No abstract is available for this editorial. but a brief section is reproduced here.
Feeding mice high-fructose corn syrup, a widely used sweetener in human diets, has been found to drive an increase in the surface area of the gut that is associated with enhanced absorption of dietary nutrients and weight gain.
The incidence of obesity has been steadily increasing, tripling globally between 1975 and 2016, at a high cost to public health1. Obesity predisposes individuals to various diseases, including cancer, and the number of obesity-associated deaths globally each year1 (estimated at 2.8 million) is similar in scale to the reported COVID-19-associated deaths in the ongoing pandemic.
Although fat-rich diets have taken much of the blame for the rise in obesity, excess consumption of processed sugars, and high-fructose corn syrup (HFCS) in particular, is strongly implicated in diet-induced obesity. Whether and how fructose causes obesity in humans remains a hotly debated question2,3.
In a report in Nature that should make one think twice before gulping down sugar-sweetened drinks with fatty snacks, Taylor et al.4 propose that HFCS promotes obesity by boosting the ability of the intestine to absorb nutrients.
Evidence has emerged5–8 that the small intestine acts as the gatekeeper for the mammalian body against the harmful effects of fructose, the main one being the aberrant accumulation of fat (termed steatosis) in the liver.
Moderate amounts of fructose — for example, those ingested when consuming fruits — are taken up and broken down by intestinal cells. Excess amounts, such as those that might be ingested after drinking a sugary beverage, overwhelm the intestine’s absorptive capacity and the fructose either ‘leaks’ into the bloodstream to reach the liver intact, or it spills over from the small intestine and reaches the colon5.
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