Evaluating acute inflammation's effects on hepatic triglyceride content in experimentally induced hyperlipidemic dairy cows in late lactation.

Autor:	Horst EA; Department of Animal Science, Iowa State University, Ames 50011., van den Brink LM; Department of Animal Science, Iowa State University, Ames 50011., Mayorga EJ; Department of Animal Science, Iowa State University, Ames 50011., Al-Qaisi M; Department of Animal Science, Iowa State University, Ames 50011., Rodriguez-Jimenez S; Department of Animal Science, Iowa State University, Ames 50011., Goetz BM; Department of Animal Science, Iowa State University, Ames 50011., Abeyta MA; Department of Animal Science, Iowa State University, Ames 50011., Kvidera SK; Department of Animal Science, Iowa State University, Ames 50011., Caixeta LS; Department of Veterinary Population Medicine, University of Minnesota, St. Paul 55108., Rhoads RP; Department of Animal and Poultry Sciences, Virginia Tech University, Blacksburg 24061., Baumgard LH; Department of Animal Science, Iowa State University, Ames 50011. Electronic address: baumgard@iastate.edu.
Jazyk:	angličtina
Zdroj:	Journal of dairy science [J Dairy Sci] 2020 Oct; Vol. 103 (10), pp. 9620-9633. Date of Electronic Publication: 2020 Aug 06.
DOI:	10.3168/jds.2020-18686
Abstrakt:	Inflammation appears to be a predisposing factor and key component of hepatic steatosis in a variety of species. Objectives were to evaluate effects of inflammation [induced via intravenous lipopolysaccharide (LPS) infusion] on metabolism and liver lipid content in experimentally induced hyperlipidemic lactating cows. Cows (765 ± 32 kg of body weight; 273 ± 35 d in milk) were enrolled in 2 experimental periods (P); during P1 (5 d), baseline data were obtained. At the start of P2 (2 d), cows were assigned to 1 of 2 treatments: (1) intralipid plus control (IL-CON; 3 mL of saline; n = 5) or (2) intralipid plus LPS (IL-LPS; 0.375 μg of LPS/kg of body weight; n = 5). Directly following intravenous bolus (saline or LPS) administration, intralipid (20% fat emulsion) was intravenously infused continuously (200 mL/h) for 16 h to induce hyperlipidemia during which feed was removed. Blood samples were collected at -0.5, 0, 4, 8, 12, 16, 24, and 48 h relative to bolus administration, and liver biopsies were obtained on d 1 of P1 and at 16 and 48 h after the bolus. By experimental design (feed was removed during the first 16 h of d 1), dry matter intake decreased in both treatments on d 1 of P2, but the magnitude of reduction was greater in LPS cows. Dry matter intake of IL-LPS remained decreased on d 2 of P2, whereas IL-CON cows returned to baseline. Milk yield decreased in both treatments during P2, but the extent and duration was longer in LPS-infused cows. Administering LPS increased circulating LPS-binding protein (2-fold) at 8 h after bolus, after which it markedly decreased (84%) below baseline for the remainder of P2. Serum amyloid A concentrations progressively increased throughout P2 in IL-LPS cows (3-fold, relative to controls). Lipid infusion gradually increased nonesterified fatty acids and triglycerides in both treatments relative to baseline (3- and 2.5-fold, respectively). Interestingly, LPS infusion blunted the peak in nonesterified fatty acids, such that concentrations peaked (43%) higher in IL-CON compared with IL-LPS cows and heightened the increase in serum triglycerides (1.5-fold greater relative to controls). Liver fat content remained similar in IL-LPS relative to P1 at 16 h; however, hyperlipidemia alone (IL-CON) increased liver fat (36% relative to P1). No treatment differences in liver fat were observed at 48 h. In IL-LPS cows, circulating insulin increased markedly at 4 h after bolus (2-fold relative to IL-CON), and then gradually decreased during the 16 h of lipid infusion. Inducing inflammation with simultaneous hyperlipidemia altered the characteristic patterns of insulin and LPS-binding protein but did not cause fatty liver. (Copyright © 2020 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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