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A total of 768 1-d-old Ross 308 male broiler chickens with an average body weight of 43.64 ± 0.59 g were used in a 5-wk feeding trial. The chickens were distributed into 4 treatments of 12 replications per treatment with 16 chickens per pen. Dietary treatments included the following: TRT1, basal diet; TRT2, —40 kcal diet + 0.05% emulsifier; TRT3, —60 kcal diet + 0.05% emulsifier; TRT4, —80 kcal diet + 0.05% emulsifier. The emulsifier contained 80% sodium stearoyl-2-lactylate and 20% tween 20. In our study, the treatment diets had no significant effect on growth performance, meat quality, relative organ weight, serum lipid profiles, and excreta microbiota. However, the birds were able to grow as well with less energy when the emulsifier was added. The supplementation of emulsifier in the low-energy diet linearly decreased cholesterol (P = 0.099) and LDL/C (P = 0.074). The fat digestion of broilers fed with TRT2, TRT3, and TRT4 was significantly higher than broilers fed with TRT1 diet. Our study result shows that the emulsifier used for the experiment is beneficial in the low-energy diet of broiler chickens.

Clostridium perfringens, an α-toxin producing gram-positive bacterium, is an enteric pathogen for poultry. Because subclinical C. perfringens infections often result in damage of the intestinal mucosa, decreased nutrient digestion, and poor performance, efforts should be taken to find an effective strategy that controls overgrowth of C. perfringens. For this purpose, the efficacy of a sodium lauroyl lactylate (LauL) as a feed additive to prevent C. perfringens colonization in broilers was determined. First, the effect of LauL was compared with capric and lauric mono- and diglycerides (MDG) and capric and lauric free fatty acids in Clostridium-infected chickens. Clostridial lesion scoring at d 16 showed that MDG and LauL were both effective in reducing the severity of lesions. When taking into account results on BW gain and mortality, LauL was more effective than MDG. For this reason, a dose response study was made to determine the optimal dietary dosage of LauL. In this experiment, it was shown that a LauL dose higher than 0.15% should be used to expect positive effects on lesion severity and mortality. None of the LauL doses led to a significant better response on growth performance. In a third trial, efficacy of LauL was compared with commercial products that limit bacterial activity in the intestinal tract (Aromabiotic Poul 60) or coccidiosis (chemical coccidiostat, Clinacox). None of the products were able to reduce the number or severity of lesions, and no effect on production performance was observed. Thus, despite the clear positive effect seen in experiment 1, and in experiment 2 with LauL doses higher than 0.15%, supplementing this lactylate to the diet does not consistently reduce C. perfringens colonization in broiler chickens because no such effects were observed in experiment 3. These results, however, provide a scientific basis for future studies to further investigate lactylates as potential additives to reduce the severity of necrotic enteritis in broilers in a C. perfringens challenge model.