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Digestive Enzymes Leak out of the Intestine and cause Loss of Cell and Tissue Functions
We investigate a mechanism for aging due to tissue autodigestion. Immunohistochemistry, reveals in old, but not in young, the accumulation of pancreatic trypsin, elastase, lipase, and amylase in numerous organs including the mesentery, liver, lung, heart, kidney, brain, and skin.
The mucin layer in the mucosal barrier of the small intestine is attenuated in the old and does not fully repair itself after each meal.
The Mucin layer on villi in the small intestine of young and old.
Accumulation of Pancreatic Trypsin in the heart muscle of young (4 months) and old (24 months)
Pancreatic trypsin leaks across intestinal villi with depleted mucin.
The accumulation of digestive enzymes in the old is accompanied by global damage to collagen.
Proteolytic cleavage of the extracellular domain of the insulin receptor causes insulin resistance and hyperglycemia in the old.
Blockade of pancreatic trypsin in the old by a two-week oral treatment with a serine protease inhibitor reduces trypsin accumulation, collagen damage, as well as insulin receptor cleavage, and hyperglycemia. More
Our measurements support the idea that the breakdown of tissues in aging is due to autodigestion and a side-effect of the fundamental requirement for digestion.
Our measurements support the idea that the breakdown of tissues in aging is due to autodigestion and a side-effect of the fundamental requirement for digestion.
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