title: Physiological response to acute endotoxemia in swine: effect of genotype on energy metabolites and leptin.
abstract: Certain high lean gain swine genotypes have greater sensitivity to pathogen and nonpathogen stressors evident by reduced productivity and increased mortality during disease stress or in suboptimal production environments. Saline (control) and an immunologic challenge (LPS; 25 microg lipopolysaccharide/kg BW) were administered to three genetic populations (each pig used as its own control): high lean (H), moderate lean terminal cross (MT), and moderate lean maternal cross (MM). LPS induced anorexia, and significantly increased body temperature and circulating TNF-alpha, cortisol, and NEFA in all genotypes (P < 0.0004). LPS reduced circulating glucose, insulin, and IGF-1 in all genotypes (P < 0.05). The LPS-induced hypoglycemia was significantly greater in MM versus MT and H pigs (P < 0.03). The hypoinsulinemia was significantly greater in MM versus H pigs (P < 0.02). MM pigs recovered from hypoinsulinemia slower than MT pigs (P < 0.03). Control insulin was higher in H versus MT pigs (P < 0.08), but relative to basal, the insulin response to LPS was similar. Plasma haptoglobin response to LPS was lower for MM versus MT and H pigs (P < 0.02), and tended to be lower in MT versus H pigs (P < 0.09). LPS treatment caused similar decreases in plasma IGF-1 concentrations among genotypes. Ten hours after LPS treatment, leptin mRNA abundance in adipose tissue was significantly reduced (relative to control) in MM and H pigs (P < 0.02) but not in MT pigs (P > 0.05). Physiological differences in leptin, a potent regulator of food intake and energy metabolism, may be important factors in the genetic variation in sensitivity to environmental stress.
authors.affiliation: Department of Animal Sciences, Purdue University, West Lafayette, IN, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Leininger
authors.forename: C P
authors.initials: CP
authors.lastname: Portocarrero
authors.forename: A P
authors.initials: AP
authors.lastname: Schinckel
authors.forename: M E
authors.initials: ME
authors.lastname: Spurlock
authors.forename: C A
authors.initials: CA
authors.lastname: Bidwell
authors.forename: J N
authors.initials: JN
authors.lastname: Nielsen
authors.forename: K L
authors.initials: KL
authors.lastname: Houseknecht
mesh_terms: D000273:Adipose Tissue / Q000737:chemistry; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003124:Colorimetry / Q000662:veterinary; D003433:Crosses, Genetic; D004591:Electrophoresis, Polyacrylamide Gel / Q000662:veterinary; D019446:Endotoxemia / Q000235:genetics / Q000503:physiopathology / Q000662:veterinary*; D004797:Enzyme-Linked Immunosorbent Assay / Q000662:veterinary; D004927:Escherichia coli Infections / Q000235:genetics / Q000503:physiopathology / Q000662:veterinary*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005838:Genotype; D006854:Hydrocortisone / Q000097:blood; D007091:Image Processing, Computer-Assisted; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D020738:Leptin / Q000096:biosynthesis* / Q000097:blood; D008297:Male; D009693:Nucleic Acid Hybridization; D012313:RNA / Q000737:chemistry / Q000302:isolation & purification; D011863:Radioimmunoassay / Q000662:veterinary; D013552:Swine; D013553:Swine Diseases / Q000097:blood / Q000235:genetics / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D012313:RNA; D007334:Insulin-Like Growth Factor I; D006854:Hydrocortisone