Biomedical Engineering Reference
In-Depth Information
observed with sodium ascorbate was attributed to: (1) a viscosity reduction
of the polymer combination in the stomach, thus implying that chitosan
mixed with a lipid might be better than chitosan alone; (2) an increase in
oil holding capacity of the chitosan gel; and (3) chitosan-fat gel being more
l exible and less likely to leak the entrapped fat in the intestinal tract.
h ree-fold fecal bile acid excretion in acid micelles
in toto
, with con-
sequent assimilation of bile acids, cholesterol, monoglycerides and fatty
acids.
In
rats kept on diets containing 7.5 % chitosan, compared to cellu-
lose-fed animals was observed [248]. But in several studies, rats on diets
containing 5 % chitosan did not have increased fecal bile acid excretion
[249, 250]. However, increased fecal bile acid excretion due to dietry chito-
san, has been observed in humans and rabbits [251, 252]. It is reported that,
in vitro
bile acid binding capacity of chitosan was approximately one-half
or equal to that of cholestyramine, a strong synthetic anion exchanger and
a hypocholesterolemic agent [250, 253, 254]. Chitosan was compared with
cholestyramine and oat gum for its lipid lowering ef ects and on intestinal
morphology in rats. All the three agents lowered liver cholesterol signii -
cantly; chitosan did so without producing any deleterious changes in the
intestinal mucosa [255]. h us prevalent evidence supports a reduction in
lipid absorption, by dearth of bile acid, since chitosan engages it by binding.
Chitosan, upon reaction with bile acids (cholate, taurocholate, etc.), forms
insoluble salts that collect lipids by hydrophobic interaction [256-258]. Yet
another explanation for lipid lowering ef ect is provided by the i nding that,
in vitro
chitosan inhibits pancreatic lipase activity by acting as an alterna-
tive substrate [259-261]. Han
et al.
assessed the ef ect of chitosan treatment
on the activity of pancreatic lipase,
in vitro
, and on the degree of fat storage
induced in mice by oral administration of a high fat diet for 9 weeks [262].
Chitosan prevented the increase in body weight, hyperlipidemia and fatty
liver induced by a high fat diet. However, the antiobesity ef ects of chito-
san in high fat treated mice were attributed to the inhibition of intestinal
absorption of dietary fat with no ef ect being observed on pancreatic lipase
activity.
LeHoux and Grondin investigated the ef ects of chitosan on plasma
and liver cholesterol levels, liver weight and 3-hydroxy-3-methylglutaryl
coenzyme A (HMG-CoA) reductase, a key regulatory enzyme of choles-
terogenesis, in rats fed on a sterol diet (1 % cholesterol and 0.2 % cholic
acid) [263]. Chitosan, at a level of 5 %, lowered plasma and liver cholesterol
levels by 54 % and 64 %, respectively. High molecular weight chitosan (750
kDa) had less hypocholesterolemic potential than a 70 kDa preparation.
Incorporation of chitosan (70 kDa, DA 7.5 %) for 3 weeks, in a sterol diet,
completely prevented any decrease in plasma high-density lipoproteins
