1. Introduction
For optimal production performance, proper levels of energy along with appropriate dietary protein is a prerequisite in broiler diets [
1]. Energy requirements cost about 70% of the total budget of poultry rations. Fats provide 2.25 times more energy than proteins and carbohydrates, and are composed of triacylglycerols, diacylglycerols, phospholipids and free fatty acids [
2]. Besides the provision of essential fatty acids, fats are the vehicle for vitamins, alleviate heat stress [
3], and improve diet palatability and absorption of fat-soluble vitamins [
4]. Vegetable oils contain polyunsaturated fatty acids (PUFAs) with a better digestibility [
5] and greater tendency of oxidation [
6] and can be used up to 8% in poultry feed. The dietary inclusion level of oil, however, depends, beside other factors, on its peroxide value (POV) that is an indicator of its rancidity [
7]. High risk of oxidation due to prolonged contact with air, sunlight, metallic catalysts and poor storage conditions limits the use of oil in poultry feed [
8]. Heating and deep frying of vegetable oils at various temperatures, likewise, also results in thermal oxidation reactions that lead to physical and chemical alterations [
9] and the production of various lipid peroxidation products [
10]. Peroxides are generated through a peroxidation process of unsaturated fatty acids leading to the production of secondary oxidation products including ketones, other low molecular weight acids [
4] and malondialdehyde that are the markers for lipid peroxidation [
11]. These products of oxidation react with lipids, fat-soluble vitamins and proteins in the diet thus reducing its nutrient content. Few of these oxidation products are toxic and have harmful effects on intestinal absorptive cells [
12], resulting in decreased growth of broilers [
5]. The influence of dietary oxidised vegetable oil on poultry production has been extensively reviewed [
13]. Poultry rations supplemented with oxidized oil may cause oxidative stress [
14], due to greater reactive oxygen species and may lead to poor growth performance in birds [
15]. Dietary oxidized oil enhances the cholesterol and low-density lipoprotein levels, with a reduced serum immune globulin contents [
16], digestive functioning [
17], and poorer meat quality [
18].
The influence of dietary oil oxidation on growth performance has been studied in broilers [
19] and various aquatic animals [
20,
21]. There is, however, contrary data available about the use of oxidized vegetable oil in animal feed. Mazur-Kuśnirek et al. [
15], for instance, observed no significant influence on growth performance of broilers fed oxidized (POV = 55.7 mEq kg
−1) oil-based diets. Hence, recovered oil from the restaurants or the food industry may be used in animal feed as a valuable energy source [
22]. It has been reported that the addition of 1 to 2% oil reduces the dustiness of the feed, whereas 4 to 5% oil in the diet increases dietary energy for broiler chickens and young fattening turkeys. In contrast, consumption of oxidized fat resulted in a decline in feed palatability as well as intake [
23], and finally poor growth in broilers [
5].
The current trial was, therefore, performed to evaluate the impact of various levels of oxidized vegetable oil on zootechnical performance and carcass characteristics, gut morphology, nutrients utilization, serum cholesterol and meat fatty acid composition in broilers. It was hypothesized that used vegetable oil from food processing facilities and restaurants can replace the expensive fresh oil in broiler diets as an energy source without compromising their zootechnical performance.
3. Discussion
The current trial was performed to evaluate the impact of dietary oxidized vegetable oil on the growth performance and carcass characteristics, digestibility of CP and fat, gut morphology, serum cholesterol, and meat fatty acid profile in broilers consuming either fresh or oxidized vegetable oil-containing diets. Growth performance, carcass characteristics, gut morphology, serum cholesterol, utilization of crude protein and fat, and meat fatty acid profile were evaluated as descriptive variables.
The observed poorer growth performance in broilers consuming MOO and HOO based diets during starter period (0 to 21 days), grower phase (22 to 35 days) and overall (0 to 35 days) course of the study is in consistent with the studies in broilers reported earlier [
5,
24]. Tan et al. [
25] reported poorer FCR in broilers consuming oxidized fish oil (POV = 140 mEq kg
−1) based diet in comparison with those consuming a diet containing fresh fish oil during 0 to 14 days of age. Lindblom et al. [
26], similarly, documented reduced growth performance in the broiler groups consuming oxidized palm (POV = 607.4 mEq kg
−1), soybean (POV = 616.2 mEq kg
−1) and flaxseed (POV = 128.2 mEq kg
−1) oil in their diets than those consuming fresh oil counterparts. The reduction in FI and growth performance of broilers consuming dietary oxidized oil may be linked with its lower palatability and digestibility [
27]. Lipid oxidation generates different oxidation products including esters, ketones, polymerized oils and aldehydes, which may cause the production of rancid odors and flavors that are ultimately associated with the decreased palatability of the diet [
23]. Such oxidation products present in oxidized oil may lead to a lower energy value and fat retention of the diet, ultimately causing harmful effects on body weight of the broilers [
5]. These oxidative compounds, if consumed, may damage the nutrients, mainly unsaturated fatty acids and antioxidative status of vitamin E leading to a greater oxidative stress. The lower concentration of PUFAs and tocopherols along with the fatty acid polymerization in the oxidized oil may cause reduced fatty acid digestibility [
28] and ultimately poor growth performance. The reduced growth, additionally, may also be associated with the destruction of fat-soluble vitamins (A, D, E and K), amino acids and pigments by rancid fats [
27]. Oxidized oils in several animal species resulted in a reduced FI, depressed growth, and introduced disease [
19,
29,
30]. Depressed growth performance by the consumption of oxidized fats may be due to the higher proliferation of hepatic cells, additionally, greater epithelial cell turnover and immunoglobulins concentration in gastrointestinal tract of broilers and pigs [
31].
The decreased growth performance can also be attributed to reduce VH that exerts negative effects on the nutrients absorption by reducing the surface area available for digestive enzymes secretions in broilers [
32]. This reduction in VH can also be due to the toxic properties of the oxidation products that cause destruction to the brush border membranes of the intestine. In the current study, the broilers consuming LOO based diets indicated no significant reduction in growth performance (FI and BWG) throughout the course of the experiment (0 to 35 days). Tan et al. [
11] reported that the growth performance remained unaffected in broilers after consuming soybean oil of various oxidation levels (POV = 3.69, 25.37, 56.83 and 73.21 mEq kg
−1). This may possibly be due to the lower inclusion and oxidation levels of the oil in experimental diets. The decreased carcass weight in broilers consuming oxidized oil-containing diets is in accordance with the previous studies [
24]. The current findings regarding dressing percentage, breast yield, giblet weights and leg quarter yield in broilers are compatible with the available literature on broilers [
18,
24,
33,
34].
The absorptive efficacy is mainly regulated by the villus surface area present for the nutrients. Improved VH equivalently enhances the surface area and consequently, higher intestinal digestive and absorptive functions [
35]. The lower VH in broilers consuming oxidized vegetable oil is in accordance with reported literature on the poultry [
7,
36]. In contrast, Tan et al. [
11] indicated no significant difference in the jejunal and ileal morphology of broilers that consumed oxidized (POV = 3.69, 25.37, 56.83 and 73.21 mEq kg
−1) oil-based diet. The reduced VH in the broilers fed with different oxidation levels of dietary vegetable oil, during the current study, may possibly be due to the toxic properties of some products of oxidation including ketones, esters, aldehydes and esters that are possibly causing damage to the intestinal brush border membrane [
12]. This decrease in VH may also be due to an imbalance between the intestinal cell loss and regeneration rates [
37]. Since dietary oxidized oil increases the proliferation rate and decreases the life span of the functional cells of gastrointestinal tract [
38]. The broilers consuming oxidized oil may initiate intestinal metabolic oxidative stress [
11].
The reduced EE digestibility in the present study is in accordance with Luo et al. [
39], which indicated 8% reduction in the apparent total tract digestibility of EE in weaned pigs consuming 3% oxidized (POV = 120.85 mEq kg
−1) fish oil-based diets. Lindblom et al. [
26], similarly, documented 6% reduction of EE digestibility in growing pigs consuming soybean oil, which was heated at 90℃ for 72 hrs. Overholt et al. [
40] reported 5% reduced EE digestibility in finishing pigs fed with the diet containing soybean oil that was heated at 180℃ for 6 hrs. In contrast, no significant effects on EE digestibility by supplementation of oxidized oil (POV = 148 mEq kg
−1) in broilers [
41] and nursery pigs were reported [
42]. Lipid’s digestibility depends on the numerous factors including the extent of saturation among others. Unsaturated fatty acids due to their greater capability of micelle formation, are usually more digestible than SFA. Oxidized oils containing lower unsaturated to saturated fatty acids ratio are, therefore, less digestible [
43]. Lipid’s oxidation increases the saturation of the fats [
6,
44], and the polymers generated by oxidation influence the digestibility of the lipids [
45,
46].
In the present study, the increased serum cholesterol level in the broilers consuming oxidized vegetable oil containing diets is in consistent with Açikgöz et al. [
41], who found 5% increased concentration of cholesterol in broilers fed with the oxidized oil (POV = 148 mEq kg
−1) than the control group. Since the oxidation decreases the linoleic acid concentration in oil; therefore, the consumption of higher levels of dietary oxidised oil leads to a lower intake of linoleic acids, which may lead to an increase in total serum cholesterol level [
47]. Ghasemi-Sadabadi et al. [
7], similarly, reported 9% higher concentration of serum cholesterol in quails fed oxidized (POV = 146.03 mEq kg
−1) oil than those fed on the control diets. In contrast, Bayraktar et al. [
48] reported 8% lower cholesterol concentration in plasma of broilers that consumed oxidized oil (POV = 100 mEq kg
−1) containing diets in comparison with those fed on the control diet. Yue et al. [
30] also documented 4% lower cholesterol in serum of laying hens after consuming oxidized (POV = 88 mEq kg
−1) oil. This decreased cholesterol concentration may possibly be due to the reduced cholesterol uptake by liver, higher fecal excretion of cholesterol [
49] and enhanced levels of thyroxin in the plasma [
28].
The essential fatty acids composition of meat can be affected by certain fatty acids in the diet [
50]. In the present study, a significantly lower percentage of PUFA, C18:2 and C18:3, and greater percentage of SFA and C18:0 in thighs of the broilers after consuming LOO, MOO and HOO based diets can be associated with heating of the oil. The heating or frying cause oxidation of the oil leading to decreased concentration of PUFA, C18:2 and C18:3 [
1,
19,
51] that was reflected by the thigh tissue fatty acid profile [
52]. In line with the current study, Ghasemi-Sadabadi et al. [
7] documented a decreased concentration of PUFA, C18:2, C18:3 and C20:4 in the breast muscles of the quail that consumed oxidized (POV = 146.03 mEq kg
−1) oil. Mazur-Kuśnierek et al. [
15], similarly, reported a lower PUFA concentration in broiler’s breast muscles consuming oxidized oil (POV = 55.7 mEq kg
−1) than those fed the control diet.