30
120 min. As a result, the amylose complex produces lower plasma glucose and liver
glycogen levels than does free amylose. Murray et al. (1998) evaluated apparent
digestibility of starch in ileal-cannulated dogs that were fed enteral diets containing
debranched amylopectin-lipid V-complex or RS. They found that the ileal and total
GI tract digestibilities of the control, V-complex, and RS diets were 89%, 76%, and
43%, respectively, which indicated that the diet containing V-complex starch lowered the carbohydrate digestibility and hence the serum glucose and insulin
responses. Differential scanning calorimetry (DSC) was used to study the effect of
sodium stearoyl lactylate (SSL), lysophosphatidyl choline (LPC), and hydroxylated
lecithin (OHL) on autoclaved amylomaize starch (Czuchajowska et al. 1991).
Differential scanning calorimetry (DSC) peaks at around 95–110 °C indicated the
formation of complex compounds between amylose chains and lipid, and the peak
at about 155 °C indicated the presence of resistant starch (RS). However lower
yields of RS were observed from lipid complexed samples as compared to autoclaved and cooled control when subjected to amylolysis by thermostable bacterial
α-amylase and amyloglucosidase. Amylose recrystallization which is important in
resistant starch formation is adversely affected by complexation of amylose with
LPC and SSL. In another study, influence of endogenous lipids on wheat starch
showed that defatting of the starch samples resulted in decrease of the RS content.
On addition of SDS to defatted wheat or amylomaize starch, resistant starch yields
decreased significantly. X-ray diffraction and DSC techniques confirmed formation
of amylose-lipid complexes in the presence of both endogenous lipids as well as
added lipids (SDS) (Eerlingen et al. 1994).
In addition to the interaction of starch with lipids and proteins, it has also been
found that starch can interact with soluble fibers (β-glucans, guar gum, psyllium, or
pectin), antinutrients (enzyme inhibitors, phytates, tannins, lectins or saponins),
organic acids and sugars (Biliaderis 1991; Bjorck et al. 2000; Pi-Sunyer 2002).
Enzyme inhibitors like phytic acid, polyphenols, and lectins present in leguminous
seeds, have been found to inhibit in vitro digestion and hence the glycemic index of
starch (Thompson and Yoon 1984). Both amylases and intestinal maltase activity
are inhibited by tannic acid (Bjorck et al. 1987). Since phytic acid inhibits the amylolysis, an increase in phytate content decreases starch digestibility (Thompson and
Yoon 1984). Brennan et al. (1996) reported that the rate of starch hydrolysis slowed
down significantly when the starch granules and surrounding bread matrix were
coated with a layer of galactomannan mucilage, which acted as a physical barrier to
enzyme-starch interactions and hence the release of hydrolyzed products. Guar gum
has been found to increase the viscosity of digesta and reduce the rise in postprandial glycemic response that occurs due to the reduction in rate of gastric emptying.
Starch blockers (α- amylase inhibitors) inhibits in vitro α-amylase activity or binds
to starch substrate, indicating that these have the potential to interfere with the
digestion of starch in vivo and hence modulate the glycemic effect of SDS and RS
(Giri and Kachole 1998; Obiro et al. 2008). Potato starch gels showed decreased
yield of resistant starch in the presence of ions like calcium and potassium (Escarpa
et al. 1997) which may be reflected to the prevention of hydrogen bond formation
between amylopectin and amylose chains.
B. A. Ashwar et al.
120 min. As a result, the amylose complex produces lower plasma glucose and liver
glycogen levels than does free amylose. Murray et al. (1998) evaluated apparent
digestibility of starch in ileal-cannulated dogs that were fed enteral diets containing
debranched amylopectin-lipid V-complex or RS. They found that the ileal and total
GI tract digestibilities of the control, V-complex, and RS diets were 89%, 76%, and
43%, respectively, which indicated that the diet containing V-complex starch lowered the carbohydrate digestibility and hence the serum glucose and insulin
responses. Differential scanning calorimetry (DSC) was used to study the effect of
sodium stearoyl lactylate (SSL), lysophosphatidyl choline (LPC), and hydroxylated
lecithin (OHL) on autoclaved amylomaize starch (Czuchajowska et al. 1991).
Differential scanning calorimetry (DSC) peaks at around 95–110 °C indicated the
formation of complex compounds between amylose chains and lipid, and the peak
at about 155 °C indicated the presence of resistant starch (RS). However lower
yields of RS were observed from lipid complexed samples as compared to autoclaved and cooled control when subjected to amylolysis by thermostable bacterial
α-amylase and amyloglucosidase. Amylose recrystallization which is important in
resistant starch formation is adversely affected by complexation of amylose with
LPC and SSL. In another study, influence of endogenous lipids on wheat starch
showed that defatting of the starch samples resulted in decrease of the RS content.
On addition of SDS to defatted wheat or amylomaize starch, resistant starch yields
decreased significantly. X-ray diffraction and DSC techniques confirmed formation
of amylose-lipid complexes in the presence of both endogenous lipids as well as
added lipids (SDS) (Eerlingen et al. 1994).
In addition to the interaction of starch with lipids and proteins, it has also been
found that starch can interact with soluble fibers (β-glucans, guar gum, psyllium, or
pectin), antinutrients (enzyme inhibitors, phytates, tannins, lectins or saponins),
organic acids and sugars (Biliaderis 1991; Bjorck et al. 2000; Pi-Sunyer 2002).
Enzyme inhibitors like phytic acid, polyphenols, and lectins present in leguminous
seeds, have been found to inhibit in vitro digestion and hence the glycemic index of
starch (Thompson and Yoon 1984). Both amylases and intestinal maltase activity
are inhibited by tannic acid (Bjorck et al. 1987). Since phytic acid inhibits the amylolysis, an increase in phytate content decreases starch digestibility (Thompson and
Yoon 1984). Brennan et al. (1996) reported that the rate of starch hydrolysis slowed
down significantly when the starch granules and surrounding bread matrix were
coated with a layer of galactomannan mucilage, which acted as a physical barrier to
enzyme-starch interactions and hence the release of hydrolyzed products. Guar gum
has been found to increase the viscosity of digesta and reduce the rise in postprandial glycemic response that occurs due to the reduction in rate of gastric emptying.
Starch blockers (α- amylase inhibitors) inhibits in vitro α-amylase activity or binds
to starch substrate, indicating that these have the potential to interfere with the
digestion of starch in vivo and hence modulate the glycemic effect of SDS and RS
(Giri and Kachole 1998; Obiro et al. 2008). Potato starch gels showed decreased
yield of resistant starch in the presence of ions like calcium and potassium (Escarpa
et al. 1997) which may be reflected to the prevention of hydrogen bond formation
between amylopectin and amylose chains.
B. A. Ashwar et al.