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Thomas M. Badger

Researcher at University of Arkansas for Medical Sciences

Publications -  305
Citations -  13313

Thomas M. Badger is an academic researcher from University of Arkansas for Medical Sciences. The author has contributed to research in topics: Soy protein & Offspring. The author has an hindex of 63, co-authored 299 publications receiving 12304 citations. Previous affiliations of Thomas M. Badger include University of Arkansas & United States Department of Agriculture.

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Maternal obesity at conception programs obesity in the offspring

TL;DR: To examine whether in utero exposure to maternal obesity increases the risk of obesity in offspring, an overfeather analysis was developed.
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On the Actions of the Growth Hormone-Releasing Hexapeptide, GHRP

TL;DR: Evidence indicates that these opiates and GHRP administered together synergistically release GH, demonstrating the independent action(s) ofGHRP and the opiates, and the complementary, rather dramatic synergistic interaction of G HRP, GHRH, and dermorphin or GHRp, G HRh, and 2549 in releasing GH again strongly supports the independent actions of these compounds.
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Maternal obesity is associated with a lipotoxic placental environment.

TL;DR: RNA-sequencing on term placenta from obese women indicates that maternal obesity leads to a lipotoxic placental environment that is associated with decreased regulators of angiogenesis and increased markers of inflammation and oxidative stress.
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Mice fed a lipogenic methionine-choline-deficient diet develop hypermetabolism coincident with hepatic suppression of SCD-1.

TL;DR: It is found that MCD feeding causes profound hepatic suppression of the gene encoding stearoyl-coenzyme A desaturase-1 (SCD-1) in the liver, which likely contributes to hypermetabolism and weight loss.
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Dietary exposure to soy or whey proteins alters colonic global gene expression profiles during rat colon tumorigenesis

TL;DR: The identification of transcripts co- or differentially-regulated by SPI and WPH diets suggests common as well as unique anti-tumorigenesis mechanisms of action which may involve growth factor, neuroendocrine and immune system genes.