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Biochemical, Molecular, and Genetic Mechanisms

Daily Injection of Tumor Necrosis Factor- Increases Hepatic Triglycerides and Alters Transcript Abundance of Metabolic Genes in Lactating Dairy Cattle^1–3,

Department of Animal Sciences and Industry, Kansas State University, Manhattan, KS 66506

To determine whether inflammation can induce bovine fatty liver, we administered recombinant bovine tumor necrosis factor- (rbTNF) to late-lactation Holstein cows. Cows (n = 5/treatment) were blocked by feed intake and parity and randomly assigned within block to control (CON; saline), rbTNF at 2 µg/(kg·d), or pair-fed control (saline, intake matched) treatments. Treatments were administered once daily by subcutaneous injection for 7 d. Plasma samples were collected daily for analysis of glucose and FFA and a liver biopsy was collected on d 7 for triglyceride (TG) and quantitative RT-PCR analyses. Data were analyzed using treatment contrasts to assess effects of tumor necrosis factor- (TNF) and decreased feed intake. By d 7, feed intake of both rbTNF and pair-fed cows was 15% less than CON (P < 0.01). Administration of rbTNF resulted in greater hepatic TNF mRNA and protein abundance and 103% higher liver TG content (P < 0.05) without affecting the plasma FFA concentration. Hepatic carnitine palmitoyltransferase 1 transcript abundance tended to be lower (P = 0.09) and transcript abundance of fatty acid translocase and 1-acyl-glycerol-3-phosphate acyltransferase was higher (both P < 0.05) after rbTNF treatment, consistent with increased FFA uptake and storage as TG. Transcript abundance of glucose-6-phosphatase (P < 0.05) and phosphoenolpyruvate carboxykinase 1 (P = 0.09), genes important for gluconeogenesis, was lower for rbTNF-treated cows. These findings indicate that TNF promotes liver TG accumulation and suggest that inflammatory pathways may also be responsible for decreased glucose production in cows with fatty liver.

^* To whom correspondence should be addressed. E-mail: bbradfor{at}ksu.edu.

Manuscript received 6 April 2009. Initial review completed 16 May 2009. Revision accepted 2 June 2009.

Published online 23 June 2009.