50
et al. 2006) and thus ultimately by the way of negative feedback triggers the utilization of excessive fat and hence a lower insulin response is expected (Nugent 2005).
In order to maintain a normal and regular glucose response a balance is therefore
required between consumption of dietary sources containing glucose and end
removal of glucose from the system. In such a case resistant starch offers a reliable
window to help control blood glucose levels due to a reduced influx of glucose
because of slow digestion and reduction in the absorbable glucose in the human
gastrointestinal system. A study conducted by Shi et al. (2017) clearly demonstrated
the inhibitory effect of resistant starch on hyperglycemic status associated with
enhanced levels of gut microflora population which lead to high secretions of short
chain fatty acids via resistant starch fermentation secreting propionate and butyrate,
which may have an inhibitory effect on obesity induced diabetes. Resistant starch
(RS) therefore functions as a new food ingredient that has a low glycemic index. RS
itself contains almost zero calories (Alphons 1998) and when used as a low-calorie
food additive that in turn can control weight effectively. The ingestion of RS can
decrease insulin secretion and control postprandial blood glucose to prevent diabetes (Weickert and Mohlig 2005). The metabolism of RS occurs 5–7 h after consumption, in contrast to normally cooked starch, which is digested almost
immediately. Digestion over a 5–7 h period reduces postprandial glycemia and insulinemia and has the potential for increasing the period of satiety (Raben et al. 1994;
Reader 1997). As RS has a low glycemic response, adding it as an ingredient to
foods will help lower the overall GI value of the food (particularly if it is replacing
existing readily absorbed forms of carbohydrate) (Jyoshna and Hymavathi 2017). In
a study on humans, it was reported that the consumption of RS3 lowered serum
glucose and insulin levels in comparison with other carbohydrates(simple sugars,
oligosaccharides, and common starch). The investigation further showed that food
rich in RS reduced postprandial blood glucose and might help in providing improved
metabolic control in type II diabetes (Reader 1997). Another study showed that RS
reduces levels of glucose dependent insulinotropic polypeptide m-RNA along the
jejunum and ileum in both normal and type 2 diabetes rats (Shimada et al. 2008).
Chemically-modified resistant starches (RS4) have also been reported to produce
different glucose responses. In another human intervention study 11 human participants were fed with two test meals containing 1–2% acetylated potato starch and
beta cyclodextrin enriched potato starch (2–3%), and it was observed that participants who were fed with diet containing 2–3% beta cyclodextrin enriched potato
starch showed lower body glucose levels. This may be due to the more distal absorption of beta cyclodextrin in the intestine or to delayed gastric emptying (Raben et al.
1997). Raben et al. (1994) investigated the effect of RS on postprandial plasma
concentration of glucose lipids and harmones and on subjective satiety and palatability ratings. In this study 10 healthy human participants were fed with test meals
consisting of 50 g pre gelatinized starch (0% RS) or 50 g raw potato starch (54%
RS) together with 500 g artificially sweetened syrup. The postprandial plasma concentrations of glucose, lactate, insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1, and epinephrine were significantly lower in those participants
who were fed with meals containing raw potato starch (54% RS). This study
G. Akhtar et al.
et al. 2006) and thus ultimately by the way of negative feedback triggers the utilization of excessive fat and hence a lower insulin response is expected (Nugent 2005).
In order to maintain a normal and regular glucose response a balance is therefore
required between consumption of dietary sources containing glucose and end
removal of glucose from the system. In such a case resistant starch offers a reliable
window to help control blood glucose levels due to a reduced influx of glucose
because of slow digestion and reduction in the absorbable glucose in the human
gastrointestinal system. A study conducted by Shi et al. (2017) clearly demonstrated
the inhibitory effect of resistant starch on hyperglycemic status associated with
enhanced levels of gut microflora population which lead to high secretions of short
chain fatty acids via resistant starch fermentation secreting propionate and butyrate,
which may have an inhibitory effect on obesity induced diabetes. Resistant starch
(RS) therefore functions as a new food ingredient that has a low glycemic index. RS
itself contains almost zero calories (Alphons 1998) and when used as a low-calorie
food additive that in turn can control weight effectively. The ingestion of RS can
decrease insulin secretion and control postprandial blood glucose to prevent diabetes (Weickert and Mohlig 2005). The metabolism of RS occurs 5–7 h after consumption, in contrast to normally cooked starch, which is digested almost
immediately. Digestion over a 5–7 h period reduces postprandial glycemia and insulinemia and has the potential for increasing the period of satiety (Raben et al. 1994;
Reader 1997). As RS has a low glycemic response, adding it as an ingredient to
foods will help lower the overall GI value of the food (particularly if it is replacing
existing readily absorbed forms of carbohydrate) (Jyoshna and Hymavathi 2017). In
a study on humans, it was reported that the consumption of RS3 lowered serum
glucose and insulin levels in comparison with other carbohydrates(simple sugars,
oligosaccharides, and common starch). The investigation further showed that food
rich in RS reduced postprandial blood glucose and might help in providing improved
metabolic control in type II diabetes (Reader 1997). Another study showed that RS
reduces levels of glucose dependent insulinotropic polypeptide m-RNA along the
jejunum and ileum in both normal and type 2 diabetes rats (Shimada et al. 2008).
Chemically-modified resistant starches (RS4) have also been reported to produce
different glucose responses. In another human intervention study 11 human participants were fed with two test meals containing 1–2% acetylated potato starch and
beta cyclodextrin enriched potato starch (2–3%), and it was observed that participants who were fed with diet containing 2–3% beta cyclodextrin enriched potato
starch showed lower body glucose levels. This may be due to the more distal absorption of beta cyclodextrin in the intestine or to delayed gastric emptying (Raben et al.
1997). Raben et al. (1994) investigated the effect of RS on postprandial plasma
concentration of glucose lipids and harmones and on subjective satiety and palatability ratings. In this study 10 healthy human participants were fed with test meals
consisting of 50 g pre gelatinized starch (0% RS) or 50 g raw potato starch (54%
RS) together with 500 g artificially sweetened syrup. The postprandial plasma concentrations of glucose, lactate, insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1, and epinephrine were significantly lower in those participants
who were fed with meals containing raw potato starch (54% RS). This study
G. Akhtar et al.