Atherosclerosis is accelerated in diabetes mellitus mainly due to the reduced availability and function of endothelial progenitor cells (EPCs). The purpose of this study was to determine the protective effects of the anthocyanin cyanidin-3-O-β-glucoside (C3G) on EPC function and endothelial repair in diabetic apolipoprotein E-deficient (apoE(-/-)) mice. Diabetes mellitus was induced in 8-wk-old male apoE(-/-) mice with streptozotocin. Diabetic apoE(-/-) mice were fed the AIN-93 diet or an AIN-93 diet supplemented with C3G (0.2% wt:wt) for 6 wk. Sham-injected apoE(-/-) mice fed the AIN-93 diet served as nondiabetic controls. The endothelium-dependent relaxation response to acetylcholine in the aortas of C3G-fed mice was greater by 51% compared with diabetic mice fed the AIN-93 diet (P < 0.05) and was similar to that in nondiabetic apoE(-/-) mice. The capacity of in vitro adhesion to fibronectin, migration, and tube formation was significantly impaired in diabetic EPCs (decreased by 83, 61.9, and 74.5%, respectively, compared with nondiabetic controls; all P < 0.01), which was significantly rescued in response to C3G (increased by 3.9-, 2-, and 1.8-fold compared with diabetic EPCs, respectively; all P < 0.05). At the molecular level, the phosphorylation levels of AMP-activated protein kinase (AMPK) Thr 172 and endothelial nitric oxide synthase (eNOS) Ser1177 were higher in EPCs derived from the C3G-treated diabetic mice compared with those in nondiabetic mice. Furthermore, compared with nondiabetic controls, diabetic apoE(-/-) mice had a 3.5-fold increase in the aortic lesion area, which was lowered by 45% in C3G-fed diabetic mice. This study extends our current knowledge that C3G improves the impairment of EPC function, enhances endothelial repair, and thus limits accelerated atherogenesis caused by diabetes. Our findings emphasize the potential utility of anthocyanin in the prevention and treatment of diabetic vascular complications.

High dietary zinc concentrations are used to prevent or treat diarrhea in piglets and humans, but long-term adaptation to high zinc supply has yet not been assessed. Intestinal zinc uptake is facilitated through members of zinc transporter families SLC30 (ZnT) and SLC39 (ZIP). Whereas in rodents, regulation of zinc homeostasis at low or adequate zinc supply has been described, such mechanisms are unclear in piglets. A total of 54 piglets were fed diets containing 57 [low dietary zinc (LZn)], 164 [normal dietary zinc (NZn)], or 2425 [high dietary zinc (HZn)] mg/kg dry matter dietary zinc. After 4 wk, 10 piglets/group were killed and jejunal tissues taken for analysis of zinc transporters SLC30A1 (ZnT1), SLC30A2 (ZnT2), SLC30A5 (ZnT5), SLC39A4 (ZIP4), divalent metal transporter 1 (DMT1), and metallothionein-1 (MT). Weight gain was higher (P < 0.05) in pigs fed HZn compared with the LZn and NZn groups during the first 2 wk. Food intake did not differ between groups. The digesta and jejunal tissue zinc concentrations were higher (P < 0.05) in the HZn compared with NZn and LZn pigs. Expression of ZnT1 was higher (P < 0.05) and ZIP4 lower (P < 0.05) in HZn pigs compared with the 2 other groups, whereas expression of ZnT5 and DMT1 did not differ between treatments. Expression of ZnT2 was lower (P < 0.05) in the LZn compared with HZn and NZn groups. The mRNA expression and protein abundance of MT was higher (P < 0.05) in HZn compared with NZn and LZn groups. Studies with intestinal porcine cell line intestinal epithelial cell-J2 confirmed the dose-dependent downregulation of ZIP4 and upregulation of ZnT1 and MT (P < 0.05) with increasing zinc concentration within 24 h. In conclusion, high dietary zinc concentrations increase intracellular zinc, promote increased zinc export from intestinal tissues into extracellular compartments, and decrease the zinc uptake from the gut lumen. The adaptive process appears to be established within 24 h; however, it does not prevent tissue zinc accumulation.

Cross-sectional studies have established a relationship between poverty and food insecurity, but little is known about the acute changes within households that lead to changes in food insecurity. This study examined how changes in income, employment status, and receipt of welfare related to change in severity of food insecurity during 1 y among low-income families. In 2005-2007, 501 families living in market and subsidized rental housing were recruited through door-to-door sampling in high-poverty neighborhoods in Toronto. One year later, families were re-interviewed. The final longitudinal analytic sample included 331 families. Within-household change in income, employment, and welfare receipt were examined in relation to change in severity of food insecurity. Severity was denoted by the aggregate raw score on the Household Food Security Survey Module (HFSSM). Analyses were stratified by housing subsidy status owing to differences in characteristics between households. Food insecurity was a persistent problem among families; 68% were food insecure at both interviews. Severity was dynamic, however, as 73.4% answered more or fewer questions affirmatively on the HFFSM between baseline and follow-up. Among market-rent families, a $2000 gain in income during the year and gain of full-time employment were associated with a 0.29 and 1.33 decrease in raw score, respectively (P < 0.01). This study suggests that improvements in income and employment are related to improvements in families' experiences of food insecurity, highlighting the potential for income- and employment-based policy interventions to affect the severity of household food insecurity for low-income families.

Recent studies have indicated that omega-3 (n3) polyunsaturated fatty acids (PUFAs) decrease adipose tissue inflammation in rodents and in morbidly obese humans. We investigated whether a diet rich in n3 PUFAs from both marine and plant sources reduces adipose tissue and systemic inflammation in overweight to moderately obese adults. We conducted a randomized, single-blind, parallel-design, placebo-controlled feeding trial. Healthy men and women with a body mass index between 28 and 33 kg/m(2) consumed a diet rich in n3 PUFAs (3.5% of energy intake; n = 11) from plant and marine sources or a control diet (0.5% of energy intake from n3 PUFAs; n = 13). These diets were consumed for 14 wk (under ad libitum conditions for 12 wk). All foods were provided for the entire study period. Subcutaneous abdominal adipose tissue and fasting plasma were collected after the first 2 wk with the control diet and again at the end of the 14-wk dietary period. The primary outcome of this ex post analysis was the adipose tissue gene expression of 13 key mediators of inflammation. Adipose tissue gene expression of inflammatory mediators did not differ between the 2 groups, after adjustment for weight change. Furthermore, none of the 5 plasma markers of systemic inflammation differed significantly as an effect of diet treatment. We conclude that a relatively high dose of n3 PUFAs from plant and marine sources did not significantly lower adipose tissue or systemic inflammation in overweight to moderately obese healthy men and women over 14 wk.

Body nitrogen retention is dependent on the amount of dietary protein consumed, as well as the fat and carbohydrate content in the diet, due to the modulation of amino acid oxidation. PPARα is a transcription factor involved in the upregulation of the expression of enzymes of fatty acid oxidation. However, the role of putative PPARα response elements (PPREs) in the promoter of several amino acid-degrading enzymes (AADEs) is not known. The aim of this work was to study the effect of the synthetic ligand (Wy 14643) and the natural ligands (palmitate, oleate or linoleate) in rats fed graded concentrations of dietary protein (6, 20, or 50 g/100 g of total diet composition) on the expression of the AADEs histidase, serine dehydratase, and tyrosine aminotransferase. Thus, we fed male Wistar rats diets containing 6, 20, or 50% casein for 10 d. The results showed that addition of Wy 14643 to the diet significantly reduced the expression of the AADE. Furthermore, the incubation of hepatocytes with natural ligands of PPARα or feeding rats with diets containing soybean oil, safflower oil, lard, or coconut oil as sources of dietary fat significantly repressed the expression of the AADEs. Gene reporter assays and mobility shift assays demonstrated that the PPRE located at -482 bp of the histidase gene actively bound PPARα in rat hepatocytes. These data indicate that PPARα ligands may reduce amino acid catabolism in rats.