Ulcerative colitis . Is it really an
autoimmune disease or something else ?
with Andreas Klein
Last month we saw that ulcerative colitis ( UC ) patients suffer continuing diarrhoea , ( unrelieved by over-the-counter medications ), and often pass blood and puss in their stool . This article was inspired by ground-breaking UC research done in 1980 by Australian Associate professor
MOVE
William Roediger now at the University of Adelaide . Up until this work researchers had been unable to find any ‘ microbe causing the mucosal changes ’ seen in UC or offer a satisfactory explanation for UC ’ s cause .
Roediger ’ s work gave us our first insight into a cause . Initially , let us define a few terms :
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1 . Epithelial cells are all the different cell types that make up our body ’ s mucous coverings
2 . Stem cells are primordial cells that live in most tissues . When any adult tissue cells die , these need to be replaced with new adult cells . Stem cells receive a signal to divide , to make new cells which then develop to become the adult cells that need to be replaced . Tissue stem cells can differentiate into most of the different cell types that a tissue requires to function properly .
3 . Goblet cells are adult cells living in mucosal tissue , such as the colon . They make and secrete the mucus that covers and protects all mucosal cells from microbes
4 . Mitochondria are tiny organelles inside cells . Their job is to burn fuels ( carbs , proteins , fats ) to make the energy that allows all cells to function .
When scientist examine the mucous membranes of UC patients ’ colons , they find that mitochondria inside mucosal / epithelial cells have difficulty making energy , stem cells of the colonic mucosa have difficulty becoming mature goblet cells and a lack of goblet cells leads to a depletion in the protective mucous covering , giving microbes access to “ unprotected ” mucosal cells .
In 1980 Roediger was the first to show that the colonic mucosal cells of UC patients have lost their ability to make energy from their normal fuel – a fat called butyrate , which is made by the colonic bacteria as they ferment fibre .
UC had up until this point had been defined as an “ autoimmune disease .” Roediger ’ s findings lead him to redefine UC as an “ energy deficiency disorder ” that specifically affects the mucosal cells that line the large intestine .
Energy production via respiration is the most efficient form of energy production in all body cells . Respiration involves cells burning fuels and producing carbon dioxide in the process . Roediger found the following :
1 . The cells harvested from nonulcerated normal tissue found between UC ulcer-lesions , in patients suffering acute UC , had great difficulty utilising oxygen to burn glucose or butyrate - they had difficulty using respiration to make cellular energy . Whilst colonic cells harvested from normal control patients and UC patients in remission used normal levels of oxygen to make energy .
Butyrate is the preferred fuel for energy production by ( most ) colonic mucosal cells . Colonic cells harvested from patients not suffering UC utilised butyrate easily to make energy in remission from UC were only able burn half the normal amount of butyrate ; suffering acute UC were completely unable to burn butyrate for energy . This finding suggests that energy production of UC patients has become abnormal .
2 . Normally , when healthy colonic mucosal cells use butyrate for energy production , in doing so , they produce ketone bodies , which are a type of fat . The amount of ketone bodies produced by colonic mucosal cells therefore shows how well they make energy from butyrate . Colonic cells harvested from patients not suffering UC produced normal levels of ketone bodies , in remission from UC produce significantly less ketone bodies and suffering acute UC produced truly little ketone bodies . This again suggests that energy production of UC patients has become abnormal .
3 . Unlike healthy patients , colonic mucosal cells of both UC patients in remission , and UC patients with acute UC , appear to only be able to use glucose ( not butyrate ) as a fuel and both produce excessive levels of lactic acid . The importance if this finding is that lactic acid is produced mainly when cells metabolise glucose non-aerobically ( i . e ., when glucose is not burnt in mitochondria using oxygen ). This finding suggests that colonic mucosal cells both from UC patients in remission and from UC patients suffering acute UC , have difficulty burning fuel aerobically ; they cannot utilise respiration for energy production because their mitochondria are not working properly .
The above suggests that colonic mucosal cells from UC patients seem to rely on anerobic energy production , with the cells from acute UC patients even more reliant on anerobic energy production than those from UC patients in remission .
According to Roediger , the key to the mystery of why the mitochondria of colonic mucosal cells from patients suffering acute or quiescent UC cannot make enough energy , has to do with a molecule called coenzyme A . Colonic mucosal cells can only burn fuels such as butyrate and glucose aerobically ( i . e . via respiration using oxygen ) when levels of coenzyme A are sufficiently high . Next month we will a look at why coenzyme A levels may be low in patients suffering from UC .
26 ISSUE 150 // NOVEMBER 2022 theindependentmagazine . com . au THE HAWKESBURY INDEPENDENT