Fructose has been associated with the increased prevalence of obesity and non-alcoholic fatty liver disease. In the recent work by Jang et al. a stable isotope tracer approach was used to interrogate the flux and metabolism of fructose and glucose in mice. While some previous work had suggested fructose is primarily metabolized in the liver, this work shows that the primary site of metabolism is the intestine, but that this is saturable above 0.5 g/kg in mice, or they project about a 3 g fructose dose in humans. Below this limit, the majority of fructose is metabolized within the intestine with key end-products including glucose (~40%), lactate (~20%), and alanine (~10%). Interestingly, in contrast to hepatic gluconeogenesis, intestinal glucose production is enhanced in the fed state, suggesting that other foods can protect from fructose “escape” from the small intestine. This work suggests a reconsideration of both normal fructose metabolism, and its relationship to the pathogenesis of metabolic syndrome. In humans, clarifying the limit wherein fructose escapes the intestinal metabolism, and how that limit is modified by other components of a meal should answer some of these questions.
Fructose has been associated with the increased prevalence of obesity and non-alcoholic fatty liver disease. In the recent work by Jang et al. a stable isotope tracer approach was used to interrogate the flux and metabolism of fructose and glucose in mice. While some previous work had suggested fructose is primarily metabolized in the liver, this work shows that the primary site of metabolism is the intestine, but that this is saturable above 0.5 g/kg in mice, or they project about a 3 g fructose dose in humans. Below this limit, the majority of fructose is metabolized within the intestine with key end-products including glucose (~40%), lactate (~20%), and alanine (~10%). Interestingly, in contrast to hepatic gluconeogenesis, intestinal glucose production is enhanced in the fed state, suggesting that other foods can protect from fructose “escape” from the small intestine. This work suggests a reconsideration of both normal fructose metabolism, and its relationship to the pathogenesis of metabolic syndrome. In humans, clarifying the limit wherein fructose escapes the intestinal metabolism, and how that limit is modified by other components of a meal should answer some of these questions.
These comments are crossposted on the Faculty of 1000 at doi:10.3410/f.732607607.793543134.
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