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posted by mrpg on Thursday August 23 2018, @11:11AM   Printer-friendly
from the smoke-gets-in-your-brain dept.

Arthur T Knackerbracket has found the following story:

An international team of researchers has uncovered a destructive mechanism at the molecular level that causes a well-known phenomenon associated with obesity, called leptin resistance.

They found that mice fed a high-fat diet produce an enzyme named MMP-2 that clips receptors for the hormone leptin from the surface of neuronal cells in the hypothalamus. This blocks leptin from binding to its receptors. This in turn keeps the neurons from signaling that your stomach is full and you should stop eating.

This is the first time that a destructive molecular mechanism has been observed and described.

Scientists showed that when MMP-2 is blocked, leptin can still bind to the receptors and signal satiety. They hope that in the future, clinicians will be able to treat leptin resistance in humans by blocking MMP-2. They also have evidence that their findings have a broader scope.

-- submitted from IRC


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  • (Score: 2) by opinionated_science on Thursday August 23 2018, @03:22PM

    by opinionated_science (4031) on Thursday August 23 2018, @03:22PM (#725232)

    these articles are poorly thought out.

    Human metabolism can use glucose(glycogen) very effectively. The problem is glucose is *toxic*, so having more than you need will random kill cells e.g. nerve endings in your eye, or remote bit like your fingers and toes.... Excess blood glucose is controlled by insulin which stimulates capture and conversion to fat.

    Human metabolism can ALSO use fat very effectively, but it yields a higher energy at a slower pace. Excess fat, however can be dumped by the gallon using Bile salts produced by the liver. You may have to sit down for this one....

    In summary, it is NOT the super fatty causing the problem. It is because the effects on nutrition are masked by the inflammation caused by the "sugar" overload. And sugar is in *eveything* processed....

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