Not sure on the direction here, but those papers got me curious of what the effects of protease's would be on sugar or visa-versa. This popped up: www.plantphysiol.org/content/125/3/1485.full
"In plants, under sugar deprivation, proteins have been shown to be degraded, thus supplying carbon skeletons to respiration and biosynthetic processes"
"The induction of proteases may be reversed by the addition of sugars in the incubation medium (James et al., 1993; Chevalier et al., 1995). This suggests that the expression of these proteins is directly related to the supply of sugars to the cell."
And a caution to messing around with protease inhibitors: www.thebody.com/content/art13559.html
I just found it interesting that although it has to do with plants, sugar deprivation was causing proteins to be degraded - and this of course lead to the thought about
diet high in sugar and carbs and an increase in bacteria and proteases from bacteria eating the sugars and well.. I have no idea. Just found it an interesting statement.
Also gets me thinking about
a sugar deprivation possibly leading to the breakdown of protein in the structure of the mucus web or something...
Also - I found this very, very interesting in regards to the infiltration of Neutrophils in the mucus of UC. Turns out Neutrophils secrete Proteases - It has to do with COPD - but at the same time... And Cysteine Proteases: pharmrev.aspetjournals.org/content/56/4/515.full#title51
Skip down to this section A. Neutrophil Elastase.
It also says:
B. Other Serine Proteases
Neutrophils also store two other serine proteases, cathepsin G and proteinase 3, in their specific granules (Rao et al., 1991). These other serine proteases have similar properties to NE and induce mucus secretion in a similar way (Sommerhoff et al., 1990; Witko-Sarsat et al., 1999). Proteinase-3 is potently expressed on the surface of neutrophils after activation with cytokines (Campbell et al., 2000). Proteinase 3 is potently inhibited by α1-AT (Duranton and Bieth, 2003), but it is only poorly inhibited by SLPI in comparison to NE, and indeed proteinase 3 destroys the activity of SLPI (Rao et al., 1993). The neutrophil elastase inhibitors currently in development also inhibit these other serine proteases (Ohbayashi, 2002).
C. Cysteine Proteases
Lysosomal cysteine proteases (cathepsins) may also be involved in COPD (Chapman et al., 1997; Turk et al., 2001). Cathepsin S expression is induced by IFN-γ in several cell types, including smooth muscle cells. Overexpression of IFN-γ induces emphysema in mice, and there is increased expression of cathepsins B, D, H, L, and S (Wang et al., 2000). Cathepsin inhibitors markedly reduce the emphysema induced in IL-13 transgenic mice, indicating the elastolytic potential of this cathepsin (Zheng et al., 2000). Several other cathepsins also have elastolytic activity, including cathepsins B, K, and L, which are expressed in alveolar macrophages (Reddy et al., 1995; Punturieri et al., 2000) and cathepsin W in CD8+ T cells (Linnevers et al., 1997). Cathepsins B, L, and S inactivate SLPI (Taggart et al., 2001).
The role of cathepsins in COPD is uncertain. Increased concentrations of cathepsin L have been detected in BAL fluid of patients with emphysema (Takeyabu et al., 1998), and alveolar macrophages from patients with COPD secrete more cysteine protease activity than macrophages from normal smokers or nonsmokers (Russell et al., 2002b). The endogenous inhibitors of cathepsins are cystatins and stefins, but little is known about
their role in COPD. Cystatin C concentrations are increased in BAL fluid of patients with COPD (Takeyabu et al., 1998).
Again I always find it intriguing that COPD and Cystic Fibrosis are so similar to IBD with regards to mucus changes and bacterial penetration and seem to involve all of the same problems. In COPD and CF the super thick mucus traps bacteria and they cannot be expelled because the mucus is to heavy - so many die from complications such as pneumonia.
Diagnosed Crohns-Colitis about
8 years ago - Past Meds: Antibiotics, Prednisone, Methotrexate, Remicade - Current Meds: No meds at the moment -Trying Amino Acid Balancing Therapy Actually achieved full clinical remission for about
2 years using Remicade, Diet (SCD) and Exercise
“The only person you're destined to become, is the person you decide to be"... wise words