The aim of this study was to investigate whether dietary protein intake during gestation less than or greater than recommendations affects gilts growth and body composition, gestation outcome, and colostrum composition. German Landrace gilts were fed gestation diets (13.7 MJ of ME/kg) containing a low (n = 18; LP, 6.5% CP), an adequate (n = 20; AP, 12.1%), or a high (n = 16; HP, 30%) protein content corresponding to a protein:carbohydrate ratio of 1:10.4, 1:5, and 1:1.3, respectively, from mating until farrowing. Gilts were inseminated by semen of pure German Landrace boars and induced to farrow at 114 d postcoitum (dpc; Exp. 1). Energy and protein intake during gestation were 33.3, 34.4, and 35.8 MJ of ME/d (P < 0.001) and 160, 328, and 768 g/d, respectively, in LP, AP, and HP gilts (P < 0.001). From insemination to 109 dpc, BW gain was least in LP (42.1 kg), intermediate in HP (63.1 kg), and greatest in AP gilts (68.3 kg), whereas increase of backfat thickness was least in gilts fed the HP diet compared with LP and AP diets (3.8, 5.1, 5.0 mm; P = 0.01). Litter size, % stillborn piglets, and mummies were unaffected (P > 0.28) by the gestation diet. Total litter weight tended to be less in the offspring of LP and HP gilts (14.67, 13.77 vs. 15.96 kg; P = 0.07), and the percentage of male piglets was greater in litters of HP gilts (59.4%; P < 0.01). In piglets originating from LP and HP gilts, individual birth weight was less (1.20, 1.21 vs. 1.40 kg; P = 0.001) and birth weight/crown-rump length ratio was reduced (45.3, 46.4 vs. 50.7 g/cm; P = 0.003). Colostrum fat (7.8, 7.4 vs. 8.1%) and lactose concentrations (2.2, 2.1 vs. 2.6%) tended to be reduced in LP and HP gilts (P = 0.10). In Exp. 2, 28 gilts (LP, 10; AP, 9; HP, 9) were treated as in Exp. 1 but slaughtered at 64 dpc. At 64 dpc, LP gilts were 7% lighter than AP gilts (P = 0.03), whereas HP gilts were similar to AP gilts. Body composition was markedly altered in response to LP and HP feeding with less lean (P < 0.01) and greater fat content (P = 0.02 to 0.04) in LP and less fat content (P = 0.02 to 0.04) in HP gilts. Fetal litter weight and number, and embryonic survival at 64 dpc were not affected by the diets. These results indicated that gestation diets containing protein at 50 and 250% of recommendations and differing in protein:carbohydrate ratio led to marked changes in protein and fat metabolism in gilts resulting in fetal growth retardation of 15%, which mainly occurred during the second half of gestation.

No abstract

Inulin stimulates intestinal bifidobacteria in humans and rodents but its effect in pigs is inconsistent. We assessed the effect of inulin on the intestinal microbiota by fluorescent in situ hybridization in growing pigs (age 9-12 wk). Pigs (n = 64) were assigned to 2 types of basal diets [wheat and barley (WB) or corn and wheat gluten (CG)] with or without 3% inulin (WBI or CGI) for 3 and 6 wk (n = 8/group) to test whether naturally occurring dietary fibers influence the inulin effect. Intestinal organic acids, pH values, and residual inulin were determined. The composition of the microbiota was highly individual. The duration of feeding did not affect any of the variables tested; therefore, data for the 2 periods were pooled. Bifidobacteria were detected in less than half of the pigs. Inulin did not stimulate lactobacilli and bifidobacteria numbers irrespective of the basal diet, although 20-50% of inulin was degraded in the jejunum. The number of pigs with colonic bifidobacteria was higher in those fed diets containing inulin (40 vs. 13%; P < 0.05). Total colonic short-chain fatty acid (SCFA) concentrations were lower in both inulin-fed groups due to reduced acetate (P < 0.05). Proportions of colonic butyrate were higher in pigs fed inulin-supplemented diets (P < 0.05). Colonic pH tended to be lower in the WB groups (WB; 6.6 +/- 0.6), and was higher due to inulin (CGI, 7.1 +/- 0.1; P < 0.05). In conclusion, inulin affected intestinal SCFA and the number of pigs harboring bifidobacteria; this effect was independent of the basal diet.

No abstract

Our results in a previous study indicated that the portal absorption of intragastrically fed alpha-ketoglutarate (AKG) was limited in young pigs. Our aim was to quantify the net portal absorption, first-pass metabolism, and whole-body flux of enterally infused AKG. In study 1, we quantified the net portal nutrient absorption in young pigs (n = 9) given an intraduodenal infusion of milk replacer [10 mL/(kg . h)] and either saline (control) or 930 micromol/(kg . h) AKG for 4 h. In study 2, we quantified the luminal disappearance of a duodenal AKG bolus in young pigs (n = 7). In study 3, we quantified the whole-body kinetics of (13)C-AKG metabolism when infused either enterally (n = 9) or intravenously (n = 9) in young pigs. In study 1, when compared with the control group, enteral AKG infusion increased (P < 0.01) the arterial (13.8 +/- 1.7 vs. 27.4 +/- 3.6 micromol/L) and portal (22.0 +/- 1.4 vs. 64.6 +/- 5.9 micromol/L) AKG concentrations and the net portal absorption of AKG [19.7 +/- 2.8 vs. 95.2 +/- 12.0 micromol/(kg . h)]. The mean fractional portal appearance of enterally infused AKG was 10.23 +/- 1.3%. In study 2, the luminal disappearance of AKG was 663 micromol/(kg . h), representing 63% of the intraduodenal dose. In study 3, the whole-body (13)C-AKG flux [4685 +/- 666 vs. 801 +/- 67 micromol/(kg . h)] was higher (P < 0.05) when given enterally than intravenously, but (13)CO(2) recovery was not different (37.3 +/- 1.0 vs. 36.2 +/- 0.7%dose). The first-pass splanchnic (13)C-AKG utilization was approximately 80%, of which 30% was oxidized to (13)CO(2). We conclude that the intestinal absorption of AKG is limited in young pigs largely due to substantial first-pass gastrointestinal metabolism.