In livestock diets, energy is one of the most expensive nutritional components of feed formulation. Because lipids are a concentrated energy source, inclusion of lipids are known to affect growth rate and feed efficiency, but are also known to affect diet palatability, feed dustiness, and pellet quality. In reviewing the literature, the majority of research studies conducted on the subject of lipids have focused mainly on the effects of feeding presumably high quality lipids on growth performance, digestion, and metabolism in young animals. There is, however, the wide array of composition and quality differences among lipid sources available to the animal industry making it essential to understand differences in lipid composition and quality factors affecting their digestion and metabolism more fully. In addition there is often confusion in lipid nomenclature, measuring lipid content and composition, and evaluating quality factors necessary to understand the true feeding value to animals. Lastly, advances in understanding lipid digestion, post-absorption metabolism, and physiological processes (e.g., cell division and differentiation, immune function and inflammation); and in metabolic oxidative stress in the animal and lipid peroxidation, necessitates a more compressive assessment of factors affecting the value of lipid supplementation to livestock diets. The following review provides insight into lipid classification, digestion and absorption, lipid peroxidation indices, lipid quality and nutritional value, and antioxidants in growing pigs.

The increased inclusion of unsaturated fats in pig diets has raised issues related to pork carcass fat quality. The objective of this experiment was to more precisely measure how differing levels of daily fatty acid intake alters the fatty acid composition in 3 different fat depots. A total of 42 gilts and 21 barrows (PIC 337×C22/29) with an average initial weight of 77.80±0.38 kg were allotted randomly based on sex and BW to 7 treatments: 3 and 6% of each of tallow (TAL; iodine value [IV]=41.9), choice white grease (CWG; IV=66.5), or corn oil (CO; IV=123.1) and a control (CNTR) corn-soybean meal-based diet with no added fat. Pigs were individually housed to allow accurate measurement of individual feed intake, in particular, daily dietary fatty acid and energy intake. Fat samples were collected from the jowl, belly, and loin at slaughter. Diet and carcass fat samples were analyzed for IV. Belly weights were recorded at slaughter along with a subjective belly firmness score (1=firmest to 3=least firm). Carcass lipid IV was increased (P<0.001) by increasing the degree of unsaturation of the dietary fat source (66.8, 70.3, and 76.3 for TAL, CWG, and CO, respectively). Carcass lipid IV for TAL and CWG was not affected (P>0.05) by inclusion levels; however, carcass lipid IV was greater (P<0.001) in pigs fed 6 than 3% CO (80.0 vs. 72.6), and carcasses of gilts had greater IV (P<0.001) than carcasses of barrows (71.5 vs. 69.1). Increasing the level of TAL and CO but not CWG from 3 to 6% decreased the apparent total tract digestibility of GE, resulting in a source×level interaction (P<0.05). Dietary fat source had no effect (P≥0.66) on apparent total tract digestibility of either DM or GE, but feeding 6% dietary fat increased G:F (P=0.006) over pigs fed 3% fat (0.358 vs. 0.337). Of all the fatty acids measured, only linoleic acid intake presented a reasonable coefficient of determination (R2=0.61). Overall, IV product (IVP) was approximately equal to linoleic acid intake as a predictor of carcass IV (R2=0.93 vs. R2=0.94). When inclusion of dietary fat and PUFA intake increased, IVP placed more emphasis on the dietary fat inclusion level rather than the dietary fat composition. Linoleic acid intake corrected the overemphasis placed on dietary fat inclusion by IVP. To conclude, linoleic acid intake showed a strong relationship with carcass IV and can be used as a predictor.

Heat stress (HS) results in major losses to the pork industry via reduced growth performance and, possibly, carcass fat quality. The experimental objective was to measure the effects of HS on the pig's response to dietary fat in terms of lipid digestion, metabolism, and deposition over a 35-d finishing period. A total of 96 PIC 337 × C22/C29 (PIC, Inc., Hendersonville, TN) barrows (initial BW of 100.4 ± 1.2 kg) were randomly allotted to 1 of 9 treatments arranged as a 3 × 3 factorial: thermoneutral (TN; constant 24°C; ad libitum access to feed), pair-fed thermoneutral (PFTN; constant 24°C; limit fed based on previous HS daily feed intake), or HS (cyclical 28°C nighttime, 33°C from d 0 to 7, 33.5°C from d 7 to 14, 34°C from d 14 to 21, 34.5°C from d 21 to 28, and 35°C from d 28 to 35 daytime; ab libitum access to feed) and diet (a corn-soybean meal-based diet with 0% added fat [CNTR], CNTR with 3% added tallow [TAL; iodine value {IV} = 41.8], or CNTR with 3% added corn oil [CO; IV = 123.0]). No interactions between environment and diet were evident for any major response criteria ( ≥ 0.063). Rectal temperature increased due to HS (39.0°C for HS, 38.1°C for TN, and 38.2°C for PFTN; < 0.001). Heat stress decreased ADFI (27.8%; < 0.001), ADG (0.72 kg/d for HS, 1.03 kg/d for TN, and 0.78 kg/d for PFTN; < 0.001), and G:F (0.290 for HS, 0.301 for TN, and 0.319 for PFTN; = 0.006). Heat stress barrows required 1.2 Mcal of ME intake more per kilogram of BW gain than PFTN ( < 0.001). Heat stress tended to result in the lowest apparent total tract digestibility of acid hydrolyzed ether extract (AEE; 59.0% for HS, 60.2% for TN, and 61.4% for PFTN; = 0.055). True total tract digestibility (TTTD) of AEE of CO-based diets (99.3%) was greater than that of CNTR (97.3%) and TAL-based diets (96.3%; = 0.012). Environment had no impact on TTTD of AEE ( = 0.118). Environment had no impact on jowl IV at market (69.2 g/100 g for HS, 69.3 g/100 g for TN, and 69.8 g/100 g for PFTN; = 0.624). Jowl IV at market increased with increasing degree of unsaturation of the dietary fat (68.5 g/100 g for CNTR, 68.2 g/100 g for TAL, and 71.5 g/100 g for CO; < 0.001). Heat stress decreased mRNA abundance of and ( ≤ 0.041). Heat stress and CO increased mRNA abundance of ( ≤ 0.047), and CO increased abundance of ( = 0.011). In conclusion, HS does not alter the pig's response to dietary fat. However, HS leads to reduced ADG, ADFI, G:F, and caloric efficiency and a suppression of mRNA abundance of genes involved in the lipolytic cascade, which resulted in a phenotype that was fatter than PFTN.

The objective was to determine the energy concentration of a diverse array of dietary fat sources and, from these data, develop regression equations that explain differences based on chemical composition. A total of 120 Genetiporc 6.0 × Genetiporc F25 (PIC, Inc., Hendersonville, TN) individually housed barrows were studied for 56 d. These barrows (initial BW of 9.9 ± 0.6 kg) were randomly allotted to 1 of 15 dietary treatments. Each experimental diet included 95% of a corn-soybean meal basal diet plus 5% either corn starch or 1 of 14 dietary fat sources. The 14 dietary fat sources (animal-vegetable blend, canola oil, choice white grease source A, choice white grease source B, coconut oil, corn oil source A, corn oil source B, fish oil, flaxseed oil, palm oil, poultry fat, soybean oil source A, soybean oil source B, and tallow) were selected to provide a diverse and robust range of unsaturated fatty acid:SFA ratios (U:S). Pigs were limit-fed experimental diets from d 0 to 10 and from d 46 to 56, providing a 7-d adaption for fecal collection on d 7 to 10 (13 kg BW) and d 53 to 56 (50 kg BW). At 13 kg BW, the average energy content of the 14 sources was 8.42 Mcal DE/kg, 8.26 Mcal ME/kg, and 7.27 Mcal NE/kg. At 50 kg BW, the average energy content was 8.45 Mcal DE/kg, 8.28 Mcal ME/kg, and 7.29 Mcal NE/kg. At 13 kg BW, the variation of dietary fat DE content was explained by DE (Mcal/kg) = 9.363 + [0.097 × (FFA, %)] - [0.016 × omega-6:omega-3 fatty acids ratio] - [1.240 × (arachidic acid, %)] - [5.054 × (insoluble impurities, %)] + [0.014 × (palmitic acid, %)] ( = 0.008, = 0.82). At 50 kg BW, the variation of dietary fat DE content was explained by DE (Mcal/kg) = 8.357 + [0.189 × U:S] - [0.195 × (FFA, %)] - [6.768 × (behenic acid, %)] + [0.024 × (PUFA, %)] ( = 0.002, = 0.81). In summary, the chemical composition of dietary fat explained a large degree of the variation observed in the energy content of dietary fat sources at both 13 and 50 kg BW.

The objective was to investigate the of effect chemical composition of dietary fat on transcription of genes involved in lipid metabolism in adipose tissue and the liver via transcriptional profiling in growing pigs. A total of 48 Genetiporc 6.0 × Genetiporc F25 (PIC, Inc., Hendersonville, TN) barrows (initial BW of 44.1 ± 1.2 kg) were randomly allotted to 1 of 6 dietary treatments. Each experimental diet included 95% of a corn-soybean meal basal diet and 5% cornstarch (control; CNTR), animal-vegetable blend (AV), coconut oil (COCO), corn oil (COIL), fish oil (FO), or tallow (TAL). Pigs were sacrificed on d 10 (final BW of 51.2 ± 1.7 kg) to collect tissues. Expression normalization across samples was performed by calculating a delta cycle threshold (ΔCt) value using . Delta delta cycle threshold (ΔΔCt) values were expressed relative to the CNTR treatment. In adipose tissue, adding dietary fat, regardless of the source, decreased the mRNA abundance of compared with the CNTR ( = 0.014). Pigs fed a COIL-based diet tended to have greater adipose tissue expression of ( = 0.071) than pigs fed the other dietary fat sources tested. Abundance of mRNA was greater in adipose tissue of barrows a fed COIL-based diet than barrows fed CNTR or FO-based diets ( = 0.047). In the liver, adding dietary fat, regardless of source, increased the mRNA abundance of , , , , , and ( ≤ 0.020) and tended to increase the abundance of ( = 0.071) and ( = 0.086) compared with the CNTR. Pigs fed a TAL-based diet had greater hepatic transcription of than pigs fed CNTR-, COCO-, or FO-based diets ( = 0.013). Hepatic transcription of tended to be greater in pigs fed COCO than in pigs fed other dietary fat sources ( = 0.074). Dietary omega-3 fatty acid content tended to negatively correlate with mRNA abundance of ( = 0.065) in adipose tissue and ( = 0.063) in the liver. Dietary fat SFA content was negatively correlated with in the liver ( ≤ 0.039). Dietary fat MUFA content tended to be positively correlated with , , and mRNA abundance in the liver ( ≤ 0.100). To conclude, the intake of omega-3 fatty acids suppressed the mRNA abundance of genes involved in lipolysis in both adipose tissue and the liver. Dietary SFA are greater inhibitors of lipogenesis in adipose tissue than omega-6 fatty acids. Intake of medium-chain fatty acids alters hepatic lipid metabolism differently than intake of long-chain fatty acids.