28 research outputs found

    A trans10-18:1 enriched fraction from beef fed a barley grain-based diet induces lipogenic gene expression and reduces viability of HepG2 cells.

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    Beef fat is a natural source of trans (t) fatty acids, and is typically enriched with either t10-18:1 or t11-18:1. Little is known about the bioactivity of individual t-18:1 isomers, and the present study compared the effects of t9-18:1, cis (c)9-18:1 and trans (t)-18:1 fractions isolated from beef fat enriched with either t10-18:1 (HT10) or t11-18:1 (HT11). All 18:1 isomers resulted in reduced human liver (HepG2) cell viability relative to control. Both c9-18:1 and HT11were the least toxic, t9-18:1had dose response increased toxicity, and HT10 had the greatest toxicity (P<0.05). Incorporation of t18:1 isomers was 1.8-2.5 fold greater in triacylglycerol (TG) than phospholipids (PL), whereas Δ9 desaturation products were selectively incorporated into PL. Culturing HepG2 cells with t9-18:1 and HT10 increased (P<0.05) the Δ9 desaturation index (c9-16:1/16:0) compared to other fatty acid treatments. HT10 and t9-18:1 also increased expression of lipogenic genes (FAS, SCD1, HMGCR and SREBP2) compared to control (P<0.05), whereas c9-18:1 and HT11 did not affect the expression of these genes. Our results suggest effects of HT11 and c9-18:1 were similar to BSA control, whereas HT10 and t-9 18:1 (i.e. the predominant trans fatty acid isomer found in partially hydrogenated vegetable oils) were more cytotoxic and led to greater expression of lipogenic genes

    Health effects of ruminant trans fatty acids with emphasis on type 2 diabetes

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    Recent government bans on industrial trans fatty acids (TFA) in developed countries has left naturally occurring TFA from ruminant products (e.g., dairy, beef, and lamb) as the sole source of TFA in the food supply. In contrast to industrial TFA, which have undisputed adverse health effects, ruminant TFA such as trans vaccenic acid (TVA; trans11-18:1), rumenic acid (RA; cis9, trans11-18:2) and trans palmitoleic acid (TPA; trans9-16:1) have been associated with reduced risk for some diseases such as type 2 diabetes. The present review summarizes the findings from observational, animal and human studies investigating the effects of ruminant TFA on metabolic parameters related to type 2 diabetes, and provides an update on the current knowledge of their biosynthesis, intake and factors affecting their concentrations in ruminant derived foods. Overall, observational studies and a small number of animal studies suggest that ruminant TFA may be protective against type 2 diabetes, whereas the same benefits have not been observed in other animal studies or in human clinical trials. Additional clinical and mechanistic studies are needed to better understand the isomer-specific effects of ruminant TFA. Until then, production practices resulting in increased levels of this group of fatty acids in ruminant milk and meat should be carefully reconsidered

    A ketogenic diet in combination with gemcitabine increases survival in pancreatic cancer KPC mice

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    Pancreatic ductal adenocarcinoma (PDAC) continues to be a major health problem. A ketogenic diet (KD), characterized by a very low carbohydrate and high fat composition, has gained attention for its anti-tumor potential. We evaluated the effect and mechanisms of feeding a strict KD alone or in combination with gemcitabine in the autochthonous LSL-KrasG12D/+; LSL-Trp53 R172H/+; Pdx1-Cre (KPC) mouse model. For this purpose, both male and female pancreatic tumor-bearing KPC mice were allocated to a control diet (CD; %kcal: 70% carb, 14% protein, 16% fat), a KD (%kcal: 14% protein, 1% carb, 85% fat), a CD + gemcitabine (CG), or a KD + gemcitabine (KG) group. Mice fed a KD alone or in combination with gemcitabine showed significantly increased blood β-hydroxybutyrate levels compared to mice fed a CD or CG. KPC mice fed a KG had a significant increase in overall median survival compared to KPC mice fed a CD (increased overall median survival by 42%). Interestingly, when the data was disaggregated by sex, the effect of a KG was significant in female KPC mice (60% increase in median overall survival), but not in male KPC mice (28% increase in median overall survival). Mechanistically, the enhanced survival response to a KD combined with gemcitabine was multifactorial, including inhibition of ERK and AKT pathways, regulation of fatty acid metabolism and the modulation of the gut microbiota. In summary, a KD in combination with gemcitabine appears beneficial as a treatment strategy in PDAC in KPC mice, deserving further clinical evaluation

    Red blood cells are superior to plasma for predicting subcutaneous trans fatty acid composition in beef heifers

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    The trans (t)-18:1 content in beef has become more of interest as partially hydrogenated vegetable oils are removed from foods. Predicting t-18:1 early in the feeding period would be useful if limitations are put on t-18:1 in beef. To determine which blood component is better related to backfat, proportions of t10-18:1 and t11-18:1 (vaccenic acid) were measured in heifer red blood cells (RBC) and plasma (N = 14) after 0, 28, 56, and 76 d on a barley-grain-based diet, and correlated with post-slaughter subcutaneous fat (SCF). Total t-18:1 declined in both RBC and plasma during late finishing (P < 0.05). At 28 d, t11-18:1 decreased and t10-18:1 increased in RBC and plasma (P < 0.05). By 76 d, t10-18:1 declined to 0 d levels. RBC and plasma t-18:1 compositions were highly correlated (t10-18:1, r ≥ 0.7, P ≤ 0.02; t11-18:1, r ≥ 0.51, P ≤ 0.06). Correlations with post-slaughter backfat were, however, consistently greater for RBC compared with plasma. The use of RBC t-18:1 composition may, therefore, be superior to plasma for predicting t-18:1 in SCF, and the length of finishing could be useful for manipulating t-18:1 in beef. The time required for changes in t18:1 in RBC to reflect in changes in SCF still, however, needs to be determined to establish optimal durations for beneficial modification.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author
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