight. The question arises if melatonin is involved in the phase-setting of annual rhythms of feeding and growth and if low summer melatonin production is permissive for high summer growth in this species. The present study was therefore set out to compare the seasonal appetite and growth rhythms in Arctic charr with constantly high plasma melatonin levels from February throughout the Arctic summer (melatonin implanted, average mid-day plasma melatonin levels 1,106 ± 147 pg/ml) with those of fish with natural plasma melatonin levels (vehicle implanted and untreated fish with average mid-day plasma melatonin levels of 94 ± 13 and 58 ± 6 pg/ml, respectively). Feed intake, body mass or body length, as well as the timing of the seasonal growth rhythm, were not affected by the high summer plasma melatonin level. Further, Arctic charr fasted for 3 months had a 24 h plasma profile of melatonin which was consistently higher throughout the scotophase compared to fed charr. Although the daily melatonin production seems to be affected by the energy status of the fish, melatonin does not seem to be directly involved in regulation of the seasonal feeding and growth rhythm in the high-latitude, anadromous Arctic charr.     

Cannabinoid CB2 Receptor Potentiates Obesity-Associated Inflammation,Insulin Resistance and Hepatic Steatosis

Background

Obesity-associated inflammation is of critical importance in the development of insulin resistance and non-alcoholic fatty liver disease. Since the cannabinoid receptor CB2 regulates innate immunity, the aim of the present study was to investigate its role in obesity-induced inflammation, insulin resistance and fatty liver.

Methodology

Murine obesity models included genetically leptin-deficient ob/ob mice and wild type (WT) mice fed a high fat diet (HFD), that were compared to their lean counterparts. Animals were treated with pharmacological modulators of CB2 receptors. Experiments were also performed in mice knock-out for CB2 receptors (Cnr2 −/−).

Principal Findings

In both HFD-fed WT mice and ob/ob mice, Cnr2 expression underwent a marked induction in the stromal vascular fraction of epididymal adipose tissue that correlated with increased fat inflammation. Treatment with the CB2 agonist JWH-133 potentiated adipose tissue inflammation in HFD-fed WT mice. Moreover, cultured fat pads isolated from ob/ob mice displayed increased Tnf and Ccl2 expression upon exposure to JWH-133. In keeping, genetic or pharmacological inactivation of CB2 receptors decreased adipose tissue macrophage infiltration associated with obesity, and reduced inductions of Tnf and Ccl2 expressions. In the liver of obese mice, Cnr2 mRNA was only weakly induced, and CB2 receptors moderately contributed to liver inflammation. HFD-induced insulin resistance increased in response to JWH-133 and reduced in Cnr2 −/− mice. Finally, HFD-induced hepatic steatosis was enhanced in WT mice treated with JWH-133 and blunted in Cnr2 −/− mice.

Conclusion/Significance

These data unravel a previously unrecognized contribution of CB2 receptors to obesity-associated inflammation, insulin resistance and non-alcoholic fatty liver disease, and suggest that CB2 receptor antagonists may open a new therapeutic approach for the management of obesity-associated metabolic disorders.