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

Abstract

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.

Menthol Targeting AMPK Alleviates the Inflammatory Response of Bovine Mammary Epithelial Cells and Restores the Synthesis of Milk Fat and Milk Protein

“…In addition, BMECs, as one of the main cells of mammary tissue, are not only important immune cells, but also a major cell population for lactation in cows ( 28 , 35 ). When mastitis occurs in cows, mastitis is well known to seriously affect milk production and quality ( 11 , 19 , 34 ). Yusaku Tsugami et al.…”

“…It is well known that the inflammatory response is a self-protective mechanism of the body, that has the function of removing pathogenic bacteria, eliminating bacterial toxins and repairing damaged tissues ( 10 ). When the autoimmunity of the body is able to clear and kill pathogenic bacteria and repair the damage, mastitis will recover on its own; otherwise, the inflammatory response will become more intense, not only damaging the mammary tissue and reducing milk production; but also even endangering the life of cow ( 11 ). Several studies have shown that the inflammatory response is closely linked to autophagy, that autophagy plays a key role in maintaining inflammatory homeostasis, and that enhancing autophagy can reduce damage to the inflammatory response ( 12 – 14 ).…”

Die Leberverfettung der Milchkuh: Teil 1

“…Es ergab sich zu Beginn der Infu sion ein transienter Anstieg von NEFA, aber keine Erhöhung des Leberfettgehalts. Diese Arbeitsgruppe hat diese Untersuchungen fortgesetzt [103] und Kühen intravenös Fett oder Fett plus LPS für 16 h infundiert. Die Infusion verursacht in beiden Gruppen einen Anstieg der NEFA im Blut und eine heftige Entzündungsreaktion in der Gruppe Fett plus LPS.…”

“…Dieser akute Versuch bestätigt zwar die Auslösung einer Entzündungsreaktion durch LPS, aber nicht die Arbeitshypothese einer Beteiligung von LPS an der Pathogenese der Leberverfettung. Die Autoren schließen aber eine eventuell chronische Wirkung von LPS an diesem Krankheitsgeschehen nicht aus [103].…”

“…Ohne NEFA und die der Mobilisation zugrundeliegenden hormonellen Veränderungen wird es wahrscheinlich keine Leberverfettung, Entzündung, oxidativen und endoplasmatischen Stress geben. Unterstützt wird diese zur Diskussion gestellte Annahme durch die Versuche mit einer LPS-Infusion [102,103]. LPS + Fettinfusion lösen ausgeprägte Entzündungsreaktionen aus, aber keine Leberverfettung [103].…”