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With rising energy costs and climate change concerns, energy efficiency will be important in maintaining competitiveness and reducing the environmental impact of industrial activities. In this paper we study the Chilean industrial sector, which is the largest consumer of energy within the country. Energy demand and CO 2 emissions in Chile have grown rapidly in recent years while energy supply is mostly imported and subject to disruption. Therefore, it is important to understand energy consumption in this sector and determine which sub-sectors have the greatest potential to reduce energy consumption. We used the Index Decomposition Analysis (IDA), applying the Logarithmic Mean Divisia Index method I (LMDI-I), to quantify the impact of diverse driving factors on energy consumption. Furthermore, a panel data analysis was used to determine whether there are differences in energy intensity across firms with different characteristics. Our results show that energy intensity has risen over time although energy consumption remains stable. This fact supports the idea that energy efficiency policies could play an important role for the industrial sector. Additionally, energy consumption and energy intensity follow different patterns in each sub-sector; therefore we conclude that the application of differentiated sectoral policies is preferable over a single global policy.

Punicic acid (PUA) is a conjugated linolenic acid isomer that has shown promise in suppressing gut inflammation. The goal of this study is to elucidate the mechanisms by which PUA modulates mucosal immunity and prevents or ameliorates gut inflammation. The expression of peroxisome proliferator-activated receptor (PPAR) α, γ and δ and their responsive genes was examined in the colonic mucosa of two mouse models of experimental inflammatory bowel disease (IBD). Immune cell-specific PPAR γ null, PPAR δ null and wild-type (WT) mice were administered control or PUA-supplemented diets and challenged with 2.5% DSS. The phenotype of immune cell subsets was examined in the mucosal and peripheral immune system. The prophylactic efficacy of PUA was also examined in an IL-10−/− model of IBD. PUA intake upregulated colonic PPAR δ, keratinocyte growth factor and the orphan nuclear receptor RORγt expression and suppressed colonic and M1 macrophage-derived TNF-α. In the mesenteric lymph nodes (i.e., mucosal inductive sit...

Background & aims: Intra-abdominal fat is pathogenically involved in both type 2 diabetes and inflammatory bowel disease (IBD). However, little is known about the interrelationships between these two widespread and devastating diseases. The goal of this study is to investigate the effect of obesity in the severity of colitis and, in turn, examine the impact of IBD on glucose tolerance during obesity. In this context, we have explored the role of infiltrating macrophages in the severity of diabetes and IBD. Methods: The infiltration of macrophages and T cells into intra-abdominal WAT, liver and the colonic lamina propria was examined in db/db and lean mice after a 7-day dextran sodium sulfate (DSS) challenge by tissue fractionation and flow cytometry. Disease activity indices (DAI), weight loss and colonic histology were examined during the course of the DSS challenge, and colonic pro-inflammatory cytokine expression was quantified by real-time RT-PCR. To determine the impact of obesity and intestinal inflammation on glucose tolerance, mice were administered an intraperitoneal glucose tolerance test. Results: We found that obesity increases the severity of experimental IBD. Following a DSS challenge, obese mice express greater concentrations of colonic TNF-a mRNA than lean mice. In addition, experimental IBD in combination with obesity worsens glucose tolerance beyond the effect caused by obesity alone. F4/80hiCCR2hi macrophages infiltrate the lamina propria of mice with DSS colitis and the WAT of obese mice. Conclusions: Infiltration of F4/80hiCCR2hi macrophages into intra-abdominal fat worsens the severity of experimental IBD during obesity. In turn, experimental IBD in obese mice repressed skeletal muscle PPAR g and GLUT4 mRNA expression, upregulated MCP-1 and worsened type 2 diabetes.

Summary Background & aims Catalpic acid (CAT) is a conjugated linolenic acid (CLN) isomer containing trans -9, trans -11, cis -13 double bonds in an 18-carbon chain and it is found primarily in the seed oil of ornamental and medicinal trees and shrubs of the family Bignoniaceae. The objective of this study was to investigate whether CAT decreases obesity and ameliorates insulin sensitivity and glucose tolerance in mice fed high-fat diets. Methods To test the efficacy of CAT in decreasing obesity and diabetes we used both a model of diet-induced obesity (DIO) and a genetic model of obesity (i.e., mice lacking the leptin receptor). Blood was collected on days 0, 7, 14, 21 and 28 for determining fasting glucose and insulin concentrations in plasma. In addition, a glucose tolerance test was administered on day 28. Results We found that dietary CAT (1g/100g) decreased fasting plasma glucose and insulin concentrations, ameliorated the glucose normalizing ability following glucose challenge and decreased abdominal white adipose tissue accumulation. In white adipose tissue (WAT), CAT upregulated peroxisome proliferator-activated receptor (PPAR) α and its responsive genes [i.e., stearoyl-coenzyme A desaturase (SCD1) and enoyl-coenzyme A hydratase (ECH)], increased concentrations of high-density lipoprotein (HDL) cholesterol and decreased plasma triglyceride (TG) levels. Conclusions CAT decreased abdominal fat deposition, increased HDL cholesterol, decreased TG concentrations, decreased glucose and insulin homeostasis and modulated WAT gene expression in a manner reminiscent of the actions of the PPAR α-activating fibrate class of lipid-lowering drugs.