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posted by mrpg on Monday August 28 2017, @07:00AM   Printer-friendly
from the mice-were-happy-though dept.

Original article in Deutsches Zentrum für Diabetesforschung e.V. (DZD):

In mice that are given a high-fat diet, an increased production of the enzyme DPP4* by the liver promotes an increase in body fat, the development of fatty liver disease and insulin resistance. These were the findings of a current study by DZD-researchers in Potsdam and Tübingen. "In combination with our observations from additional human and cell studies, these results indicate that increased DPP4 production by the liver is the cause rather than the consequence of a fatty liver and insulin resistance," says the head of the study, Annette Schürmann from the German Institute for Human Nutrition Research (DIfE), a partner of the German Center for Diabetes Research (DZD). The research team led by Schürmann has now published its findings in Molecular Metabolism.

"DPP4 inhibitors** are well known from the treatment of diabetes. Therefore, in our opinion, they could be used in the future not only to improve the sugar metabolism but also to treat non-alcoholic fatty liver disease***," adds the lead author of the study, Christian Baumeier from DIfE.

[...] In addition, the scientists observed that human beings suffering from insulin resistance and non-alcoholic fatty liver disease have a greater amount of active DPP4 in their blood than healthy people.

Background information:

* DPP4 is the acronym for dipeptidyl peptidase 4. The enzyme cleaves, among others, some intestinal hormones (incretins) glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptides (GIP), which as a result lose their effectiveness. This leads to high blood glucose values; the function of the insulin-producing cells in the pancreas is also negatively influenced.

** DPP4 inhibitors are already used as a drug in the treatment of diabetes in order to prolong the effect of the two endogenous incretins GLP-1 and GIP. Their aim is to increase insulin secretion after food intake in people with type 2 diabetes.

*** Non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in Europe and the United States and a frequent side effect of obesity and type 2 diabetes. Depending on the country, around 25 to 45 percent of adults are affected. Left untreated, a fatty liver can develop into liver cirrhosis with life-threatening consequences. Complete remission is possible, with weight reduction playing a major role (sources: the present study by Baumeier et al., 2017, and Deutsches Ärzteblatt, volume 111; issue 26; June 27, 2014).

-- submitted from IRC


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  • (Score: 2, Insightful) by The Mighty Buzzard on Monday August 28 2017, @10:01AM (4 children)

    By which, of course, I mean "correlation is not causation". Unless they've got more going on than was reported, I gotta call bullshit. It sounds more like guesswork than proven theory to me and I don't want medicated by guesswork if it's all the same to you.

    --
    My rights don't end where your fear begins.
    • (Score: 1, Informative) by Anonymous Coward on Monday August 28 2017, @10:55AM (2 children)

      by Anonymous Coward on Monday August 28 2017, @10:55AM (#560149)

      "In combination with our observations from additional human and cell studies, these results indicate that increased DPP4 production by the liver is the cause rather than the consequence of a fatty liver and insulin resistance"

      I'm sure you reviewed their cell studies didn't you, Blizzhard?

      • (Score: 5, Touché) by c0lo on Monday August 28 2017, @11:53AM

        by c0lo (156) Subscriber Badge on Monday August 28 2017, @11:53AM (#560171) Journal

        I'm sure you reviewed their cell studies didn't you, Blizzhard?

        Given that he's rarely wrong (and always unrepentant), I trust that he did more than that: reproduced the experiment but disproved the causation - the paper is pending, any time soon.

        (grin)

        --
        https://www.youtube.com/watch?v=aoFiw2jMy-0 https://soylentnews.org/~MichaelDavidCrawford
      • (Score: 3, Funny) by The Mighty Buzzard on Monday August 28 2017, @02:08PM

        Sorry, no. Flawed methodology if that's what they're going off of. The proper method would be to introduce elevated levels of DPP4 into the mice artificially and contrast that with a control group that was otherwise identical. Don't try to out-science me, boy.

        --
        My rights don't end where your fear begins.
    • (Score: 1, Insightful) by Anonymous Coward on Monday August 28 2017, @06:40PM

      by Anonymous Coward on Monday August 28 2017, @06:40PM (#560393)

      I think this one is a 5 step process instead of the traditional 3 steps. At first glance, steps 1 and 2 may seem superfluous, suggesting the traditional 3 step process, but IANASomethingorother.

      1. Fat makes you fat!
      2. Sugar makes you fat! Fat doesn't make you fat!
      3. Fat makes you fat! ← You are here
      4. ???
      5. Profit! (for big pharma when they start making skinny pills)

  • (Score: 1, Insightful) by Anonymous Coward on Monday August 28 2017, @06:45PM (1 child)

    by Anonymous Coward on Monday August 28 2017, @06:45PM (#560398)

    For those wondering if it applied to low carb diets,
    "(HFD, 45 kcal% fat, 35 kcal% carbohydrates and 20 kcal% protein, D12451, Research Diets) for 27 weeks.",
    the carbs were still considerable.

    By the way here is a direct link to to the study, for those who enjoy reading the science directly and not the summary:
    http://www.molmetab.com/article/S2212-8778(17)30531-8/fulltext [molmetab.com]

    • (Score: 0) by Anonymous Coward on Monday August 28 2017, @07:33PM

      by Anonymous Coward on Monday August 28 2017, @07:33PM (#560437)

      yes, the whole study is unnecessary and misleading. they basically set the test subjects up to get the results they got. "let's replicate the American diet and verify the enzyme responsible for this mechanism". big deal. if you eat a bunch of fat while still eating carbs, sugar and protein in high percentages then the fat won't be used for fuel and will build up and cause side effects like insulin resistance. that is the whole point of gong on a ketogenic diet! you drastically reduce the carbs, protein and sugar and your body burns the fat for fuel like it's supposed to. i like how they are representing this study in a way to further their propaganda.

      let's strip all the good (and more expensive) fuel out of the food, "tell them fat is what is making them fat, water the shit down(pasteurized, skim "milk") or substitute the cheapest pig slop we can make and they'll even eat more of it because they never get full! Whahahaha!" "they'll also die of a long list of degenerative diseases like cancerous little piggies n their pens"

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