scispace - formally typeset
M

Martin J. J. Ronis

Researcher at LSU Health Sciences Center New Orleans

Publications -  200
Citations -  8492

Martin J. J. Ronis is an academic researcher from LSU Health Sciences Center New Orleans. The author has contributed to research in topics: Soy protein & Osteoblast. The author has an hindex of 53, co-authored 196 publications receiving 7769 citations. Previous affiliations of Martin J. J. Ronis include University of Arkansas for Medical Sciences & Louisiana State University.

Papers
More filters
Posted ContentDOI

The Dietary Total-Fat Content Affects the In Vivo Circulating C15:0 and C17:0 Fatty Acid Concentrations Independently to the Dietary Fatty Acid Compositions; Highlighting Dietary Routes that may Attenuate the Development of Metabolic Disease

TL;DR: The dietary total-fat content and fat-type have a very complex influence on the relative compositions of circulating fatty acids, which are independent to the actual dietary fatty acid composition.
Journal ArticleDOI

Binge ethanol exposure in mice represses expression of genes involved in osteoblast function and induces expression of genes involved in osteoclast differentiation independently of endogenous catalase.

TL;DR: In this paper, the role of endogenous catalase in skeletal ethanol toxicity was investigated in wild-type mice with a newly designed binge ethanol model, in which 12-week-old mice were exposed to four consecutive days of gavage with ethanol at 3, 3, 4, and 4.5 g ethanol/kg body weight.
Journal ArticleDOI

Preface to DMR special edition "cytochrome P450: new horizons".

TL;DR: Despite the fact that P450 research is now a mature field, many questions remain to be addressed, and the purpose of the current special issue: “Cytochrome P450: New Horizons” is to cover current research into some of these questions and to raise awareness among those not currently working in the field.
Journal ArticleDOI

Effects of N -Acetylcysteine on Non-Alcoholic Steatohepatitis (NASH) in Rats Fed via Total Enteral Nutrition

TL;DR: A "two-hit" model for NASH exists in which development of steatosis constitutes the "first hit" and sensitizes the liver to potential "second hits" resulting in NASH.