|JOHNSON, CASEY - North Dakota State University|
|THAVARAJAH, DIL - North Dakota State University|
|THAVARAJAH, PUSHPARAJAH - North Dakota State University|
Submitted to: Food Research International
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/17/2012
Publication Date: 11/29/2012
Publication URL: http://handle.nal.usda.gov/10113/58099
Citation: Johnson, C.R., Thavarajah, D., Combs, G.F., Thavarajah, P. 2012. Lentil (Lens culinaris L.): A prebiotic carbohydrate-rich whole food legume. Food Research International. 51(2013) 107–113.
Interpretive Summary: The paper addressed the contents in lentils of prebiotic carbohydrates capable of surviving digestion and being utilized by the hindgut microflora in humans. It presents the results of analyses of prebiotic carbohydrates in 10 varieties of lentils grown commercially at several sites in North Dakota, USA, in 2011. These showed significant variations, some varying by variety, others by location, and two (sorbitol and mannitol) varying by both variety and location. These results show that lentils contain nutritionally significant amounts of prebiotic carbohydrates and, that it may be possible to enhance those amounts through breeding and locational sourcing.
Technical Abstract: Changes in dietary selenium and selenoprotein status may influence both anti- and pro-cancer pathways, making the outcome of interventions different from one study to another. To characterize such outcomes in a defined setting, we undertook a controlled hepatocarcinogenesis study involving varying levels of dietary selenium and altered selenoprotein status using mice carrying a mutant (A37G) selenocysteine tRNA transgene (TrsptG37) and/or TGFa. The use of TrsptG37 allowed us to alter selenoprotein expression in a selenoprotein and tissue specific manner and, at sufficient dietary selenium, separate the effect of diet and selenoprotein status, whereas TGFa was employed as the driver of hepatocarcinogenesis. We subjected these mice to diets deficient in selenium (0.02 ppm selenium) or supplemented with 0.1, 0.4 or 2.25 ppm selenium as selenite or 30 ppm triphenylselenonium chloride (TPSC), a non-metabolized selenium compound. TrsptG37 transgenic and TGFa/TrsptG37 bi-transgenic mice maintained on selenium-deficient or TPSC diets developed early morbidity and mortality prior to tumor formation, and showed a characteristic neurologically lethal phenotype. Pathological analyses revealed widespread disseminated pyogranulomatous inflammation, wherein pyrogranulomas occurred in liver, lungs, heart, spleen, small and large intestine, and mesenteric lymph nodes in the TrsptG37 transgenic and TGFa/TrsptG37 bi-transgenic mice fed the selenium-deficient or TPSC diets. The incidence of hepatocarcinogenesis was significantly increased in mice carrying the TGFa transgene; however, neither dietary selenium nor selenium status, separately or in combination, influenced hepatocarcinogenesis in these animal models. Thus, dietary selenium and selenoprotein status do not affect hepatocarcinogenesis driven by TGFa, but their deficiency leads to widespread pyogranuloma formation.