**4. Environmental stressors**

Environmental stressors on pigs can impact lipid metabolism and overall carcass quality. Impacts of environmental stressors, including thermal stress and housing density, are through both direct effects of decreased growth efficiency and indirect effects of altered regulation of *de novo* lipogenesis. Managerial and nutritional strategies during critical growth periods may alleviate the impact of these environmental stressors. Additionally, the regulation of *de novo* lipogenesis is influenced by the health status of the animal. Insults to health through disease or constant stress decrease feed intake and reduce *de novo* lipid synthesis. This decrease in *de novo* synthesis shifts the ratios of fatty acids in the adipose tissue to more unsaturated FA, further reducing lipid quality.

#### **4.1. Spatial allocation, growth, and carcass composition**

Decreasing space allocation reduces growth performance and the minimal spatial requirements for grow-finish pigs have been examined [36, 71]. Housing densities between 0.76 and 0.93 m2/pig have been reported as the threshold for grow-finish swine, below which ADG and ADFI are reduced [71].

Stress from spatial allocation is not a simple reflection of floor space, it is also reflective of pen dimensions, size, location of feeders and waters, and size of the pigs. One allometric calculation for spatial allocation is f = k x BW.667 (f = floor allowance, m2; k = coefficient of housing area; BW = body weight, kg) which accounts for the relationship between body weight and surface area [71]. In a study using this approach, housing densities of 0.578, 0.761 and 0.942 m2/pig corresponding to housing area coefficients of 0.030, 0.039 and 0.048, respectively; resulted in decreased ADG and ADFI in pigs housed at floor area allowances with coefficients between 0.030 and 0.039 [71]. These results were within in the range of other reported housing threshold values [71].

### **4.2. Heat stress, pork quality and animal growth**

The thermal neutral zone of a mammal is the range of ambient temperatures within which the animal can control its core body temperature without elevating its metabolic rate [72]. Within the thermoneutral zone of mammals, core body temperature is maintained without expending additional energy to warm or cool basal body temperature [72, 73]. If the environmental conditions are below this zone, additional energy of metabolism is devoted to generating heat to maintain the desired core temperature [72]. Conversely, at temperatures above this zone, the animal must dissipate energy to maintain core body temperature through additional heat loss mechanisms such as evaporative heat loss, convection, and conduction [72]. When environmental temperature rises above the point where heat production and heat loss are balanced, the animal is in a state of heat stress [74]. In swine, evaporative heat loss is limited due to their inability to sweat; therefore, heat loss is primarily by respiration, evaporation, and exposure to cool air and wet surfaces for convection and conduction, respectively [72, 73, 75]. As an adaptive mechanism to further cool the body and maintain a homeothermic temperature, the animal decreases feed intake in order to decrease the thermal effect of feeding [74].

222 Lipid Metabolism

observed after feeding CLA [65, 66].

**4. Environmental stressors** 

which ADG and ADFI are reduced [71].

other reported housing threshold values [71].

**4.2. Heat stress, pork quality and animal growth** 

tissue to more unsaturated FA, further reducing lipid quality.

**4.1. Spatial allocation, growth, and carcass composition** 

Reductions in SCD-1 expression were observed with CLA feeding in both mouse liver and cultured preadipocytes [48]. Previous studies indicate that CLA tends to decrease both SCD-1 [65] and decreases the ∆9 desaturase index in pigs [65, 66]. Decreasing SCD-1 mRNA expression, and thereby decreasing the amount of saturated fatty acids being converted to unsaturated fatty acids, may be responsible for the increased levels of saturated fatty acids

The c10 t12 isomer of CLA decreases the expression of PPARγ in adipose tissue and increases the expression of PPARα in liver tissue [67, 68, 69]. By acting as a PPARγ modulator, CLA is able to prevent lipid accumulation as shown in cultured adipocytes [70]. Conjugated linoleic acid also acts as a PPARα activator and induces accumulation of PPARresponsive mRNAs in hepatic cells [67] serving to upregulate PPAR-responsive pathways.

Environmental stressors on pigs can impact lipid metabolism and overall carcass quality. Impacts of environmental stressors, including thermal stress and housing density, are through both direct effects of decreased growth efficiency and indirect effects of altered regulation of *de novo* lipogenesis. Managerial and nutritional strategies during critical growth periods may alleviate the impact of these environmental stressors. Additionally, the regulation of *de novo* lipogenesis is influenced by the health status of the animal. Insults to health through disease or constant stress decrease feed intake and reduce *de novo* lipid synthesis. This decrease in *de novo* synthesis shifts the ratios of fatty acids in the adipose

Decreasing space allocation reduces growth performance and the minimal spatial requirements for grow-finish pigs have been examined [36, 71]. Housing densities between 0.76 and 0.93 m2/pig have been reported as the threshold for grow-finish swine, below

Stress from spatial allocation is not a simple reflection of floor space, it is also reflective of pen dimensions, size, location of feeders and waters, and size of the pigs. One allometric calculation for spatial allocation is f = k x BW.667 (f = floor allowance, m2; k = coefficient of housing area; BW = body weight, kg) which accounts for the relationship between body weight and surface area [71]. In a study using this approach, housing densities of 0.578, 0.761 and 0.942 m2/pig corresponding to housing area coefficients of 0.030, 0.039 and 0.048, respectively; resulted in decreased ADG and ADFI in pigs housed at floor area allowances with coefficients between 0.030 and 0.039 [71]. These results were within in the range of

The thermal neutral zone of a mammal is the range of ambient temperatures within which the animal can control its core body temperature without elevating its metabolic rate [72]. The optimum temperature for a finishing pig between 54.5 and 118.2 kg of body weight is 18.3°C, with a desirable temperature range between 10°C to 23.9°C [76]. The heat stress index (HSI; Figure 5), published by Iowa State University [77], is a practical guideline outlining temperature and humidity ranges for growing pigs. The HSI classifies environmental temperature and humidity conditions into three zones: alert, danger, and emergency. Within the alert range, producers are advised to monitor animal behavior, increase ventilation, and ensure that water is readily available. The danger range requires additional cooling by spraying or misting with water and increasing air flow. Under emergency conditions, producers are advised to avoid transporting animals, withdraw feed during the hottest part of the day, and reduce light levels. For example, when relative humidity is between 45 and 60%, 25.6°C is the alert threshold, 27.2°C is the danger threshold and 30°C is the emergency threshold.

For grow-finish swine, housing temperatures above 23.9°C decrease voluntary feed intake and growth rate compared to optimum housing temperatures [76, 78]. Voluntary decreases in feed intake decrease metabolic heat production to help maintain homeothermy [79]. Pigs challenged with heat-stress will have decreased feed consumption and average daily gain; however, feed efficiency is maintained when compared to control animals [80].

Nienaber et al. [81] noted that elevated temperature decreased daily feed consumption in both cattle and swine, through decreases in meal size and frequency. Feed intake was reduced by 55 g per degree of temperature increase above 22ºC [82]. A similar decrease in feed intake observed by Collin et al. [75] was coupled to reductions in thermic effect of feeding and heat production.

Humidity is also influential in the animal's ability to dissipate heat by evaporative heat loss [74]. In a study comparing 50, 65, and 80% humidity levels, respiration rate and rectal temperatures were increased at lower temperatures and 80% humidity compared to when humidity was 50 and 65% [74]. Increasing environmental humidity decreases the efficiency of evaporative cooling, resulting in symptoms of heat-stress occurring at lower temperatures.

Impacts of Nutrition and Environmental Stressors on Lipid Metabolism 225

Interactions between environmental stressors can amplify or alleviate the impact of an individual stressor. Pigs challenged with increased temperature and decreased spatial allocation demonstrated that both temperature and spatial allocation affected growth performance and carcass quality [63]. Temperature stress decreased ADG, ADFI, and G:F ratios. Pigs housed at minimum required spatial allocation of 0.66 m2/pig [36] and high environmental temperatures (32.2°C) had a 50% reduction in ADFI and an 85% reduction in ADG when compared with pigs housed in their thermal neutral zone; when pigs were housed at increased spatial allocation (0.93 m2/pig) and a temperature above 23.9°C, there was a 29% reduction of ADFI and a 36% reduction in ADG. Additionally, the level of saturation in adipose tissue was decreased in heat stressed pigs; however, increasing the spatial allocation in the 32.2°C environment ameliorated these effects and increased the fatty acid saturation to match the 23.9°C-housed pigs. The effects of spatial allocation on carcass quality demonstrate that challenging pigs with elevated temperature and reduced spatial allocation decreased feed intake, as demonstrated in the literature [87], and also decreased carcass lipid firmness. These relationships demonstrate that almost 50% of the negative growth performance effects of temperature can be ameliorated by a 28% increase in spatial allocation. In addition, an increase in housing allocation during heat stress may ameliorate the negative effects of temperature on belly weight, carcass quality, and growth performance.

The belly is the most expensive cut of the carcass, thus, the quality of bacon produced from the belly is linked to overall carcass value. Bacon is scored according to lean content and slice thickness to identify premium quality slices [88]. Premium slices have greater than 50% lean content and are wider than 1.9 cm at all points [88]. Accordingly, bacon slices are graded as either number one slices, number two slices, or as ends and pieces [88]. Pork bellies that are classified below standard based on these characteristics represent a decrease in carcass value. The swine industry has shifted to genetically lean lines with decreased backfat and thus, bellies of have become thinner, leaner, and softer [89, 90]. Thinner bellies are generally softer, produce fewer grade one slices, and present more problems with processing and storage [89, 90]. Providing saturated fat in the diet of pigs increases belly thickness and improves belly firmness [90]. Likewise, feeding CLA improves belly firmness in finishing pigs [59, 90].

Many processors utilize IV as numerical evaluation of carcass fat quality and thus have target IV values. An IV greater than 65, for some processors may be unacceptably high [58], while an IV greater than 75 may be the threshold for other processors. Increased IV [29] and decreased saturated to unsaturated fatty acid ratios [21] indicate decreases in carcass quality due to decreased fat firmness. High levels of unsaturated fatty acids result in rapid oxidation which decreases shelf life [91]. Furthermore, high levels of unsaturated fatty acids in the diets also produce bacon which is smeary, separates and causes processing difficulties

**5. Carcass quality** 

**5.1. Bacon quality** 

**5.2. Carcass lipid quality** 

**Figure 5.** Heat Stress Index for Swine published by Iowa State University [77].

Physiological response to stressors, such as heat, results in the activation of the stressactivated sympathetic nervous system and the release of catecholamines and glucocorticoids [83]. When animals are exposed to a stressor, the hypothalamus releases corticotrophinreleasing hormone which stimulates adrenocorticotropin hormone (ACTH) from the pituitary gland [84]. The release of ACTH stimulates the adrenal cortex to release cortisol [84]. Cortisol regulates growth, immunity, and intermediary metabolism including gluconeogenesis, glycogen synthesis, and lipogenesis [7, 85]. The regulation of these processes by stressactivated hormones is one source of altered metabolism during periods of stress that may contribute to changes in feed intake, weight gain, and carcass lipid quality.

Decreases in acetyl-CoA-carboxylase and stearoyl-CoA-desaturase in adipose and liver tissues have been noted in heat-stressed pigs [79]. Kouba et al. [79] noted a decrease in acetyl-CoA-carboxylase activity in heat-stressed pigs and a decrease in *de novo* fatty acid synthesis. Acetyl-CoA-carboxylase and stearoyl-CoA-desaturase catalyze the first step of the synthesis of fatty acids and the synthesis of monounsaturated fatty acids from saturated fatty acids, respectively, and therefore would be key points of potential change in lipid metabolism.

Kouba et al. [86] noted 20-35 kg pigs maintained at 31°C compared to 20°C had slightly thicker backfat with a greater lipid content and an increase in lipoprotein lipase expression in backfat and an increase in VLDL-lipid concentration in heat-stressed pigs. The increase in fat thickness of heat-stressed pigs was thus attributed to increases in lipid metabolism in the liver, and in adipose tissue, noted through increased VLDL production and LPL activity, respectively. Increased lipid circulation between liver and adipose tissue is also part of the adaptation of pigs to high environmental temperatures [86].

Interactions between environmental stressors can amplify or alleviate the impact of an individual stressor. Pigs challenged with increased temperature and decreased spatial allocation demonstrated that both temperature and spatial allocation affected growth performance and carcass quality [63]. Temperature stress decreased ADG, ADFI, and G:F ratios. Pigs housed at minimum required spatial allocation of 0.66 m2/pig [36] and high environmental temperatures (32.2°C) had a 50% reduction in ADFI and an 85% reduction in ADG when compared with pigs housed in their thermal neutral zone; when pigs were housed at increased spatial allocation (0.93 m2/pig) and a temperature above 23.9°C, there was a 29% reduction of ADFI and a 36% reduction in ADG. Additionally, the level of saturation in adipose tissue was decreased in heat stressed pigs; however, increasing the spatial allocation in the 32.2°C environment ameliorated these effects and increased the fatty acid saturation to match the 23.9°C-housed pigs. The effects of spatial allocation on carcass quality demonstrate that challenging pigs with elevated temperature and reduced spatial allocation decreased feed intake, as demonstrated in the literature [87], and also decreased carcass lipid firmness. These relationships demonstrate that almost 50% of the negative growth performance effects of temperature can be ameliorated by a 28% increase in spatial allocation. In addition, an increase in housing allocation during heat stress may ameliorate the negative effects of temperature on belly weight, carcass quality, and growth performance.

### **5. Carcass quality**

224 Lipid Metabolism

**Figure 5.** Heat Stress Index for Swine published by Iowa State University [77].

contribute to changes in feed intake, weight gain, and carcass lipid quality.

adaptation of pigs to high environmental temperatures [86].

Physiological response to stressors, such as heat, results in the activation of the stressactivated sympathetic nervous system and the release of catecholamines and glucocorticoids [83]. When animals are exposed to a stressor, the hypothalamus releases corticotrophinreleasing hormone which stimulates adrenocorticotropin hormone (ACTH) from the pituitary gland [84]. The release of ACTH stimulates the adrenal cortex to release cortisol [84]. Cortisol regulates growth, immunity, and intermediary metabolism including gluconeogenesis, glycogen synthesis, and lipogenesis [7, 85]. The regulation of these processes by stressactivated hormones is one source of altered metabolism during periods of stress that may

Decreases in acetyl-CoA-carboxylase and stearoyl-CoA-desaturase in adipose and liver tissues have been noted in heat-stressed pigs [79]. Kouba et al. [79] noted a decrease in acetyl-CoA-carboxylase activity in heat-stressed pigs and a decrease in *de novo* fatty acid synthesis. Acetyl-CoA-carboxylase and stearoyl-CoA-desaturase catalyze the first step of the synthesis of fatty acids and the synthesis of monounsaturated fatty acids from saturated fatty acids, respectively, and therefore would be key points of potential change in lipid metabolism.

Kouba et al. [86] noted 20-35 kg pigs maintained at 31°C compared to 20°C had slightly thicker backfat with a greater lipid content and an increase in lipoprotein lipase expression in backfat and an increase in VLDL-lipid concentration in heat-stressed pigs. The increase in fat thickness of heat-stressed pigs was thus attributed to increases in lipid metabolism in the liver, and in adipose tissue, noted through increased VLDL production and LPL activity, respectively. Increased lipid circulation between liver and adipose tissue is also part of the

#### **5.1. Bacon quality**

The belly is the most expensive cut of the carcass, thus, the quality of bacon produced from the belly is linked to overall carcass value. Bacon is scored according to lean content and slice thickness to identify premium quality slices [88]. Premium slices have greater than 50% lean content and are wider than 1.9 cm at all points [88]. Accordingly, bacon slices are graded as either number one slices, number two slices, or as ends and pieces [88]. Pork bellies that are classified below standard based on these characteristics represent a decrease in carcass value.

The swine industry has shifted to genetically lean lines with decreased backfat and thus, bellies of have become thinner, leaner, and softer [89, 90]. Thinner bellies are generally softer, produce fewer grade one slices, and present more problems with processing and storage [89, 90]. Providing saturated fat in the diet of pigs increases belly thickness and improves belly firmness [90]. Likewise, feeding CLA improves belly firmness in finishing pigs [59, 90].

#### **5.2. Carcass lipid quality**

Many processors utilize IV as numerical evaluation of carcass fat quality and thus have target IV values. An IV greater than 65, for some processors may be unacceptably high [58], while an IV greater than 75 may be the threshold for other processors. Increased IV [29] and decreased saturated to unsaturated fatty acid ratios [21] indicate decreases in carcass quality due to decreased fat firmness. High levels of unsaturated fatty acids result in rapid oxidation which decreases shelf life [91]. Furthermore, high levels of unsaturated fatty acids in the diets also produce bacon which is smeary, separates and causes processing difficulties

#### 226 Lipid Metabolism

[88]. As discussed above, dietary fatty acid composition contributes to the carcass fatty acid composition; therefore, feeding more saturated dietary lipid sources will result in firmer carcass lipids with decreased IV [21].

Impacts of Nutrition and Environmental Stressors on Lipid Metabolism 227

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[12] Ntambi, J. M., M. Miyazaki, and A. Dobrzyn. 2004. Regulation of stearoyl-CoA

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## **5.3. Shelf-life of meat products**

Shelf-life is defined as the period of time between packaging of a product and its end use when product properties remain acceptable to the consumer [92]. Shelf-life properties may include appearance, texture, flavor, color, and nutritive value [93]. One of the major factors affecting the shelf-life of meat products is rancidity or lipid oxidation, which occurs when fatty acids react to oxygen sources in the environment [94]. Oxidation produces low molecular weight aldehydes, acids, and ketones that cause the meat to exhibit distinct odors and flavors, typically unacceptable to consumers [94]. The level of unsaturation greatly affects the susceptibility of fat to oxidation with high degrees of unsaturation resulting in rapid oxidation and subsequently decreased shelf-life [95].
