Dietary isoleucine content defines the metabolic and molecular response to a Western diet.

The amino acid composition of the diet has recently emerged as a critical regulator of metabolic health. Consumption of the branched-chain amino acid isoleucine is positively correlated with body mass index in humans, and reducing dietary levels of isoleucine rapidly improves the metabolic health of diet-induced obese male C57BL/6J mice. However, it is unknown how sex, strain, and dietary isoleucine intake may interact to impact the response to a Western Diet (WD). Here, we find that although the magnitude of the effect varies by sex and strain, reducing dietary levels of isoleucine protects C57BL/6J and DBA/2J mice of both sexes from the deleterious metabolic effects of a WD, while increasing dietary levels of isoleucine impairs aspects of metabolic health. Despite broadly positive responses across all sexes and strains to reduced isoleucine, the molecular response of each sex and strain is highly distinctive. Using a multi-omics approach, we identify a core sex- and strain- independent molecular response to dietary isoleucine, and identify mega-clusters of differentially expressed hepatic genes, metabolites, and lipids associated with each phenotype. Intriguingly, the metabolic effects of reduced isoleucine in mice are not associated with FGF21 - and we find that in humans plasma FGF21 levels are likewise not associated with dietary levels of isoleucine. Finally, we find that foods contain a range of isoleucine levels, and that consumption of dietary isoleucine is lower in humans with healthy eating habits. Our results demonstrate that the dietary level of isoleucine is critical in the metabolic and molecular response to a WD, and suggest that lowering dietary levels of isoleucine may be an innovative and translatable strategy to protect from the negative metabolic consequences of a WD.

Factors contributing to non-randomness in species Co-occurrences on Islands.

There has been dispute whether patterns of species co-occurrence on islands are largely random. We present a new method for testing this question; this method lets one not only examine whether a whole fauna is non-randomly structured, but also identify in which direction and by how much each particular species combination deviates from expectations based on randomness. Application of this method to the whole Bismarck and New Hebridean avifaunas, and to two particular guilds, shows that some pairs of species have more exclusive distributions than expected for random placement of species, because of competition, differing distributional strategies, or different geographical orgins. Other pairs of species have more coincident distributions than expected, because of shared habitat, single-island endemism, shared distributional strategies, or shared geographical origins. Much of the information about non-random co-occurrence is contained in the incidence graphs for occurrence of individual species. Finally, our present understanding of assembly rules is summarized.

Examination of the "null" model of connor and simberloff for species co-occurrences on Islands.

Among birds of the Bismarck Archipelago, only certain combinations of the species in a guild coexist on islands, and some species that are very similar ecologically have mutually exclusive distributions. Diamond (1975) interpreted these patterns as biologically significant, involving effects such as competition. Connor and Simberloff (1979) claimed such patterns to be not recognizably different from random, because they were scarcely distinguishable from those generated by a "null" distribution supposedly not incorporating competition.On examining the analysis by Connor and Simberloff, we find that it actually yields the opposite conclusion: three faunas tested have grossly non-random structures, while their test is unworkable for the fourth fauna. The method of Connor and Simberloff for generating a null distribution has many fatal weaknesses: dilution of relevant data from guilds with irrelevant data from the whole species pool; hidden incorporation of effects of competition into the constraints; inability to recognize a checkerboard, the extreme example of a distribution produced by competition; reliance on inefficient Monte Carlo simulations; severe constraints that sometimes make generation of a null distribution impossible; failure to weight species combinations; and failure to identify the direction of non-randomness or the species combinations most responsible.Finally, we use other recent studies by Simberloff and coleagues to examine the value of constructing null hypotheses in community ecology.

Asymmetries in population growth regulated by intraspecific competition: Empirical studies and model tests.

The linearity assumption in the logistic model of population growth is violated for nearly all organisms. Two simple models, the θ-logistic and the θ-Ricker, are shown to account for asymmetric patterns of population growth for 27 species of Drosophila and for a variety of other organisms, where the data were derived from the literature. These models are developed so as to aid laboratory and field ecologists to anticipate the dynamics of various experimental organisms. Potential problems of data gathering and model applications for experimental ecologists and wild life management biologists are identified. Intraspecific asymmetries offer alternative explanations to the "habitat selection" model, and the "higher order interactions" or coalitions model, for interspecific competition.