Ann E. Brodie
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Ann E. Brodie has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
Ching Yuan Hu
Department of Animal Sciences, Oregon State University, Corvallis OR 97331
1 shared publication- Ching Yuan Hu
Department of Human Nutrition, Food and Animal Sciences, College of Tropical Agriculture and Human Resilience, University of Hawaii at Manoa, 1955 East-West Road, AgSci. 415J, Honolulu, HI 96822, USA
1 shared publication - Dennis E. Jewell
Department of Grain Science & Industry, Kansas State University, Manhattan, KS 66506, USA
1 shared publication Kathleen R. Ferguson
Department of Animal Sciences, Oregon State University, Corvallis OR 97331
1 shared publicationV.A. Azarenko
1 shared publicationViola A. Manning
Department of Animal Sciences, Oregon State University, Corvallis OR 97331
1 shared publication
Latest Publications
- Open Access
- 1 March 1999
- Published by Elsevier in The Journal of Nutrition
- Vol. 129 (3) , 602-606
Conjugated Linoleic Acid Inhibits Differentiation of Pre- and Post- Confluent 3T3-L1 Preadipocytes But Inhibits Cell Proliferation Only in Preconfluent Cells
Conjugated linoleic acid (CLA; 18:2) is a group of isomers (mainly 9-cis, 11-trans and 10-trans, 12-cis) of linoleic acid. CLA is the product of rumen fermentation and can be found in the milk and muscle of ruminants. Animals fed CLA have a lower body fat content. The objective of this study was to establish the possible mechanisms by which CLA affects adipogenesis. 3T3-L1 is a well-established cell line that is used extensively in studying adipocyte biology. These cells typically grow in a culture medium until they reach confluence, at which time they are induced to differentiate by hormonal treatment (d 0). Treatment of 3T3-L1 cells with 25 to 100 μmol/L CLA inhibited differentiation in a dose-dependent manner, while linoleic acid treatment did not differ from DMSO-treated controls. Continuous treatment from d −2, −1, 0 or 2 to d 8 and treatment from d −2 to d 0 and from d 0 to d 2 inhibited differentiation. Differentiation was monitored morphologically (oil Red-O staining), enzymatically (reduction of activity of glycerol-3-phosphate dehydrogenase), and by northern analysis of peroxisome proliferator-activated receptor γ2, CCAAT/enhancer binding protein α and adipocyte specific protein 2 mRNA. CLA inhibited cell proliferation of nonconfluent cells but did not affect cell division of confluent cells, as indicated by 5-bromo-2′-deoxyuridine incorporation and mitochondria metabolism. Therefore, CLA inhibited differentiation before confluence and during induction. However, cellular proliferation was only inhibited prior to induction. These results imply that fat reduction caused by CLA treatment may be attributed to its inhibition of both proliferation and differentiation of preadipocytes in animals.
- 1 March 1999
- Published by Elsevier in The Journal of Nutrition
- Vol. 129 (3) , 602-606
Open AccessConjugated Linoleic Acid Inhibits Differentiation of Pre- and Post- Confluent 3T3-L1 Preadipocytes But Inhibits Cell Proliferation Only in Preconfluent Cells
Conjugated linoleic acid (CLA; 18:2) is a group of isomers (mainly 9-cis, 11-trans and 10-trans, 12-cis) of linoleic acid. CLA is the product of rumen fermentation and can be found in the milk and muscle of ruminants. Animals fed CLA have a lower body fat content. The objective of this study was to establish the possible mechanisms by which CLA affects adipogenesis. 3T3-L1 is a well-established cell line that is used extensively in studying adipocyte biology. These cells typically grow in a culture medium until they reach confluence, at which time they are induced to differentiate by hormonal treatment (d 0). Treatment of 3T3-L1 cells with 25 to 100 μmol/L CLA inhibited differentiation in a dose-dependent manner, while linoleic acid treatment did not differ from DMSO-treated controls. Continuous treatment from d −2, −1, 0 or 2 to d 8 and treatment from d −2 to d 0 and from d 0 to d 2 inhibited differentiation. Differentiation was monitored morphologically (oil Red-O staining), enzymatically (reduction of activity of glycerol-3-phosphate dehydrogenase), and by northern analysis of peroxisome proliferator-activated receptor γ2, CCAAT/enhancer binding protein α and adipocyte specific protein 2 mRNA. CLA inhibited cell proliferation of nonconfluent cells but did not affect cell division of confluent cells, as indicated by 5-bromo-2′-deoxyuridine incorporation and mitochondria metabolism. Therefore, CLA inhibited differentiation before confluence and during induction. However, cellular proliferation was only inhibited prior to induction. These results imply that fat reduction caused by CLA treatment may be attributed to its inhibition of both proliferation and differentiation of preadipocytes in animals.
- 1 February 1997
- Published by Elsevier in Toxicology Letters
- Vol. 90 (2-3) , 91-95
Inhibition of increases of transcription factor mRNAs during differentiation of primary rat adipocytes by in vivo 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment
- 1 February 1997
- Published by Elsevier in Toxicology Letters
- Vol. 90 (2-3) , 91-95
Inhibition of increases of transcription factor mRNAs during differentiation of primary rat adipocytes by in vivo 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment