Thomas M. Badger

TL;DR: Potential effects of dietary protein source on metabolism of a wide variety of CYP1A substrates, including environmental and dietary carcinogens, many of which induce their own metabolism are suggested.

TL;DR: An ethanol-dependent regulation of rat hepatic class I ADH is demonstrated for the first time and implies adaptability of the ethanol eliminating system to high concentrations of alcohol.

TL;DR: Hippuric acid was able to stimulate bone‐forming gene expression but suppress PPARγ expression, leading to increased bone mass dose‐dependently, and PAs are capable of altering the mesenchymal stem cell differentiation program.

TL;DR: It is proposed that the pulsatile BACs are caused by an ethanol concentration-dependent regulation of an ethanol metabolizing system, perhaps CYP2E1, and found to be pulsatile during continuous alcohol infusion.

TL;DR: The results suggest that high‐fat feeding may disrupt bone development and modeling; high concentrations of NEFAs and insulin resistance occurring with high fat intake are mediators of reduced osteoblast activity and differentiation; diets high in soy protein may help prevent high dietary fat‐induced bone impairments; and the molecular mechanisms underlying the SPI‐protective effects involve isoflavone‐induced normalization of insulin signaling in bone.