The effects of 3 sweeteners on growth performance, serum biochemicals, and jejunal physiological functions of broiler chickens was investigated in a study that took place at Nanjing Agricultural University in China.
Taste is mediated by taste receptors, and in mammals, sweet substances could bind with the sweet taste receptors on the taste buds and induce the sweet signal transduction. Sweet taste receptors in mammals consist of taste receptor family 1 member 2 (T1R2) and taste receptor family 1 member 3.
Interestingly, T1R2 is missing in chickens. An increasing number of studies in mammals have suggested that sweeteners not only induce the sense of sweet taste but also exert additional biological functions in the gastrointestinal tract. Stevioside (STE) has been proven to exhibit anti-inflammatory activity in intestinal cells. Sucralose (SUC) could reduce the beneficial bacteria in the gastrointestinal tract of rats. Few studies have been focused on the physiological relationship between sweeteners and gastrointestinal tract in chickens.
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In this study, a total of 192 day-old male Ross 308 broiler chicks were randomly divided into 4 treatments with 6 replicates for each treatment. The treatments, which lasted for 21 days, were basal diet (CON), a basal diet supplemented with 250 mg/kg stevioside (STE), a basal diet supplemented with 100 mg/kg sucralose (SUC), and a basal diet supplemented with 600 mg/kg saccharin sodium (SAC).
The results showed that dietary STE supplementation increased (P < 0.05) growth performance, serum total protein, serum albumin, and jejunal antioxidant capacity of broiler chickens. This suggests that STE could potentially be applied as a growth-promoting and antioxidant feed additive in broiler chickens.
Both SUC and SAC supplementation decreased (P < 0.05) serum total protein and albumin. Dietary SAC supplementation impaired the intestinal integrity, permeability, and mucus layer of the jejunum in broiler chickens. In addition, SAC supplementation elevated (P < 0.05) the transcription expression level of jejunal bitter taste receptors and induced excessive jejunal apoptosis.