Agriculture Reference
In-Depth Information
properties in the colon (Spiller 1994; Reddy et al.,
1997). Butyric acid induced differentiation of
normal colon cells, and induced the growth arrest
and apoptosis in cancer cells (Archer et al., 1998;
Avivi-Green et al., 2002; Ruemmele et al., 2003).
These cellular activities may be responsible for
butyrate's anticancer activity. Inulin may facili-
tate the absorption of calcium, magnesium, and
iron in the colon due to the formation of short-
chain fatty acids, such as acetic, propionic, and
butyric acids, that affect pH in colon. Calcium
and magnesium are important regulators of cel-
lular activity and may help control the rate of cell
turnover. High concentrations of calcium may aid
formation of insoluble bile or salts of fatty acids
and therefore may reduce the damaging effects of
bile or fatty acids on colon cells (Topping and
Clifton 2001).
Resistant starch resists upper intestinal diges-
tion and passes into the lower intestine to be fer-
mented by microfl ora in the colon. There are
three types of resistant starch: physically trapped
starch, resistant starch granules, and retrograded
starch (Englyst et al., 1993; Muir et al., 1993).
Physically trapped starch is trapped within food
matrices that severely prevent or delay their inter-
action with digestive enzymes in the small intes-
tine. They are commonly found in whole or partly
ground grains, seeds, and legumes, and their con-
centration and distribution is affected by food
processing techniques. Resistant starch granules
have crystalline regions that are less susceptible
to digestion by acid or α-amylase enzymes. Food
processing techniques that gelatinize such starches
can aid their digestion. Retrograded starch is
formed from gelatinized starch that undergoes
the process of retrogradation. High-amylose
starch retrogrades faster than high-amylopectin
starch. High-amylose starch can be retrograded to
a form that resists dispersion in water and diges-
tion by α-amylase. Retrograded starch may be
generated during food processing (Englyst et al.,
1993; Muir et al., 1993).
The physiological functions of resistant starch
include improving glycemic response and colon
health, providing lower calorie intake, and modu-
lating fat metabolism. Food components that
moderate blood sugar levels following food con-
sumption provide health benefi ts such as reduced
risk of developing diabetes, heart disease, and
other chronic diseases. Resistant starch is fer-
mented by microfl ora in the colon to produce
short-chain fatty acids (acetate, propionate, and
butyrate) to promote colon health (Avivi-Green
et al., 2002; Ruemmele et al., 2003). Resistant
starch used in products provides bulk and helps
decrease the caloric content of foods. Resistant
starch consumption has been shown to promote
lipid oxidation and metabolism in human subjects
(Higgins et al., 2004). In their study, addition of
5.4% resistant starch to the diet signifi cantly
increased lipid oxidation by 23% when compared
to the control meal with 0% resistant starch. The
results suggested replacement of 5.4% of total
dietary carbohydrate with resistant starch signifi -
cantly increased postprandial lipid oxidation and
metabolism, and therefore could conceivably
decrease fat accumulation in the long-term.
Betaine
Trimethyl glycine, also known as glycine betaine,
or simply betaine, is found in a wide range of
dietary sources (Fig. 22.1). Betaine was fi rst dis-
covered in sugar beet juice in the 19th century.
Since then it has been found in many food sources,
with wheat, spinach (
Spinacia oleracea
L.), and
sugar beet (
Beta vulgaris
L.) being the richest
plant dietary sources. Betaine functions as an
osmolyte, protecting cells, proteins, and enzymes
from environmental stress. It also functions as a
methyl donor in the methionine cycle for conver-
sion of homocysteine to methionine, primarily in
the liver and kidneys. Betaine increases glutathi-
one levels in the liver and improves antioxidant
status. Low levels of betaine may contribute to
various diseases, including coronary, cerebral,
hepatic, and vascular diseases (Craig 2004).
CH
3
CH
3
- N - CH
2
- COO
-
.
H
2
O
CH
3
Fig. 22.1
Molecular structure of glycine betaine.
