Ganong's Review of Medical Physiology, 23rd Edition

440
SECTION V
Gastrointestinal Physiology

Figure 26–17. Their hydrophilic portions face out and their
hydrophobic portions face in. Above a certain concentration,
called the
critical micelle concentration,
all bile salts added
to a solution form micelles. Lipids collect in the micelles, with
cholesterol in the hydrophobic center and amphipathic phos-
pholipids and monoglycerides lined up with their hydrophilic
heads on the outside and their hydrophobic tails in the center.
The micelles play an important role in keeping lipids in solu-
tion and transporting them to the brush border of the intesti-
nal epithelial cells, where they are absorbed (see Chapter 27).
Ninety to 95% of the bile salts are absorbed from the small
intestine. Once they are deconjugated, they can be absorbed
by nonionic diffusion, but most are absorbed in their conju-
gated forms from the terminal ileum (Figure 26–18) by an
extremely efficient Na

• –bile salt cotransport system powered
  by basolateral Na


• 
  

  –K

  
  


• 
  

  ATPase. The remaining 5–10% of the
  bile salts enter the colon and are converted to the salts of
  deoxycholic acid and lithocholic acid. Lithocholate is rela-
  tively insoluble and is mostly excreted in the stools; only 1% is
  absorbed. However, deoxycholate is absorbed.
  The absorbed bile salts are transported back to the liver in
  the portal vein and reexcreted in the bile (enterohepatic circu-

  
  

lation) (Figure 26–18). Those lost in the stool are replaced by

synthesis in the liver; the normal rate of bile salt synthesis is

0.2 to 0.4 g/d. The total bile salt pool of approximately 3.5 g

recycles repeatedly via the enterohepatic circulation; it has

been calculated that the entire pool recycles twice per meal

and six to eight times per day. When bile is excluded from the

intestine, up to 50% of ingested fat appears in the feces. A

severe malabsorption of fat-soluble vitamins also results.

When bile salt reabsorption is prevented by resection of the

terminal ileum or by disease in this portion of the small intes-

tine, the amount of fat in the stools is also increased because

when the enterohepatic circulation is interrupted, the liver

cannot increase the rate of bile salt production to a sufficient

degree to compensate for the loss.

INTESTINAL FLUID & ELECTROLYTE

TRANSPORT

The intestine itself also supplies a fluid environment in which

the processes of digestion and absorption can occur. Then,

when the meal has been assimilated, fluid used during diges-

tion and absorption is reclaimed by transport back across the

epithelium to avoid dehydration. Water moves passively into

and out of the gastrointestinal lumen, driven by electrochem-

ical gradients established by the active transport of ions and

other solutes. In the period after a meal, much of the fluid re-

uptake is driven by the coupled transport of nutrients, such as

glucose, with sodium ions. In the period between meals, ab-

sorptive mechanisms center exclusively around electrolytes.

In both cases, secretory fluxes of fluid are largely driven by the

active transport of chloride ions into the lumen, although ab-

sorption still predominates overall.

FIGURE 26–17
Physical forms adopted by bile acids in
solution.
Micelles are shown in cross-section, and are actually thought
to be cylindrical in shape. Mixed micelles of bile acids present in hepat-
ic bile also incorporate cholesterol and phosphatidylcholine.
(Adapted
from Barrett KE:
Gastrointestinal Physiology

. McGraw-Hill, 2006.)

Charged side chain

OH group

Simple micelle Bile acid monomers

Mixed micelle

Phosphatidylcholine

Cholesterol

FIGURE 26–18

Quantitative aspects of the circulation of

bile acids.

The majority of the bile acid pool circulates between the

small intestine and liver. A minority of the bile acid pool is in the sys-

temic circulation (due to incomplete hepatocyte uptake from the por-

tal blood) or spills over into the colon and is lost to the stool. Fecal loss

must be equivalent to hepatic synthesis of bile acids at steady state.

(Adapted from Barrett KE:

Gastrointestinal Physiology

. McGraw-Hill, 2006.)

Hepatic synthesis

Sphincter of Oddi

Small intestine

Large intestine

Spillover into colon

Fecal loss ( = hepatic synthesis)

Passive uptake

of deconjugated

bile acids from colon

Return

to liver

Active

ileal

uptake

Gallbladder

Spillover from

liver into

systemic

circulation