Sucrose Limitation and Inulin Metabolism

Abstract

Obesity is associated with a low-grade inflammatory response, which among other things, is triggered by bacterial plasma lipopolysaccharide (LPS). A high-energy diet, increases the amount of LPS-producing gut microbiota, and increased LPS levels has been observed in obese individuals. By inducing changes in the gut microbiota by prebiotics, like inulin, it is possible to decrease the plasma LPS level. This is associated with the stimulation of bifidobacterial growth. We have designed a novel approach to address this issue of plasma LPS, by probioticly induce changes in the gut flora by genetically modifying a bacteria to produce plant originated inulin. We cloned the two genes encoding sucrose:sucrose fructosyltransferase (SST) and fructan:fructan fructosyltransferase (FFT) from the Jerusalem artichoke into a E. coli, where it will produce inulin by using sucrose as an acceptor molecules. In the future this construct should be introduced by a probiotic lactobacillus, into the gut.

Not a scientist? Here we present the translated version of our abstract.

Obesity and its related disorders are a worldwide problem that fx costs america billions of dollars each year. Literature suggests that a high-energy diet is the reason for obesity, not only because the body is unable to use all the energy, but in fact because the “bad” bacteria in your gut feeds on it. The jerusalem artichoke produces a sugar fiber called inulin, which apart from being non-digestible to humans, helps the good bacteria in the gut to grow and is beneficial in the prevention of colon cancer. From this information we decided to produce a beneficial (probiotic) bacteria that can convert table sugar (sucrose) into this inulin fiber. If we are successful in introducing this bacteria to the human gut, we can apply many beneficial aspects relating to obesity, such as decreased hunger, fat mass, body weight, inflammations and increased satisfaction from eating.

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