METFORMIN EFFECTS ON BROILER METABOLISM

Authors: Rosebrough, Robert; ASHWELL, CHRISTOPHER - ARS, RETIRED

Submitted to: International Journal for Vitamin and Nutrition Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/3/2005
Publication Date: 3/3/2005
Citation: Rosebrough, R.W., Ashwell, C. 2005. Dietary metformin effects on in vitro and in vivo metabolism in the chicken. Nutrition Research. 25:491-497.

Interpretive Summary: Excess fat production in the modern broiler accounts for an annual loss to the poultry industry of 800 to 950 million dollars annually. The original source of this problem relates to selection genetic practices that emphasized rapid growth at the expense of other carcass characteristics. At least part of the genetic component appears to be an aberrant appetite control mechanism. This study describes methods to chemically control appetite by modulating blood glucose and lactate. In conclusion, our modality of metformin administration (inclusion in the diet) did not change plasma glucose of birds. It should be noted that this affect may be specific to chronic dosing that introduces metformin to intermediary metabolism at a fixed rate. In contrast, metformin did increase plasma lactate which might indicate a change in the flux rate of metabolites through glycolysis, altering feed intake by some sort of feed back inhibition. The decrease in lipogenesis accompanying dietary metformin does support a restriction in lipogenic substrates.

Technical Abstract: Birds were fed diets containing 0, 0.25, 0.5 & 1 and 0, 2.5, 5 & 10 g metformin/kg diet in two separate experiments to determine if metformin (1,1 dimethylbiguanidine hydrochloride) regulated plasma glucose and, possibly, feed intake in broiler chickens. Feed intakes in the first experiment were equal, but, in the second experiment, metformin at 5 and 10 g/kg reduced feed intake. The first series of diets had no effect on plasma glucose and lactate. The second series of dietary treatments did not affect plasma glucose but did increase plasma lactate, uric acid and triglycerides linearly. In the second experiment, there were significant decreases in lipogenesis that accompanied increasing doses of metformin. The increase in plasma lactic acid suggests that metformin stimulates pyruvate kinase in the bird, as it does in mammals. The lack of effect on plasma glucose also suggests that regulation occurs downstream of pyruvate in the bird. These findings may explain metformin's ability to reduce hepatic triglyceride synthesis and suppress appetite. On the other hand, chronic feeding of metformin does not elicit the same effects in birds that it does in mammals.