title: Acute experimental mastitis is not causal toward the development of energy-related metabolic disorders in early postpartum dairy cows.
abstract: Twenty Holstein cows in early lactation (7 d in milk) were administered 100 microg of Escherichia coli lipopolysaccharide (LPS) dissolved in 10 mL of sterile 0.9% NaCl saline (treatment; TRT) or 10 mL of sterile saline (control) into both right mammary quarters to test the hypothesis that acute experimental mastitis would have negative impacts on aspects of energy metabolism that might lead to the development of metabolic disorders. A primed continuous intravenous infusion (14-micromol/kg of BW priming dose; 11.5-micromol/kg of BW per h continuous infusion) of 6,6-dideuterated glucose was used to determine pre- and posttreatment glucose kinetics using steady-state tracer methodologies. The LPS-treated cows displayed productive, clinical, and physiological signs of moderate to severe inflammation; control cows displayed no signs of immune activation. Pretreatment glucose rates of appearance (Ra) into plasma were similar (715 and 662 +/- 33 mmol/h for TRT and control, respectively) between treatment groups. Intramammary LPS infusion into TRT cows resulted in increased glucose Ra relative to control cows (mean glucose Ra from 150 through 270 min after intramammary infusion were 815 and 674 +/- 21 mmol/h for TRT and control cows, respectively). Furthermore, plasma concentrations of glucose increased, whereas plasma nonesterified fatty acids, glycerol, and beta-hydroxybutyrate concentrations decreased, in TRT relative to control cows. Interestingly, plasma insulin concentration increased dramatically in TRT cows and occurred prior to the small increase in plasma glucose concentration. Although these results only represent the early stages of inflammation, they are not consistent with a causal relationship between mastitis and energy-related metabolic disorders and instead suggest a coordinated protective effect by the immune system on metabolism during the early stages of mammary insult.
authors.affiliation: Department of Animal Science, Cornell University, Ithaca, NY 14853, USA.
authors.forename: M R
authors.initials: MR
authors.lastname: Waldron
authors.forename: A E
authors.initials: AE
authors.lastname: Kulick
authors.forename: A W
authors.initials: AW
authors.lastname: Bell
authors.forename: T R
authors.initials: TR
authors.lastname: Overton
mesh_terms: D020155:3-Hydroxybutyric Acid / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002417:Cattle; D002418:Cattle Diseases / Q000209:etiology*; D004032:Diet; D004734:Energy Metabolism; D004926:Escherichia coli; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005234:Fatty Liver / Q000209:etiology / Q000662:veterinary; D005260:Female; D005990:Glycerol / Q000097:blood; D007328:Insulin / Q000097:blood; D007662:Ketosis / Q000209:etiology / Q000662:veterinary*; D007774:Lactation / Q000276:immunology; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008321:Mammary Glands, Animal; D008414:Mastitis, Bovine / Q000150:complications* / Q000276:immunology / Q000382:microbiology; D008892:Milk / Q000737:chemistry; D011644:Puerperal Disorders / Q000209:etiology / Q000662:veterinary*
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D008070:Lipopolysaccharides; D005990:Glycerol; D020155:3-Hydroxybutyric Acid