The health risks associated with consumption of diets high in trans fats from industrially produced hydrogenated fats are well documented. However, trans fatty acids are not a homogeneous group of molecules, and less is known about the health effects of consuming diets containing vaccenic acid (VA), a positional and geometric isomer of oleic acid, the predominant trans isomer in ruminant fats. The presence of VA in industrial trans fats has raised the question of whether VA produces the same adverse health effects as industrially produced trans fats. VA is also the major trans fat in ruminant fats, and questions have arisen as to whether consuming this trans fat has the same effects on health risk. The purpose of this paper is to critically review the published studies in humans, animals, and cell lines. Epidemiological, but not rodent, studies suggest that VA intake or serum concentrations may be associated with increased cancer risk. However, epidemiological, clinical, and rodent studies to date have not demonstrated a relationship with heart or cardiovascular disease, insulin resistance, or inflammation. VA is the only known dietary precursor of c9,t11 conjugated linoleic acid (CLA), but recent data suggest that consumption of this trans fat may impart health benefits beyond those associated with CLA.
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Vaccenic acid (VA) is a ruminant-derived trans-fat and precursor of conjugated linoleic acid (CLA). The objective of the present study was to explore the effects of VA on immune function in a model of the metabolic syndrome, JCR:LA-cp rats. Lean (2:1 mix of þ /cp and þ /þ) and obese (cp/cp) rats, aged 8 weeks, were fed a control (0 % VA) or a VA diet (1·5 % (w/w) VA) for 3 weeks (twenty rats per group). Splenocytes and mesenteric lymph node (MLN) immune cell phenotypes (flow cytometry), ex vivo cytokine production (ELISA) and phospholipid fatty acid concentrations were measured. Obese rats had higher proportions of splenic macrophages, total T-cells, helper T-cells (total and percentage CD25 þ ), cytotoxic T-cells (total and percentage CD25 þ ) and produced higher concentrations of IL-6 to concanavalin A (ConA) compared with lean rats. Obese rats had lower proportions of MLN T-cells, new T-cells (CD3 þ CD90 þ ) and cytotoxic T-cells, but higher proportions of helper cells that were CD45RC þ , CD25 þ and CD4lo, and produced higher concentrations of IL-2, IL-10, interferon g and TNFa in response to ConA compared with lean rats. VA was higher in plasma phospholipids and both VA and CLA (cis-9, trans-11) were higher in MLN phospholipids compared with control-fed rats. Lean VA-fed rats had lower proportions of MLN and splenocyte CD45RC þ helper cells, and helper T-cells. Splenocytes from VA-fed rats produced 16-23 % less IL-2, IL-10 and TNFa compared with controls. VA normalised production of MLN IL-2 and TNFa in obese rats to levels similar to those seen in lean rats. These results indicate that dietary VA favourably alters the pro-inflammatory tendency of mesenteric lymphocytes from JCR:LA-cp rats.
The aim of the present study was to determine if the consumption of barley tortillas varying in fibre and/or starch composition affected postprandial glucose, insulin, glucagon-like peptide-1 (GLP-1) or peptide YY concentrations. A double-blind, randomised, controlled trial was performed with twelve healthy adults. They each consumed one of five barley tortillas or a glucose drink on six individual visits separated by at least 1 week. Tortillas were made from 100 % barley flour blends using five different milling fractions to achieve the desired compositions. All treatments provided 50 g of available carbohydrate and were designed to make the following comparisons: (1) low-starch amylose (0 %) v. high-starch amylose (42 %) with similar b-glucan and insoluble fibre content; (2) low b-glucan (4·5 g) v. medium b-glucan (7·8 g) v. high b-glucan (11·6 g) with similar starch amylose and insoluble fibre content; and (3) low insoluble fibre (7·4 g) v. high insoluble fibre (19·6 g) with similar starch amylose and b-glucan content. Blood was collected at fasting and at multiple intervals until 180 min after the first bite/sip of the test product. Amylose and insoluble fibre content did not alter postprandial glucose and insulin, but high-b-glucan tortillas elicited a lower glucose and insulin response as compared to the low-b-glucan tortillas. The tortillas with high insoluble fibre had a higher AUC for GLP-1 as compared to the tortillas with low insoluble fibre, whereas amylose and b-glucan content had no effect. Results show that processing methods can be used to optimise barley foods to reduce postprandial blood glucose responses and factors that may influence satiety.
Lingonberry grown in northern Manitoba, Canada, contains exceptionally high levels of anthocyanins and other polyphenols. Previous studies from our lab have shown that lingonberry anthocyanins can protect H9c2 cells from ischemia-reperfusion injury and anthocyanin-rich diets have been shown to be associated with decreased cardiovascular disease and mortality. Oxidative stress can impair function and trigger apoptosis in cardiomyocytes. This study investigated the protective effects of physiologically relevant doses of lingonberry extracts and pure anthocyanins against hydrogen-peroxide-induced cell death. Apoptosis and necrosis were detected in H9c2 cells after hydrogen peroxide treatment via flow cytometry using FLICA 660 caspase 3/7 combined with YO-PRO-1 and then confirmed with Hoechst staining and fluorescence microscopy. Each of the 3 major anthocyanins found in lingonberry (cyanidin-3-galactoside, cyanidin-3-glucoside, and cyanidin-3-arabinoside) was protective against hydrogen-peroxide-induced apoptosis in H9c2 cells at 10 ng·mL (20 nmol·L) and restored the number of viable cells to match the control group. A combination of the 3 anthocyanins was also protective and a lingonberry extract tested at 3 concentrations produced a dose-dependent protective effect. Lingonberry anthocyanins protected cardiac cells from oxidative-stress-induced apoptosis and may have cardioprotective effects as a dietary modification.
The present study investigated the effect of dietary Zn deficiency during sexual maturation on sperm integrity and testis phospholipid fatty acid composition. Male weanling Sprague -Dawley rats were randomised into four dietary groups for 3 weeks: Zn control (ZC; 30 mg Zn/kg); Zn marginally deficient (ZMD; 9 mg Zn/kg); Zn deficient (ZD; ,1 mg Zn/kg); pair fed (PF; 30 mg Zn/kg) to the ZD group. Morphology of cauda epididymal sperm and lipid profiles of testis phospholipids were analysed. The rats fed the ZD diet had a lower testis weight (P, 0·02). Seminal vesicles and prostate weight were also lower in the ZD and PF groups. Rats fed the ZD diet, but not the ZMD diet, had 34 -35 % more abnormal spermatozoa and 24 % shorter sperm tail length than the ZC and PF rats (P, 0·001). Testis cholesterol concentration was higher in the ZD rats compared with the ZC and PF rats (P,0·04). Testes were highly enriched with n-6 fatty acids by showing n-6 : n-3 fatty acid ratios of 27:1 in phosphatidylcholine (PC) and 23:1 in phosphatidylethanolamine (PE). The dominant fatty acid in testes was docosapentaenoic acid (22 : 5n-6), comprising 15 and 24 % of PC and PE, respectively. This fatty acid was significantly lower in the ZD rats, whereas 18 : 2n-6 was higher compared with the rats in the other diet groups. These results demonstrate that severe Zn deficiency adversely affects sperm integrity and modulates testis fatty acid composition by interrupting essential fatty acid metabolism. This suggests that Zn deficiency-associated abnormal testicular function is perhaps preceded by altered membrane fatty acid composition, especially of a major fatty acid, 22 : 5n-6.
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