Experiments have made important contributions to our understanding of human behavior, including behavior relevant for understanding social-ecological systems. When there is a conflict between individual and group interests in social-ecological systems, social dilemmas occur. From the many types of social-dilemma formulations that are used to study collective action, common-pool resource and public-good dilemmas are most relevant for social-ecological systems. Experimental studies of both common-pool resource and public-good dilemmas have shown that many predictions based on the conventional theory of collective action, which assumes rational, self-interested behavior, do not hold. More cooperation occurs than predicted (Ledyard 1995), “cheap talk” increases cooperation (Ostrom 2006), and participants are willing to invest in sanctioning free riders (Yamagishi 1986, Ostrom et al. 1992, Fehr and Gächter 2000, Chaudhuri 2011). Experiments have also demonstrated a diversity of motivations, which affect individual decisions about cooperation and sanctioning (see Fehr and Fischbacher 2002 and Sobel 2005 for reviews, and Bowles 2008 for policy implications).

Type 2 diabetes (T2D) is a complex metabolic disease that is more prevalent in ethnic groups such as Mexican Americans, and is strongly associated with the risk factors obesity and insulin resistance. The goal of this study was to perform whole genome gene expression profiling in adipose tissue to detect common patterns of gene regulation associated with obesity and insulin resistance. We used phenotypic and genotypic data from 308 Mexican American participants from the Veterans Administration Genetic Epidemiology Study (VAGES). Basal fasting RNA was extracted from adipose tissue biopsies from a subset of 75 unrelated individuals, and gene expression data generated on the Illumina BeadArray platform. The number of gene probes with significant expression above baseline was approximately 31,000. We performed multiple regression analysis of all probes with 15 metabolic traits. Adipose tissue had 3,012 genes significantly associated with the traits of interest (false discovery rate, FDR ≤ 0.05). The significance of gene expression changes was used to select 52 genes with significant (FDR ≤ 10^-4) gene expression changes across multiple traits. Gene sets/Pathways analysis identified one gene, alcohol dehydrogenase 1B (ADH1B) that was significantly enriched (P < 10^-60) as a prime candidate for involvement in multiple relevant metabolic pathways. Illumina BeadChip derived ADH1B expression data was consistent with quantitative real time PCR data. We observed significant inverse correlations with waist circumference (2.8 x 10[superscript -9]), BMI (5.4 x 10^-6), and fasting plasma insulin (P < 0.001). These findings are consistent with a central role for ADH1B in obesity and insulin resistance and provide evidence for a novel genetic regulatory mechanism for human metabolic diseases related to these traits.

The structure and dynamics of ecosystems can affect the information available to resource users on the state of the common resource and the actions of other resource users. We present results from laboratory experiments that showed that the availability of information about the actions of other participants affected the level of cooperation. Since most participants in commons dilemmas can be classified as conditional cooperators, not having full information about the actions of others may affect their decisions. When participants had more information about others, there was a more rapid reduction of the resource in the first round of the experiment. When communication was allowed, limiting the information available made it harder to develop effective institutional arrangements. When communication was not allowed, there was a more rapid decline of performance in groups where information was limited. In sum, the results suggest that making information available to others can have an important impact on the conditional cooperation and the effectiveness of communication.

Our previous studies show reduced abundance of the β-subunit of mitochondrial H+-ATP synthase (β-F1-ATPase) in skeletal muscle of obese individuals. The β-F1-ATPase forms the catalytic core of the ATP synthase, and it is critical for ATP production in muscle. The mechanism(s) impairing β-F1-ATPase metabolism in obesity, however, are not completely understood. First, we studied total muscle protein synthesis and the translation efficiency of β-F1-ATPase in obese (BMI, 36±1 kg/m²) and lean (BMI, 22±1 kg/m²) subjects. Both total protein synthesis (0.044±0.006 vs 0.066±0.006%·h^-1) and translation efficiency of β-F1-ATPase (0.0031±0.0007 vs 0.0073±0.0004) were lower in muscle from the obese subjects when compared to the lean controls (P<0.05). We then evaluated these same responses in a primary cell culture model, and tested the specific hypothesis that circulating non-esterified fatty acids (NEFA) in obesity play a role in the responses observed in humans. The findings on total protein synthesis and translation efficiency of β-F1-ATPase in primary myotubes cultured from a lean subject, and after exposure to NEFA extracted from serum of an obese subject, were similar to those obtained in humans. Among candidate microRNAs (i.e., non-coding RNAs regulating gene expression), we identified miR-127-5p in preventing the production of β-F1-ATPase. Muscle expression of miR-127-5p negatively correlated with β-F1-ATPase protein translation efficiency in humans (r = – 0.6744; P<0.01), and could be modeled in vitro by prolonged exposure of primary myotubes derived from the lean subject to NEFA extracted from the obese subject. On the other hand, locked nucleic acid inhibitor synthesized to target miR-127-5p significantly increased β-F1-ATPase translation efficiency in myotubes (0.6±0.1 vs 1.3±0.3, in control vs exposure to 50 nM inhibitor; P<0.05). Our experiments implicate circulating NEFA in obesity in suppressing muscle protein metabolism, and establish impaired β-F1-ATPase translation as an important consequence of obesity.