Magazine article Science News

Altered Mice Stay Svelte on High-Fat Diet. (Let Them Eat Cake)

Magazine article Science News

Altered Mice Stay Svelte on High-Fat Diet. (Let Them Eat Cake)

Article excerpt

A protein that links gluttony and weight gain may be a novel target for antiobesity drugs. Mice lacking this protein can indulge in fatty food but remain as slim as mice on a lower-fat diet, a new study reports. The finding suggests a new avenue to help morbidly obese people lose weight.

When food is scarce, stockpiling energy in fat cells is a survival advantage. But when food is plentiful, as in industrialized countries, genes that promote fat storage lead to obesity (SN: 4/14/01, p. 238). The molecular mechanisms that translate extra calories into fat deposition are largely unknown.

Now, researchers at Kyoto University in Japan have identified a key pathway in the process. Scientists have long known that the hormone called gastric inhibitory polypeptide (GIP) is secreted into the bloodstream by the small intestine in response to ingested foods, particularly fatty ones. GIP binds to cell-surface receptors on distant fat cells, signaling food intake.

In an upcoming Nature Medicine, the Kyoto team shows that if this sequence is disrupted, mice burn excess fat rather than store it, and they become obesity resistant.

Previous research focused on GIP's effect on pancreas cells, not on fat cells, notes Yuichiro Yamada, one of the new study's authors. Because the hormone boosts insulin release from pancreatic cells, scientists have long speculated on a role for GIP in type II diabetes, which is marked by an inefficient response to insulin. But the new study is the first to clearly link GIP and obesity, Yamada and his colleagues say.

The scientists genetically engineered mice to lack the GIP receptor. When fed a high-fat diet during their first year, unaltered mice became obese and developed insulin resistance, a precursor to diabetes. GIP-receptor-deficient mice remained lean and responsive to insulin. …

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