A new mechanism by which the consumption of sugar causes obesity and metabolic syndrome is reported in Nature Communications this week. The work suggests that the metabolic conversion of glucose into fructose in the liver is a key step in the development of glucose-induced obesity, insulin resistance and fatty liver in mice.
Consumption of carbohydrates with a high glycemic index, such as glucose, causes weight gain and metabolic problems, but the mechanism by which this occurs is not fully understood. Richard Johnson and colleagues suggest that fructose, rather than glucose, may be the culprit. They created two types of mice that either cannot convert glucose into fructose, or cannot degrade fructose in the liver. They then fed these mice a glucose-rich diet for 10 weeks. As opposed to their normal counterparts, both strains of mice were resistant to weight gain, did not develop fatty liver and had normal metabolic parameters.
Whether the hepatic generation of fructose also has a role in the development of obesity and metabolic syndrome in humans remains to be tested.
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