Biology Reference
In-Depth Information
The amylose chain of starch displays a natural twist providing a helical
conformation with six anhydroglucose units per turn ( Zobel, 1988 ) .
Hydroxyl groups of glucose residues are present on the outer surface of
the helix, while the internal cavity is a hydrophobic tube ( Zhou,
Robards, Helliwell, & Blanchard, 2007 ) . The hydrophobic complexing
agents can stay or complex within the amylose helix stabilized through
van der Waals forces with adjacent C-hydrogen of amylose ( Godet,
Tran, & Delagw, 1993; Zhou et al., 2007 ) . The effects of free fatty acids
(lauric, myristic, palmitic, stearic and oleic acids, lysolecithin and choles-
terol) on the hydrolysis of starch, amylose, and amylopectin using
-amylase
and amyloglucosidase have been reported in the literature by Crowe,
Seligman, and Copeland (2000) . Around 60% amylose was converted to
glucose in 1 h that reached up to 90% after 6 h. The addition of lauric,
myristic, palmitic, and oleic acids reduced the enzymatic hydrolysis of amy-
lose by 35%. However, neither stearic acid nor cholesterol presented an
inhibition. Lauric acid had no effect on the enzymatic breakdown of amy-
lopectin, whereas the breakdown of whole starch was inhibited 12% by
lauric acid. These experiments suggest that only the hydrolysis of the amy-
lose fraction (31% of the whole starch) is affected by lauric acid. Amylose
presents a helical conformation and can form inclusion complexes with small
hydrophobic molecules. Complexes between fatty acids such as lauric acid
and amylose can form rapidly under physiological conditions, which con-
tribute to the formation of RS ( Seligman, Copeland, Appels, & Morell,
1998 ). The formation of such complexes with lipids may result in significant
changes in the behavior of the starch, including decreased solubility,
increased gelatinization temperature, and delayed retrogradation and resis-
tance toward the action of digestive enzymes. Amylose may bind one lauric
acid molecule per
a
20 glucose units in the glucose chain, but in contrast,
very little lauric acid binds under the same conditions to amylopectin and
other branched glucans ( Crowe et al., 2000 ).
Enzymatic resistance of the pure amylose and lipid complexes has also
been reported in the literature ( Gelders, Duyck, Goesaert, & Delcour,
2005; Holm et al., 1983 ) . With the help of in vitro and in vivo digestibility
studies on amylose-lipid complexes, Holm et al. (1983) observed that com-
plexed amylose is hydrolyzed and absorbed in the gastrointestinal tract to the
same extent as free amylose but at somewhat slower rate. After studying the
influence of enzymatic action on the digestibilities of complexes formed
between amylose of different average chain lengths (degree of polymeriza-
tion) and docosanoic acid/glycerol monostearate, Gelders et al. (2005)
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