3 ms·

This is fascinating. I've always thought of type 2 diabetes as a disease of the pancreas, rather than a disease of the intestine. I found this abstract from 201

by pohl 8y ago

This is fascinating. I've always thought of type 2 diabetes as a disease of the pancreas, rather than a disease of the intestine. I found this abstract from 2013 interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830370/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3830370/ "...A growing body of evidence, however, appears to indicate that type 2 DM (T2DM) may be an operable intestinal illness—a novel revolutionary concept about an old disease."

gumby 8y ago
Diabetes is a disease (like most) characterized by symptom rather than case. If you have excess glucose in the blood it could be because you aren’t producing adequate insulin or because the cells aren’t taking it up properly (or combo). It’s somewhat easy to figure out which but the standard of care for adults exhibiting DM in the US is simply to assume it is insulin resistance.
- 0x8BADF00D 8y ago
  There’s definitely a role for mitochondrial dysfunction as well. If you store excess fat in the liver, consume sugar while overfeeding (eating at surplus of TDEE), your mitochondria will start to dysfunction w.r.t. energy.
  - gumby 8y ago
    what's the mechanism here?
    - 0x8BADF00D 8y ago
      IANAD, but based on the literature I’ve read, there are two negative feedback loops[0][1]. The first involves skeletal muscle uptake of insulin. Mitochondria in skeletal muscle will not efficiently use glycogen stores. Insulin is released inappropriately by the pancreas due to excess glucose. Body thinks we are in a catabolic state (we must be because insulin was released) so fatty acid oxidation is inhibited. Liver converts lactate into glucose, exacerbating the original mitochondrial dysfunction (what happens when you introduce too much energy into a system that cannot use it?). The second negative feedback loop involves insulin/glucagon and leptin/ghrelin. Since your body thinks it’s starving (when in reality it cannot use energy efficiently), ghrelin will be secreted. So you keep getting hungry, no matter how much you eat, and insulin spikes as a result of insulin resistance. Leptin is effectively silenced, removing the body’s ability to feel sated. [0]http://semmelweis.hu/biokemia/files/2014/09/EN_con_INS12_Mitochondria-and-diabetes2005.pdf http://semmelweis.hu/biokemia/files/2014/09/EN_con_INS12_Mit... [1]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824521/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824521/
qwerty456127 8y ago
> I've always thought of type 2 diabetes as a disease of the pancreas, rather than a disease of the intestine. It seems just so many diseases of whatever actually are diseases of the intestine and originate from unhealthy intestinal microbiome. This example is a yet another proof. Whoever interested in using this idea to improve/save their health should read Dr. Kellman's microbiome diet book (it's fairly well written, exciting, practical and includes a fair amount of references to scientific research).

by pohl 8y ago

gumby 8y ago

Diabetes is a disease (like most) characterized by symptom rather than case. If you have excess glucose in the blood it could be because you aren’t producing adequate insulin or because the cells aren’t taking it up properly (or combo). It’s somewhat easy to figure out which but the standard of care for adults exhibiting DM in the US is simply to assume it is insulin resistance.

0x8BADF00D 8y ago
There’s definitely a role for mitochondrial dysfunction as well. If you store excess fat in the liver, consume sugar while overfeeding (eating at surplus of TDEE), your mitochondria will start to dysfunction w.r.t. energy.
- gumby 8y ago
  what's the mechanism here?
  - 0x8BADF00D 8y ago
    IANAD, but based on the literature I’ve read, there are two negative feedback loops[0][1]. The first involves skeletal muscle uptake of insulin. Mitochondria in skeletal muscle will not efficiently use glycogen stores. Insulin is released inappropriately by the pancreas due to excess glucose. Body thinks we are in a catabolic state (we must be because insulin was released) so fatty acid oxidation is inhibited. Liver converts lactate into glucose, exacerbating the original mitochondrial dysfunction (what happens when you introduce too much energy into a system that cannot use it?). The second negative feedback loop involves insulin/glucagon and leptin/ghrelin. Since your body thinks it’s starving (when in reality it cannot use energy efficiently), ghrelin will be secreted. So you keep getting hungry, no matter how much you eat, and insulin spikes as a result of insulin resistance. Leptin is effectively silenced, removing the body’s ability to feel sated. [0]http://semmelweis.hu/biokemia/files/2014/09/EN_con_INS12_Mitochondria-and-diabetes2005.pdf http://semmelweis.hu/biokemia/files/2014/09/EN_con_INS12_Mit... [1]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824521/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824521/

qwerty456127 8y ago

> I've always thought of type 2 diabetes as a disease of the pancreas, rather than a disease of the intestine. It seems just so many diseases of whatever actually are diseases of the intestine and originate from unhealthy intestinal microbiome. This example is a yet another proof. Whoever interested in using this idea to improve/save their health should read Dr. Kellman's microbiome diet book (it's fairly well written, exciting, practical and includes a fair amount of references to scientific research).