When The Primary Brain Is Plagued: Diabetes As Predominantly An Intestinal Disease

Discussion in 'Cancer, Degenerative Diseases' started by Amazoniac, Sep 24, 2019.

  1. Amazoniac

    Amazoniac Member

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    As you can tell from the title, those are not my words, they're Butcher's (Koch, 1926), and to be more specific, only in obedience to microbial commands, whose cells outnumber ours by a factor of 10. What if there are indeed racialist strains that thrive on skin color rather than their favorable conditions?

    - Diabetes is predominantly an intestinal disease

    "The connection between gut microbiota and energy homeostasis and low-grade inflammation contribute to dysregulation of normal glucose tolerance. In animals models, altered gut microbiota led to development of obesity, insulin resistance, and diabetes by altered fatty acid metabolism in adipose tissue and liver, modulation of gut peptide YY and glucagon-like peptide (GLP)-1 secretion, activation of the lipopolysaccharide toll-like receptor-4 axis, and modulation of intestinal barrier integrity by GLP-2.[1] Gut bacteria were recently proposed to contribute to differences in body weight, insulin sensitivity, glucose metabolism, and other cardiometabolic risk. A recent study by Karlsson et al., found that the gut microbiome with abundance of particular bacterial species in the gut could differentiate diabetic vs normal glucose tolerant individuals with a degree of accuracy similar to that of traditional predictive models. The bacterial species most predictive of T2D was not consistent across different ethnic groups.[2]"

    "Diabetes rapidly resolves following Roux-en-Y gastric bypass (RYGB) and biliopancreatic diversion (BPD). A meta-analysis of 136 studies with 22,094 patients demonstrated that T2DM resolved completely in 76.8% and resolved or improved in 86.0% of patients who had undergone bariatric surgery.[8] Complete remission of diabetes occurs in 48% of patients after laparoscopic gastric banding, 84% after RYGB, and 95% after BPD. Diabetes remission after RYGB and BPD is also durable, and recurrence of diabetes 10 years after surgery is rare. RYGB and BPD can cause complete remission of diabetes in days to weeks, long before substantial weight loss; whereas diabetes remission after laparoscopic gastric banding typically occurs over weeks to months, consistent with weight loss.[8]"

    "[An hypothesis proposes that] the exclusion of the duodenum and proximal jejunum from the transit of nutrients may prevent secretion of a putative signal that promotes insulin resistance and T2DM."

    "Recent experimental studies have suggested the rearrangement of GI anatomy as a primary mediator of the surgical control of diabetes. A study in diabetic Goto-Kakizaki (GK) rats that supports the proximal hypothesis, showed that enhancing delivery of nutrients to the hindgut without excluding nutrient flow through the proximal intestine (via a simple gastrojejunostomy (GJ)) does not improve diabetes.[9] But duodenal-jejunal bypass (DJB), with similar shortcuts of nutrients as in GJ, also includes the exclusion of the proximal intestine from the flow of nutrients, improved glucose tolerance, and fasting glycemia.[9] Glucose intolerance returned when DJB was reversed, even though the GJ was preserved. This experiments shows that the exclusion of the duodenum is critical for the effect on diabetes. However, preventing duodenal passage of nutrients by GI bypass improves glucose tolerance only in patients with diabetes, but is detrimental for glucose homeostasis when performed in nondiabetic humans (i.e. surgical exclusion of the duodenum for the treatment of peptic ulcer or gastric cancer).[8] Therefore, T2DM might be characterized by a component of duodenal-jejunal dysfunction."

    "In spite of many patients remaining overweight or frankly obese more than 80 and 90% of RYGB and BPD patients, respectively have a complete sustained remission of T2DM.[10] Consider in terms of its ability to induce disease remission, RYGB (and BPD) appear more effective in treating diabetes than obesity. A recent study showed that changes in the metabolism of the Roux limb itself may play a direct role in the improvement in glucose homeostasis after RYGB by remodeling and reprogramming intestinal glucose disposal and metabolism triggered by exposure of the Roux limb to undigested nutrients.[11]"​

    Source of Support: Nil ✓
    Conflict of Interest: None declared ✓
    Credibility from underdeveloped (and thus uncorrupted) origin: Acceptable ✓
     
  2. OP
    Amazoniac

    Amazoniac Member

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    upload_2020-4-11_15-17-3.png
    Source: the internet.
     
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