Objective: Protein leverage plays a role in driving increased energy intakes that may promote weight gain. The influence of the protein to carbohydrate ratio (P:C) in diets of C57BL/6J mice on total energy intake, fat storage, and thermogenesis was investigated. Design and Methods: Male mice (9 weeks old) were provided ad libitum access to one of five isocaloric diets that differed in P:C. Food intake was recorded for 12 weeks. After 16 weeks, white adipose tissue (WAT) and brown adipose tissue (BAT) deposits were dissected, weighed, and the expression levels of key metabolic regulators were determined in BAT. In a separate cohort, body surface temperature was measured in response to 25 diets differing in protein, fat, and carbohydrate content. Results: Mice on low P:C diets (9:72 and 17:64) had greater total energy intake and increased WAT and BAT stores. Body surface temperature increased with total energy intake and with protein, fat, and carbohydrate, making similar contributions per kJ ingested. Expression of three key regulators of thermogenesis were downregulated in BAT in mice on the lowest P:C diet. Conclusions: Low-protein diets induced sustained hyperphagia and a generalized expansion of fat stores. Increased body surface temperature on low P:C diets was consistent with diet-induced thermogenesis (DIT) as a means to dissipate excess ingested energy on such diets, although this was not sufficient to prevent development of increased adiposity. Whether BAT was involved in DIT is not clear. Increased BAT mass on low P:C diets might suggest so, but patterns of thermogenic gene expression do not support a role for BAT in DIT, although they might reflect failure of thermogenic function with prolonged exposure to a low P:C diet.Obesity (2013) 21, 85-92.

Starchy foods are digested faster and produce higher postprandial glycemia in individuals with high AMY1 CN. In contrast, having low CN is associated with colonic methane production. This trial was registered at www.anzctr.org.au as ACTRN12617000670370.

Protein kinase C epsilon (PKC 3) activation in the liver is proposed to inhibit insulin action through phosphorylation of the insulin receptor. Here, however, we demonstrated that global, but not liver-specific, deletion of PKC 3 in mice protected against dietinduced glucose intolerance and insulin resistance. Furthermore, PKC 3-dependent alterations in insulin receptor phosphorylation were not detected. Adipose-tissue-specific knockout mice did exhibit improved glucose tolerance, but phosphoproteomics revealed no PKC 3-dependent effect on the activation of insulin signaling pathways. Altered phosphorylation of adipocyte proteins associated with cell junctions and endosomes was associated with changes in hepatic expression of several genes linked to glucose homeostasis and lipid metabolism. The primary effect of PKC 3 on glucose homeostasis is, therefore, not exerted directly in the liver as currently posited, and PKC 3 activation in this tissue should be interpreted with caution. However, PKC 3 activity in adipose tissue modulates glucose tolerance and is involved in crosstalk with the liver.

Cognitive abilities underpin the capacity of individuals to build models of their environment and make decisions about how to govern resources. Here, we test the functional intelligences proposition that functionally diverse cognitive abilities within a group are critical to govern common pool resources. We assess the effect of two cognitive abilities, social and general intelligence, on group performance on a resource harvesting and management game involving either a negative or a positive disturbance to the resource base. Our results indicate that under improving conditions (positive disturbance) groups with higher general intelligence perform better. However, when conditions deteriorate (negative disturbance) groups with high competency in both general and social intelligence are less likely to deplete resources and harvest more. Thus, we propose that a functional diversity of cognitive abilities improves how effectively social groups govern common pool resources, especially when conditions deteriorate and groups need to re-evaluate and change their behaviors.

The zinc transporter (ZnT; SLC30) and Zrt- and Irt-like protein (Zip, SLC39) zinc transporter families are integral to the maintenance of intracellular zinc concentrations. Few studies have examined the expression patterns of zinc transporter genes in human primary tissues. This study investigated the expression levels of a range of zinc transporter mRNA in the peripheral blood mononuclear cells of healthy men and women (n = 40) using quantitative real-time PCR. It also explored the relationships among zinc transporter expression levels, plasma zinc concentrations, and dietary zinc intake. The relative expression of the zinc transporter mRNA varied considerably, with ZnT7, ZnT1, and Zip1 being the most abundantly expressed. ZnT1 and Zip1 mRNA were highly correlated with one another (r = 0.9; P < 0.001) and with ZnT5, ZnT7, Zip3, and Zip10 (P < 0.001). When analyzed by gender, a correlation between the mRNA of ZnT7 and Zip3 (r = 0.6; P < 0.01) was demonstrated only in women. Zip10 mRNA was correlated with ZnT1 and Zip1 (r = 0.9; P < 0.001) in men only. In a regression analysis, plasma zinc variability was not significantly explained by dietary zinc intake, gender, age, or any individual or combination of zinc transporters. This study expands what is known about both the levels of zinc transporter gene transcription in humans and the extent of its variation in healthy men and women. The positive association between the mRNA of ZnT1 and Zip1, which have reciprocal roles in zinc transport across the plasma membrane, provides insight into the coordinated control of zinc homeostasis in humans.