Antitumor Necrosis Factor Antibodies Reduce Hepatic Steatosis During Total Parenteral Nutrition and Bowel Rest in the Rat

. 2005. Strong relationships between mediators of the acute phase response and fatty liver in dairy cows. Can. J. Anim. Sci. 85: [165][166][167][168][169][170][171][172][173][174][175]. The objective of this study was to investigate the relationship between activation of acute phase response and fatty liver in transition dairy cows. Fatty liver was induced in dairy cows by feeding 8 kg of cracked corn 1 mo before the expected day of parturition. Liver and blood samples were obtained at days -4, 3, 8, 12, 14, 22, 27, and 36 postpartum. Cows that developed fatty liver (n = 4) reached peak total lipids in the liver at day 12 postpartum with 11.4% (wet wt.) compared with 6.6% in control cows (n = 4). Cows with fatty liver had greater plasma tumor necrosis factor-alpha (TNF-α), nonesterified fatty acids (NEFA), and lower lactate concentrations than did control cows at day -4. During highest concentrations of total lipids in the liver, for at least one time-point, fatty-liver cows had greater concentrations of plasma serum amyloid A (SAA), haptoglobin, and NEFA and lower concentrations of calcitonin gene-related peptide (CGRP), prostaglandin E 2 (PGE 2 ), cortisol, and TNF-α than did control cows. Concentrations of total lipids in the liver at 12 d postpartum were correlated (a) positively with plasma TNF-α, SAA, and NEFA and negatively with plasma CGRP before calving, (b) positively with plasma SAA, haptoglobin, and NEFA and negatively with plasma PGE 2 , CGRP, total cholesterol, and glucose at days 3, 8, and 12 postpartum, and (c) negatively with concentrations of plasma glucose, lactate, and total bilirubin after day 12 postpartum. In conclusion, this study indicates that the acute phase response occurs in cows with fatty liver as well as strong relationships between mediators of immune response and fatty liver. Mots clés: Réponse phase aiguë, foie gras, vaches laitièresFatty liver is a common metabolic disorder that affects almost half of all dairy cows immediately after parturition.Despite much progress in understanding metabolic events during the development of fatty liver, the precise mechanisms of the pathology remain unclear. The conventional view is that fatty liver is characterized by excess liver triacylglycerols (TAG) arising from a negative energy balance after parturition (Bauchart et al. 1998). The negative energy balance evokes a major mobilization of non-esterified fatty acids (NEFA) from adipose tissue and increased uptake of

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“…Similarly, pretreatment with anti-TNF-α monoclonal antibodies lowers concentrations of total lipids as well as TAG in liver (Pappo et al 1995).…”

Section: Discussionmentioning

confidence: 99%

Strong relationships between mediators of the acute phase response and fatty liver in dairy cows

Ametaj¹,

Bradford²,

Bobe³

et al. 2005

Can. J. Anim. Sci.

156

126

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“…This is prevented by the pretreatment of these animals with broad-spectrum MMP inhibitors. TNF-␣ antibodies in rats attenuate ethanol, and parenteral nutrition induced hepatic steatosis (30,43). Broad-spectrum synthetic MMP inhibitors are also hepatoprotective in liver ischemia perfusion injury without a clear mechanism (14).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of matrix metalloproteinases increases PPAR-α and IL-6 and prevents dietary-induced hepatic steatosis and injury in a murine model

Alwayn

Andersson

Lee³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Several methods for preventing such hepatic dysfunction have been reported, such as the use of cyclic TPN 13) or the administration of ursodeoxycholic acid, 14) metronidazole, 15) gentamicin, 16) anti-TNF antibody, 17) cholecystokinin, 18,19) glutamine, [20][21][22][23] or steroids and growth hormone. Nevertheless, the problem of hepatic dysfunction in patients receiving TPN has yet to be completely overcome, and the mechanism of TPN-induced hepatic steatosis remains unclear.…”

Section: Role Of Soybean Oil Fat Emulsion In the Pre-vention Of Tpn-imentioning

confidence: 99%

Soybean Oil Fat Emulsion to Prevent TPN-Induced Liver Damage: Possible Molecular Mechanisms and Clinical Implications

Nishimura

Yamaguchi

Naito

et al. 2006

Biological & Pharmaceutical Bulletin

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INTRODUCTIONTotal parenteral nutrition (TPN), which is recognized as one method for parenteral hyperalimentation, has been found to be an effective and relatively safe method for supplying energy and nutrients to surgical patients. Following improvements in parenteral regimens including vitamins and trace elements and in catheter techniques to reduce the septic complications associated with TPN, TPN has been widely employed to provide complete nutritional support and therapeutic benefits in a variety of pathophysiological settings in which patients are unable to eat. However, TPN-induced hepatobiliary dysfunction, which was first described by Peden et al.,1) has been recognized as a cause of severe morbidity and a life-threatening complication of TPN, especially in neonates and infants. Hepatic dysfunction with steatosis is the most common complication associated with fat-free TPN in adults, and cholestasis is more common in infants.2,3) Recently, the 3-component infusion solution containing amino acids, glucose, and soybean oil emulsion, GA-1080 (MIXID ® , Otsuka Pharmaceutical Factory, Inc.; Tokushima, Japan), has been demonstrated to be effective in overcoming such hepatic morbidity in clinical studies.4) Intravenous fat emulsions, especially soybean oil, are now available as a source of essential fatty acids in patients receiving TPN, and the "three-in-one" solution GA-1080 has been found to be clinically safe, stable, and economical. However, the multifactorial pathogenesis of TPN-induced hepatic dysfunction remains unclear, and the molecular mechanisms by which GA-1080 prevents hepatic dysfunction have not yet been identified.We have recently developed an infant rat model of hepatobiliary dysfunction.5) Using this animal model, we have clearly demonstrated the metabolic complications in the liver that may occur due to the excessive administration of fat-free TPN in infant rats. Furthermore, we have shown that including fat in the TPN regimen is very important in preventing TPN-induced hepatic dysfunction. In this review, we describe the molecular mechanisms and the clinical implications of soybean oil in TPN solutions in avoiding the hepatic complications associated with parenteral nutrition. INFANT RAT TPN MODEL WITH HEPATOBILIARY DYSFUNCTIONSince the first studies of TPN in animal models conducted in 1968 by Dudrick et al.,6) it has been known that only a limited number of species (such as the dog, cat, rabbit, and guinea pig) can tolerate the surgical procedures required for TPN, and few studies have employed rats as an animal model for TPN. In 1981, Tashiro and Meng 7) were the first to report a technique for long-term TPN in unrestrained weanling or infant (3-week-old) rats, thus establishing an animal model for pediatric TPN. Numerous studies have focused on the optimal TPN composition in mature rats, but few have addressed this issue in infant rats.We have recently developed an infant rat model with hepatic dysfunction and steatosis induced by overdose of fatfree TPN. 5) After 30 infant (3-week-ol...

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Antitumor Necrosis Factor Antibodies Reduce Hepatic Steatosis During Total Parenteral Nutrition and Bowel Rest in the Rat

Cited by 54 publications

References 16 publications

Strong relationships between mediators of the acute phase response and fatty liver in dairy cows

Strong relationships between mediators of the acute phase response and fatty liver in dairy cows

Inhibition of matrix metalloproteinases increases PPAR-α and IL-6 and prevents dietary-induced hepatic steatosis and injury in a murine model

Soybean Oil Fat Emulsion to Prevent TPN-Induced Liver Damage: Possible Molecular Mechanisms and Clinical Implications

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