Experimental results in the use of dimethylglycine sodium (na-dmg) taminizer-d® in broilers

N,N Dimethylglycine sodium (Na-DMG) is a tertiary amino acid, which is an intermediary metabolite in the path of Coline, formed in the liver mitochondria by elimination of a methyl group of betaine (Friesen et al., 2007). It can be metabolized in the liver at mitochondria level, causing both methyl groups to be transformed by transmethylation in tetrahydrofolate and generating free glycine (Mackenzie & Frisell, 1958; Slow et al., 2004). It is a small, water-soluble molecule, lipophilic enough to be rapidly absorbed across cell membranes. It is likely to be absorbed quickly and completely when administered orally (Cupp & Tracy, 2003). Huchzermeyer & De Ruyck (1986) suggest a free radical capture potential of DMG, as evidenced by a significant reduction in plasma and tissue at the level of species reactive to thiobarbituric acid (TBARS) (Yagi, 1984). Non-esterified fatty acids cause dysfunction of the endothelium (Avogaro, 2003), among other biological functions, DMG is useful in improving the use of oxygen in muscle tissue and as a nutritional supplement to improve athletic performance in humans and race horses (Revised by Cupp & Tracy, 2003;) (Holley & Cheeseman, 1993). Data are available on broilers, showing a significant improvement in the digestibility of carbohydrates and proteins when a control diet supplemented with 167 mg Na-DMG/kg was administered Na-DMG/kg (Kalmar et al.,). The improvement of digestibility coefficients achieved through the addition of an emulsifier to the diet occurs because non-fatty nutrients isolate by lets of fat and, therefore, become more accessible to the digestive enzymes and their absorption in the small intestine. This study showed that Na-DMG significantly reduces the plasma levels of non-esterified fatty acids (NEFA). The effects observed on digestibility are in line with data by Dierick & Decuypere (2004), in the sense that, beside the use of an emulsifier added to the diet during the growth stage, showing significant improvement in non-fatty AFD fractions, there is scientific evidence that the biological action of Na-DMG has a positive effect on breeder production parameters, is non-toxic to DL10 and does not accumulate in the bird, leaves no residues in poultry meat for consumption and is friendly with the environment. There is great public concern over nitrogen pollution in surface waters caused by livestock production and the high costs for the removal of manure (EFSA, 2011), Na-DMG offers a reduction in the excretion of stools and nitrogen from urine, as well as a decrease in the cost of food (Nahm, 2007). In addition, Kalmar et al. demonstrate the protective effect of DMG in the diet against the development of pulmonary hypertension syndrome, or ascites, which is related to the effects of diet and to environmental effects (Leenstra & Cahaner, 1991; Malan et al., 2003). The worldwide perspective of the pulmonary hypertension syndrome will remain constant based on the genetic evolution of birds (Decuypere, 2008). The speed of growth and feed conversion of broilers in the future, based on high energy diets, the pressure on the costs of raw materials and the search for value added will be the most critical factor to be solve, based on different intestinal function improvement options (Cools et al., in preparation; Newman et al., 2002).

The use of N,N-Dimethylglycine sodium can improve the production parameters, carcass performance, muscle mass, and reduce injuries by ascites in broilers.

            I.    Identify and assess the optimal dose of Na-DMG by means of three treatments, T0, T500, T1000.

            II.    To determine and assess the effect of Na-DMG in production parameters in broilers, heart ascitis index (HAR), viability and weight.

            III.    To identify and assess the effect on carcass performance, especially in regard to the pectoral muscles, thigh and leg.

            IV.    Identify and assess the effect of Na-DMG in idiopathic ascites in broilers.

An environmentally controlled booth, 6 meters (front) by 3 m (deep), total surface area 18 m² was used in Cadereyta, Querétaro, Mexico. We assessed the performance of Na-DMG and its effect as an additive treatment, administered orally in commercial feed, in two levels of inclusion, T500, T1000 and four phases, pre-initiator, initiator, growth, and final (AOAC 1984); National Research Council 1994) (Table 1). Start date of the experiment: October 11, 2010; completion date: November 27, 2010, age of the birds 47 days to slaughter house.

Table 1. Results of commercial diet nutritional composition

      I.            90 one-day-old Ross308 commercial chicks, mixed.

      II.            Mixing technique and level of inclusion of Na-DMG.

      III.            Three levels of treatment: T0, T500, T1000 ppm.

      IV.            Feeders and troughs of initiation, and final stage

      V.            Evaluation of performance results against standard Ross 308 (Ross 2009a; 2009b; 2009c; 2009d) and commercial zone Bajío, Mexico and NRC (1994).

                     a.     Weight gain daily, weekly and cumulative.

                     b.     Food consumption per day, week, and cumulative.

                     c.     Feed conversion per day, week, cumulative (FCR).

                     d.     Mortality and viability, day, week, and cumulative.

                     e.     Calculation of metabolizable energy by stage (Table No 1).

                     f.       Measurement of thermal factors, thermo-neutrality curves.

                    g.     Internal return rate (IRR) of investment by the use of (Na-DMG).

                    h.     Heart ascitis index (ICA), if ascites present.

     VI.            Water quality (solids, ppm).

     VII.            Effect in pigmentation using Minolta equipment.

     VIII.            Without biological agents (vaccines) or prophylactic or healing treatments.

     IX.            Evaluation of production parameters, body weight (BW).

      X.            Feed Conversion Rate (FCR)

    XI.            Nine batches of 10 birds each, with two levels of treatment, three repetitions each.

   XII.            Evaluation of the heart ascites index (ICA) with two levels of treatment of Na-DMG.

Until the fourth week of treatment significant differences (p < 0.05) are observed, in favor of the treated groups. In the fifth and sixth week the groups have a similar average (p > 0.05); differences are manifest in week 7. Due to the observed variability a randomized block design was applied.

The group that received T1000, statistically performs better than the control group (p < 0.05).

Feed conversion increases as the number of days increases. The average conversion rate is statistically significant (p < 0.05) among all treatments; being lower in T1000 and higher in T0 (Table 2).

Table 2. Feed conversion results by treatment (Total male and female)

The exponential regression model is the model that better explains bird growth in each treatment, according to the parameters of the model in each treatment, the weight expected on day 49 surpasses that of the control group by 43 g and 42 g.

In terms of carcass weight, the treated groups statistically exceed the control group (p< 0.05), however T500 and T1000 are statistically equal. Breast: The weight of the breast is significantly different in each group (p < 0.05) and is greater in the T1000 group. Thigh and leg: The weight of legs and thighs is significantly (p < 0.05) greater in T500 and T1000, compared to the T0 groups; however T500 and T1000 do not differ (p > 0.05). Carcass: The carcass weight is significantly (p < 0.05) higher in the control group. The T500 and T1000 groups do not differ (p > 0.05). Wings: The weight of the wings in the T1000 group is significantly lower (p < 0.05) than in groups T500 and T0; groups T500 and T0 do not differ (p > 0.05). Head and Tarsus: Weight of tarsus and head in the T1000 group, is significantly lower (p < 0.05) than in groups T500 and T0, whereas T500 and T0 do not differ (p > 0.05).

The total mortality caused by ascites was 5.4% (six birds), two during the experiment and four in the slaughterhouse. Birds without treatment of N,N-Dimethylglycine sodium developed ascites injuries early, and injuries were more severe than I treated birds and among the treated birds, it was observed that with dosage increase injuries were less severe (Table 3).

Table 3. Ascites Heart Index in six birds that died of ascites syndrome

        I.            The use of N.N-Dimethylglycine sodium suggests that it can improve performance results, carcass performance, especially in regard to the pectoral muscles and reduce the negative effect of idiopathic ascitis in broilers.

      II.            Further research on these results at the industrial level is needed to confirm its effect as a promoter and its qualities.

AOAC. 1984. Official methods of Analysis of the Association of Official Analytical Chemist International. In: S. Williams (ed.), 14th edn. AOAC International, Virginia, USA.

Avogaro A, De Kreutzenberg S, Kiwanuka S, Tiengo. 2003. Nonesterified fatty acids and endothelial dysfuntion. International Congress Series 1253:l39-145.

Cools A, Maes D, Buyse J, Kalmar I, Vandermeiren JA, Janssens GPJ. Effect of N,N-dimethylglycine supplementation in parturition feed of sows on metabolism, nutrient digestibility and reproductive performance: (in preparation).

Cupp MJ & Tracy TS. 2003. Dimethylglycine (N,N-dimethylglycine). pp. 149-160. In: M.J. Cupp, T.S. Tracy (eds). Dieteray supplements. Toxicology and clinical pharmacology, Humana Press, New Jersey.

Decuypere E. 2008. Ascites syndrome in broilers: physiological and nutritional perspectives. Avian pathology 37:117-126.

European Food Safety Authority (EFSA). 2011. Scientific Opinion on the safety and efficacy of (dimethylglycine sodium salt) as a feed additive for chickens for fattening, Parma, Italy. EFSA Journal 9(1):1950.

Friesen RW, Novak EM, Hasman D, Innis SM. 2007. Relationship of dimethylglycine, choline, and betaine with oxoproline in plasma of pregnant women and their newbom infants. Journal of Nutrition 137:2641-2646.

Holley AE & Cheeseman KH. 1993. Measuring free-radical reactions in-vivo. British Medical Bulletin 49(3):494-505.

Huchzermeyer FW & De Ruyck AMC. 1986. Pulmonary hypertension syndrome associated with ascites in broilers. Veterinary Record 119:94-94.

Kalmar LD, Cools A, Buyse J, Roose P, Janssens GPJ. Dietary N,N-dimethylglycine supplementation improves nutrient digestibility and attenuates pulmonary hypertension syndrome in broilers. Journal of Animal Physiology and Animal Nutrition, submitted (JAP AN-Oct-09-269).

Leenstra FEL & Cahaner A. 1991. Genotipo por interacciones de medio ambiente utilizando valores, pollos magra o grasa, procedentes de los Países Bajos e Israel, planteadas a temperatura normal o baja. Ciencia de las aves de corral 70:2028-2039.

Mackenzie CG & Frisell WR. 1958. The metabolism of dimethylglycine by liver mitochondria. Journal of Biological Chemistry 232(1):417-427.

Malan DD, Scheele CW, Buyse J, Kwakernaak C, Siebrits FK, Van Der Klis JD, Decuypere E. 2003. Metabolic rate and its relationship with ascites in chicken genotypes. British Poultry Science 44:309-315.

Nahm KH. 2007. Feed formulations to reduce N excretion and ammonia emission from poultry manure. Bioresource Technology 98:2282-2300.

National research Council (NRC). 1994. Nutrient requirements ofpoultry. 9th rey. edn.,National academy Press, Washington D.C.

Newman RE, Bryden WL, Fleck E, Ashes JR, Buttemer WA, Storlien LH, Downing JA. 2002. Dietary n-3 and n-6 fatty acids alter avian metabolism: metabolism and abdominal fat deposition. British Journal of Nutrition 88(1):11-18.

Ross 2009a. Broiler manual. URL:http://www.aviagen.com

Ross 2009b. Broiler manual - Nutrition specifications. URL:http://www.aviagen.com

Ross 2009c. Broiler performance objectives. URL:http://www.aviagen.com

Ross 2009d. Tech note ascites Effective Management Practices to Reduce the Incidence of Ascites in broilers. URL:http://www.aviagen.com

Slow S, McGregor DO, Lever M, Lee MB, George PM, Chambers ST. 2004. Dimethylglycine supplementation does not affect plasma homocysteine concentrations in pre- dialysis chronic renal failure patients. Clinical Biochemistry 37:974-976.

Yagi K. 1984. Assay for blood plasma or serum. Methods in Enzymology 105:328-331.