Compensatory gain based on lysine level in finishing pigs after being fed lysine deficient 97% corn diets for 3 or 6 wk.

The objective of this experiment was to evaluate increasing the concentration of lysine on the compensatory gain of finishing pigs during their recovery period after being fed a 97% corn holding diet for 3 or 6 wk. One thousand six hundred and eighty pigs with a starting body weight of 73.5 ±â€…2.2 kg were blocked by starting body weight and assigned to a nested arrangement. Twenty replicates of seven treatments were comprised of two restriction lengths [3 weeks (3 wk) vs. 6 weeks (6 wk)], and three lysine concentrations during recovery (Lys:ME same as control:100; control + 10%: 110; control + 20%: 120) plus one control (CONT) that remained nutrient unrestricted. Pen weight and feed intake were recorded on days 0, 21, 41, and at marketing. Whole pens were marketed when the pen average met 130 kg and carcass measurements were collected. Data were analyzed by pen with the fixed effects of restriction length and lysine within restriction length. Nutrient restriction lowered (P < 0.01) average daily gain (ADG) compared to control, with 1.2, 0.4, and 0.5 kg for control, 3 wk, and 6 wk treatments, respectively. Restricted pigs showed decreased feed intake while restricted. After the respective restriction period, pigs were allowed a recovery diet until market. Previously restricted pigs had 16.7% and 27.3% greater (P < 0.01) ADG over control pigs for 3 and 6 wk treatments, respectively, in the first 3-wk of recovery. The lysine concentration in the recovery diet impacted (P < 0.01) the ADG with pigs allowed the highest lysine concentration having a 10% greater ADG than pigs fed the lower Lys:ME concentrations, for both restriction treatments. The increase in ADG was not paralleled by an increase in feed intake over control, thus, there was an improvement (P < 0.01) in gain to feed ratio in the recovery period. Control pigs reached market weight (131.5 kg) on experiment day 49 while pigs fed corn diets for 3 wk or 6 wk were slower to market (57 and 69 days, respectively; P < 0.01). Restricted pigs had greater backfat (CONT: 1.47, 3 wk: 1.55, 6 wk: 1.65 cm; P < 0.01), and decreased loin depth (CONT: 7.32, 3 wk: 7.03, 6 wk: 6.61 cm, P < 0.02) which was also impacted (P < 0.01) by lysine concentration. In conclusion, the use of restrictive diets reduced ADG and increased days to market. The use of recovery diets in which the Lys:ME ratio was greater than control pigs, resulted in increased compensatory growth.

Feeding long-chain n-3 polyunsaturated fatty acids during gestation increases intestinal glucose absorption potentially via the acute activation of AMPK.

The current study utilized Ussing chambers to examine the impact of supplementing maternal gestation and/or lactation diets with n-3 polyunsaturated fatty acids (PUFA) provided via a protected fish oil (PFO) product on intestinal fatty acid profiles and ex vivo glucose uptake in the jejunum of weanling piglets. Jejunum tissues were enriched with n-3 PUFA as a result of feeding the sows the PFO during gestation and/or lactation (P<.05). Glucose uptake improved by twofold (P<.042) in intestinal preparations obtained from the offspring of sows fed PFO during gestation or throughout gestation/lactation versus lactation alone. This was also reflected in the jejunum protein expressions of glucose transporter 2 (GLUT2) and sodium-dependent glucose transporter 1 (SGLT1). Furthermore, adding docosahexaenoic acid (DHA) or an AMP-activated protein kinase (AMPK) agonist to the chamber buffer improved glucose uptake (P<.05) in intestinal preparations obtained from the offspring fed the control diet, devoid of the PFO product and containing minimal concentrations of n-3 PUFA. Collectively, these data indicate two important points. First, long-term exposure to n-3 PUFA via the maternal gestation diet effectively enhances glucose uptake in the weanling piglet, and the underlying mechanism may be associated with changes in the intestinal fatty acid profile. Secondly, there is an apparent direct and acute effect of DHA that is achieved within a time frame that precludes substantial changes in the intestinal fatty acid profile. Additionally, both mechanisms may involve activation of AMPK. Thus, n-3 PUFA delivered in utero and postnatally via the maternal diet may help the offspring adapt quickly to rapidly changing diets early in life and allow optimal nutrient uptake.

n-3 PUFA attenuate lipopolysaccharide-induced down-regulation of toll-like receptor 4 expression in porcine adipose tissue but does not alter the expression of other immune modulators.

The objective of this study was to test the hypothesis that the inflammatory response to lipopolysaccharide (LPS) in vivo is accompanied by down-regulation of toll-like receptor (TLR) 4 in adipose tissue, and a source of protected n-3 polyunsaturated fatty acid (PUFA) attenuates this response. Seventy-two castrated male pigs were individually fed either a control (CONT) diet, or the CONT diet containing 1.87% (LF) or 7.50% (HF) protected n-3 PUFA on a weight basis for 7 weeks. Adipose and muscle tissue biopsy samples were taken at Weeks 1, 2, 3, 4 and 7 to assess gene expression and/or confirm tissue enrichment with eicosapentaenoic acid and docosahexaenoic acid and reflected the n-3 PUFA contained in the diet. The LPS challenge was performed at week 7 and consisted of sequential injections of 10 and 2.5 mug LPS per kilogram of body weight 23 h apart. The LPS challenge resulted in a marked down-regulation (P=.004) of TLR4 at the protein level in the adipose tissue of challenged vs. control pigs, but LF and HF clearly blocked this response at the mRNA level. Although LF and HF also attenuated (P<.001) the LPS-induced acute febrile response and lowered (P<.002) serum concentrations of tumour necrosis factor alpha. Cyclooxygenase 2 and 12-lipoxygenase were readily expressed in porcine adipose tissue, but there was no effect of LF, HF or LPS on expression levels of these inflammatory mediators, or that of TNF and interleukin 6, at the conclusion of the challenge period. These findings indicate that adipose tissue responds to LPS administration in vivo by reducing TLR4 mRNA and protein abundance and that the anti-inflammatory effects of n-3 PUFA do not include down-regulation of TLR4 in adipose tissue.

In utero and postnatal exposure to long chain (n-3) PUFA enhances intestinal glucose absorption and energy stores in weanling pigs.

The aim of this research was to determine whether feeding gestating and lactating sows (n-3) PUFA [eicosapentaenoic acid (EPA) and/or docosahexenoic acid (DHA)] or coconut fat (saturated fat) influences ex vivo glucose absorption in the proximal jejunum and glucose and glycogen concentration of liver and muscle of their offspring at weaning. Sows were fed 1 of 4 diets for 150 d, which included the entire gestation and lactation periods. The diets consisted of basal corn/soybean meal (CONT), CONT + protected EPA and DHA-rich fish oil (PFO), CONT + DHA Gold fat (DHAGF), and CONT + coconut fat (COCO). All tissues were collected from piglets (n = 4 per treatment) following a 24-h period of food deprivation, which was initiated at weaning. Proximal jejunum samples were mounted in modified Ussing chambers for transport determinations. Relative to the CONT (7 muA/cm(2)), active glucose transport was greater (P = 0.013) in piglets from sows fed the PFO (30 microA/cm(2)) and DHAGF (40 microA/cm(2)) diets, but not the COCO diet (19 microA/cm(2); pooled SEM = 5). Likewise, jejunum expression of glucose transporter 2 and sodium glucose transporter 1 protein tended (P < 0.10) to be greater in piglets from dams fed the PFO and DHAGF diets, as did AMP-activated protein kinase activity. Piglets' muscle glycogen was greater than in CONT (34 +/- 5.2 mg/g wet tissue) only in piglets from dams fed the DHAGF (46 +/- 5.2 mg/g wet tissue; P < 0.05). These results indicate that (n-3) PUFA, particularly DHA, improves intestinal glucose absorption and muscle glycogen concentrations in newly weaned pigs. These findings may also have important implications for human mothers and infants.