Page 259 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Pancreas tent of the pancreatic juice (! C ). Trypsin in
the small intestinal lumen deactivates CCK re-
The exocrine part of the pancreas secretes lease via a feedback loop (! D). Secretin in-
1–2 L of pancreatic juice into the duodenum creases HCO 3 and water secretion by the duc-
–
each day. The pancreatic juice contains bicar- tules. CCK and acetylcholine (ACh) potentiate
–
2+
bonate (HCO 3 ), which neutralizes (pH 7–8) this effect by raising the cytosolic Ca concen-
HCl-rich chyme from the stomach, and mostly tration. Secretin and CCK also affect the pan-
inactive precursors of digestive enzymes that creatic enzymes.
break down proteins, fats, carbohydrates and Pancreatic enzymes are essential for diges-
other substances in the small intestine. tion. They have a pH optimum of 7–8. Insuffi-
–
Pancreatic secretions are similar to saliva in cient HCO 3 secretion (e.g., in cystic fibrosis)
that they are produced in two stages: (1) Cl is results in inadequate neutralization of chyme
–
Nutrition and Digestion creatic secretions also contain digestive pro- are secreted in their inactive form, i.e., as pro-
and therefore in impaired digestion.
secreted in the acini by active secondary trans-
+
port, followed by passive transport of Na and
Proteolysis is catalyzed by proteases, which
water (! p. 237 C1). The electrolyte composi-
tion of these primary secretions corresponds to
enzymes: trypsinogen 1–3, chymotrypsinogen A
that of plasma (! A1 and A2). Primary pan-
and B, proelastase 1 and 2 and procarboxypep-
tidase A1, A2, B1 and B2. They are not activated
enzymes and other proteins (exocytosis;
until they reach the intestine, where an entero-
–
! p. 30). (2) HCO 3 is added to the primary
–
(! D), which in turn converts chymotryp-
+
sinogen into active chymotrypsin. Trypsin also
secretory ducts; Na and water follow by pas-
10 secretions (in exchange for Cl ) in the peptidase first converts trypsinogen to trypsin
–
activates many other pancreatic proenzymes
sive transport. As a result, the HCO 3 concen-
tration of pancreatic juice rises to over including proelastases and procarboxypep-
–
100 mmol/L, while the Cl concentration falls tidases. Pathological activation of the pro-
(! A3). Unlike saliva (! p. 237 B), the osmolal- enzymes within the pancreas causes the organ
+
ity and Na /K concentrations of the pancreatic to digest itself (acute pancreatic necrosis).
+
juice remain constant relative to plasma (! A1 Trypsins, chymotrypsins and elastases are
and A2). Most of the pancreatic juice is endoproteases, i.e., they split certain peptide
secreted during the digestive phase (! A3). bonds within protein chains. Carboxypep-
tidases A and B are exopeptidases, i.e., they split
HCO 3 is secreted from the luminal membrane of
–
the ductules via an anion exchanger that simul- amino acids off the carboxyl end of the chain.
–
taneously reabsorbs Cl from the lumen (! B1). Cl – Carbohydrate catabolism. α-Amylase is
returns to the lumen via a Cl channel, which is more secreted in active form and splits starch and
–
frequently opened by secretin to ensure that the glycogen into maltose, maltotriose and α-limit
amount of HCO 3 secreted is not limited by the dextrin. These products are further digested by
–
availability of Cl (! B2). In cystic fibrosis (mu- enzymes of the intestinal epithelium
–
coviscidosis), impairment of this CFTR channel (cys- (! p. 259).
tic fibrosis transmembrane conductance regulator)
leads to severe disturbances of pancreatic function. Lipolysis. Pancreatic lipase (see p. 252ff.) is
–
The HCO 3 involved is the product of the CO 2 + OH – the most important enzyme for lipolysis. It is
reaction catalyzed by carbonic anhydrase (CA). For secreted in its active form and breaks triacyl-
+
–
each HCO 3 molecule secreted, one H ion leaves the glycerol to 2-monoacylglycerol and free fatty
+
cell on the blood side via an Na /H exchanger acids. Pancreatic lipase activity depends on the
+
(! B3). presence of colipases, generated from pro-coli-
Pancreatic juice secretion is controlled by pases in pancreatic secretions (with the aid of
cholinergic (vagal) and hormonal mechanisms trypsin). Bile salts are also necessary for fat
(CCK, secretin). Vagal stimulation seems to be digestion (! p. 248).
enhanced by CCK A receptors in cholinergic Other important pancreatic enzymes include
fibers of the acini (! A2,3, B, C and p. 234). Fat (pro-) phospholipase A 2, RNases, DNases, and a
246 in the chyme stimulates the release of CCK, carboxylesterase.
which, in turn, increases the (pro)enzyme con-
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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