White Paper | May 2021

Glycemic and Insulinemic

Response of Prebiotic
FOSSENCE®
Contents:

Introduction 1-2

Understanding Glycemic Index 3-4

and Insulin Index

Alternative food-based strategies 5-6

for Glycemic and Weight Control

Study details conducted at INQUIS 7

clinical research

Study outcomes 8-11

Summary 12

References 13
 George Bernard Shaw had said,
there is no
sincere love than
the love of
food.
Food is a major part of one’s life, and the
variety of food preparations and products
available across the world are testimony to
this.
It’s no secret that the amount of calories one
consumes versus its utilization directly impacts
weight and metabolic health. Moreover, the
modern culture of foods and its preparations
subjects one to calorie dense intakes. When
combined with a sedentary lifestyle, it may
generally result in weight gain and metabolic
disorders. Globally, in 2016, more than 1.9
billion adults were overweight, of which over
650 million were obese (WHO, 2018).
Being overweight raises the risk of various
non-communicable diseases such as
cardiovascular diseases, diabetes, osteo-
arthritis and some cancers. The global
diabetes prevalence in 2019 was
estimated to be 9.3% (463 million people)
(Saeedi P et al, 2019).
Obesity and diabetes are major causes of
morbidity and mortality, and impaired
quality of life. Therefore, attention has
now focused on the management of these
conditions, with significant importance
being given to food-related strategies. Not
only is the calorie count given attention,
but also how specific carbohydrates
impact the post-meal rise in blood sugar
called the glycemic response, on which is
based the concept of the ‘Glycemic
Index’.
Page 1
The glycemic response to a food or meal is the effect that the food or meal has on blood sugar
(glucose) levels after its consumption (Sadler M et al, 2011). Normally, blood glucose and insulin
levels rise after eating and later revert to fasting levels over a short period. This is especially true
after the consumption of meals rich in certain carbohydrates. ‘Glycemic Index’ (GI) is expressed
as an increase in blood glucose produced by a specific amount of available carbohydrate in the
food (Augustin LS et al, 2015). Foods with a high Glycemic index rapidly raise blood sugar levels
and cause substantial fluctuations in blood sugar (Bhupathiraju SN et al, 2014).

In simpler terms, the glycemic index (GI) is a rating system for foods containing carbohydrates.
It shows how quickly each food affects the blood sugar (glucose) level when it is eaten on its own
(Augustin LS et al, 2015).

It is defined as the incremental

High GI carbs
area under the curve (AUC)
cause blood sugar for the blood glucose
to spike then crash
response after consumption
Blood glucose levels

of a 50 g carbohydrate portion
of a test food expressed
Low GI carbs as a percent of the response
are digested and
released slowly for to an equivalent carbohydrate
sustained energy
amount from a reference
food ingested by the same
subject, with glucose or white
Time 1 hour 2 hours
bread as the reference food
(Wolever TM et al, 1991).
Figure 1: Blood glucose levels after eating high and low GI foods
(Rizkalla SW et al, 2002).

Page 2
Glycemic Index is classified as:
Low Medium High

55 55-70 70
or less and above

Foods with a high GI score contain
carbohydrate that is rapidly digested and
produces a sharp rise and fall in blood glucose
levels. In contrast, foods with a low GI score
contain slowly digested carbohydrate, which
produces a more gradual and relatively low rise
in blood glucose and insulin levels.
We are aware that the body produces the
hormone Insulin post meals to maintain blood
sugar within a healthy range.
Therefore, when one consumes foods,
there is an elevation of the insulin
concentration in the blood during the 2-h
period after the food is ingested. A direct
index of the postprandial insulin response to
a test food in comparison with an
isoenergetic portion of a reference food
(analogous to the glycemic index, either
glucose or white bread), is defined as a
dietary insulin index (DII) (Mirmiran P et al,
2016).

The Insulin Index (II) is a relatively new concept which measures the amount of insulin the body
produces in response to a set carbohydrate load in a particular food. This index is not
necessarily proportional to the GI, and consumption of large volumes of food with a high insulin
index may play a role in the development of insulin resistance, although the link has yet to be
conclusively established.

Insulin Index is classified as follows:

Low Medium High

<10 10-<20 20
and more

High glycemic and insulinemic responses can affect

appetite and energy metabolism, favouring body weight
and body fat gain (Pereira et al, 2015).
Page 3
Foods that have a high GI, Glycemic Load (GL) and DII are quickly digested and absorbed,
resulting in a high glycemic response, which in turn stimulates higher insulin secretion
(insulinemic response), leading to obesity and diabetes (Figure 2) (Vidya R et al, 2014).

High GI / High GL Meal

Glucose load
Blood glucose levels
Insulin demand from pancreas

Hunger Oxidative stress

leads to overeating Increased inflammation

Hyperinsulinemia
Insulin resistance
Free fatty acids

Overweight/obesity CVD

Metabolic syndrome

Type 2 diabetes mellitus

Figure 2: Physiological effects of High GI / High GL foods and link to diabetes and obesity

On the other hand, low GI foods are

LGI HGI
digested and absorbed at slower 4
* * * * *
rates, leading to lower glycemic and 3
2
insulinemic responses, which in turn
1
induces satiety, reduces food intake 0
and increases adipose tissue -1
mobilization (which is reflected as -2

reduced waist circumference after -3

Body fat (%) Waist circumference (cm)
-4
the intake of low GI meals; (Figure 3).

Figure 3: Changes in Waist circumference (WC) and Body fat (%)

Waist circumference and body fat changes (post-intervention) in response to the consumption
of two daily LGI or HGI meals for 45 consecutive days. Waist circumference (***p=0.008) and body fat
(**p=0.050) reduced after the consumption of the LGI vs. HGI meal (Mann-Whitney Test).
Adopted from: Pereira et al, 2015.

Hence, the knowledge of the GI index of a food substance may be a guiding factor for those
who wish to manage their weight or postprandial rise in blood sugar (Pereira et al, 2015).

Page 4
Alternative food-based
strategies for Glycemic
and Weight Control
Awareness among people about the role
that diet plays in the management of
obesity, diabetes and other related health
concerns is improving worldwide. Selection
of foods based on a glycemic index,
glycemic load or insulin index is now gaining
recognition in the management of weight
and hyperglycaemia. This approach is
particularly popular in the “healthy and
diabetes-friendly” packaged food category.
In keeping with the diet trend toward
high-fibre, low-glycemic carbohydrates and
carb-controlled foods, more reduced-sugar
products are showing up in groceries.
The newest ingredient on the block is the
prebiotic Fructo-oligosaccharide, or FOS,
which is now appearing in many food
products. Commonly consumed foods
such as bananas, onions, garlic, asparagus,
wheat, rye, Jerusalem artichoke, contain
FOS. Also, it can be produced enzymatically
from sugarcane molasses.
FOS has beneficial effects on health as it
stimulates the growth of some beneficial
bacteria such as Bifidobacteria.
The use of FOS as a food ingredient has
stimulated much research to know its
functionality and its effects on human
health, especially concerning its bifidogenic
character. Its potential benefits in
preventing and controlling some diseases
have been also been studied, especially
in conditions where there are conditions
of metabolic disorders such as
hyperglycaemia.
Consumer interest in food and beverages
with carbohydrates offering steady
glucose release and lower glycemic
index (GI) continues to rise. Slowly
digestible carbohydrates (SDC) like FOS
offer an ingredient solution to improve
carbohydrate quality and meet consumer
needs.
Page 5
Sh or t - c h a i n F O S
being sweet to taste has
been frequently used to replace
sugars in low-sugar food products
to lower the postprandial glycemic
response, reduce energy content,
or enrich foods with dietary fibres
(Lecerf JM et al, 2015; Respondek F
et al, 2014).

This section shall discuss the studies

about acute glycemic and insulinemic
responses of FOSSENCE® (which
contains short-chain FOS) when
administered alone or when
added or substituted for a
carbohydrate load.

Acute Glycemic and

Insulinemic responses
FOSSENCE® is a short-chain fructo-
of FOSSENCE® oligosaccharide (scFOS) that is a
sweet-tasting, soluble dietary fibre
produced by Tata Chemicals Limited
through a patented process. It is
a mixture of tri-saccharide (GF2),
tetra-saccharide (GF3) and
pentasaccharide (GF4) of glucose (G)
and fructose (F).

Unlike most simple sugars,

short-chain fructo-oligosaccharide,
a naturally occurring oligosaccharide,
remains intact through the upper
digestive tract but is degraded in the
colon by the ‘good’ gut bacteria.

Page 6
Study conducted at INQUIS
clinical research
(Formerly GI Labs, Canada)

In a randomized, controlled, cross-over study conducted in 3 phases explored Glycemic

Response and Insulin Response to ingestion of FOSSENCE®, when replaced by/added to
available-carbohydrates (avCHO) among 25 healthy adults (40±14years). In each phase GR
and IR elicited by 3-4 testmeals were measured among the fasted recruited subjects. (Table 1)
(Shah P et al, 2020).

Table 1: Interventions received by study subjects in three phases of the study

Experimental arms
Phases
1 2 3 4

Phase 1 10g Dextrose (10Dex*) 10g FOSSENCE® Water as control

(10FOS**)

Phase 2 50g Dextrose (50Dex) 50Dex+15FOS 35Dex 35Dex+15FOS

Phase 3 50g available 50WB+15FOS 35WB 35WB+15FOS

carbohydrate (avCHO)
from white bread
alone 50WB***

*Dex = Dextrose **FOS = FOSSENCE® ***WB = White Bread

On each test occasion, samples for fasting blood glucose and insulin were taken. The subjects
were then asked to consume a test meal within 10 min. Each test meal was served with a drink
of 1 cup of water.

Blood samples were collected at fasting and over 2 hours after the start of the test meal and
analyzed for glucose and insulin levels. The primary endpoint was differences in incremental
glucose area under curve (IAUC).

Page 7
The Study
Outcomes

Page 8
Phase 1

The results demonstrated that FOSSENCE® does not

increase postprandial glucose and insulin levels at
a 10g intake compared to 10g dextrose
intake and was comparable to the
response of water. The absolute and
incremental plasma glucose
levels of the subjects were
significantly lower after the intake
of water and water containing
10g FOS compared to water
containing 10g of dextrose at 15, 30
and 45 min.

2.5
Plasma Glucose (mmol/L)

2.0 10Dex
1.5 Control
10FOS
1.0

0.5

0.0
0 30 60 90 120
-0.5
Time (min)

Figure 4: Incremental Plasma Glucose

25.0
10Dex
FOSSENCE® is resistant to
20.0
Serum Insulin µU/ml

Control breakdown, not digested by

15.0
10FOS enzymes in the human small-
10.0 intestine and therefore is an
5.0 unavailable carbohydrate that
0.0 does not raise post prandial
0 30 60 90 120 blood glucose or insulin.
-5.0
Time (min)

Figure 5: Incremental Serum Insulin

Page 9
Phase 2
Relative glycemic and insulinemic response of a 50g oral glucose challenge with 15g of
FOSSENCE® added or when 15g FOSSENCE® (30% carbohydrates) was substituted for 15g of
the dextrose was evaluated.

Addition of FOSSENCE® to a carbohydrate challenge showed no significant difference

1 in glucose peak levels, incremental glucose levels or incremental insulin levels.

Substitution of carbohydrate by FOSSENCE® showed that glucose IAUC and insulin

2 IAUC for was significantly lower than of IAUC by control (p<0.002 and p<0.0003,
respectively).

3 Incremental insulin levels were significantly lower after substitution of 30% available
carbohydrates compared to control (p<0.02).

4 Peak insulin levels were significantly lower after 30% carbohydrates were substituted
with FOSSENCE® compared to control (p<0.001).

75
6.0 50Dex 50Dex
a 50Dex+FOS
Plasma Glucose (mmol/L)

Serum Insulin (µU/ml)

5.0 50Dex+FOS 55 35Dex

35Dex 35Dex+FOS
4.0
35Dex+FOS ab a
3.0 35
a a
2.0 ab a
15
1.0 a ab a
0.0 a ab
-5 0 30 60 90 120
0 30 60 90 120
-1.0 Time (min)
Time (min)

Figure 6: Incremental Plasma Glucose Figure 7: Incremental Serum Insulin

Results demonstrate that adding 15g of FOSSENCE® to glucose load does not significantly
change 2h glucose or insulin IAUC, neither does it modulate postprandial glucose or insulin
levels but 30% substitution attenuates postprandial glucose and insulin levels.

When FOSSENCE® was added to a carbohydrate challenge, peak or absolute glucose levels
did not differ significantly after the intake of and 50g Dextrose +15g FOSSENCE® or between
the intake of 35g dextrose and 35g Dextrose + 15g FOSSENCE®.

When FOSSENCE® replaced 30% of available carbohydrate, IAUC and plasma glucose
levels after the intake of 35g Dextrose + 15g FOSSENCE® were substantially lower than that
after the intake of 50g dextrose.

Page 10
Phase 3
IAUC of plasma glucose over 2 hours
were compared after the consumption 3.5
a
50WB
50WB+15FOS

Plasma Glucose (mmol/L)

of a white bread portion containing 50g 3.0
a a
35WB
2.5
a ab
available carbohydrate and the same 35WB+15FOS
2.0 b bc
white bread portion with 15g of c a
1.5
FOSSENCE® added or substituted for 1.0
a a
30% of the available carbohydrate in a
0.5 b
b
the white bread. 0.0 b
b
0 30 60 90 120
Time (min)
Addition of FOSSENCE® to
carbohydrate challenge (50WB vs Figure 8: Incremental Plasma Glucose
50WB+15FOS) resulted in no
significant difference in glucose or 60

insulin IAUC, or incremental glucose or 50 50WB

a 50WB+15FOS
insulin levels at any time point. a
Serum Insulin (µU/ml)

40 35WB
Substitution (30%) of available ab ab a 35WB+15FOS

carbohydrate by FOSSENCE®
30
bc a
a
20
(50WB vs 35WB+15FOS) resulted a
10
in significantly lower glucose
b
IAUC (p<0.0001) as well as insulin 0
b
0 30 60 90 120
IAUC (p<0.0001). Substitution of Time (min)
FOSSENCE® also reduced incremental
Figure 9: Incremental Serum Insulin
plasma glucose at 60, 90 and 120min
and serum insulin levels at 30, 45, 60,
90 and 120 min compared to 50WB
meal.

The glucose and insulin IAUCs were significantly lower after the intake of bread portion
containing 35g available carbohydrate and 35g available carbohydrate + 15g FOSSENCE®
compared to that after the intake of bread portion containing 50g available carbohydrate and
50g available carbohydrate + 15g FOSSENCE®.

Page 11
Summary

To conclude, these studies demonstrate

that FOSSENCE®, when consumed alone,
does not increase postprandial glucose
and insulin levels, suggesting its resistance
to breakdown.

When added to a carbohydrate load

(Dextrose or White Bread), FOSSENCE®
does not increase postprandial glucose
or insulin levels, while replacement
of FOSSENCE® with 30% of glycemic
carbohydrate reduces postprandial
glucose and insulin levels, indicating the
blood glucose/insulin attenuation after
FOSSENCE®-fortified meals.

FOSSENCE® has a sweet taste with

a sweetness of 30-40% to that of sugar.
The sweetness profile is without any
bitterness or any after taste.
Hence, FOSSENCE maybe advised
®

to individuals on restricted sugar intake.

Page 12
References

Augustin LS, et al. Glycemic index, glycemic load and glycemic response: An International Scientific Consensus
Summit from the International Carbohydrate Quality Consortium (ICQC). Nutr Metab Cardiovasc Dis. 2015
Sep;25(9):795-815. doi: 10.1016/j.numecd.2015.05.

Bhupathiraju SN, et al. Glycemic index, glycemic load, and risk of type 2 diabetes: results from 3 large US
cohorts and an updated meta-analysis. Am J Clin Nutr. 2014 Jul;100(1):218-32. doi: 10.3945/ajcn.113.079533.
Epub 2014 Apr 30. PMID: 24787496; PMCID: PMC4144100.

Lecerf JM, et al. Postprandial glycaemic and insulinaemic responses in adults after consumption of dairy
desserts and pound cakes containing short-chain fructo oligosaccharides used to replace sugars. J Nutr Sci,
2015; 12;4:e34. https:// doi:10.1017/jns.2015.22.

Mirmiran P, et al. Dietary insulin load and insulin index are associated with the risk of insulin resistance: a
prospective approach in tehran lipid and glucose study. J Diabetes Metab Disord. 2016 Jul 20;15:23. doi:
10.1186/s40200-016-0247-5. PMID: 27446819; PMCID: PMC4955203.

Pereira, et al. Effect of glycemic index on obesity control. Archives of endocrinology and metabolism. 2015
Jun;59(3):245-51.

Respondek F, et al. Digestive tolerance and postprandial glycaemic and insulinaemic responses after
consumption of dairy desserts containing maltitol and fructo-oligosaccharides in adults. Eur J Clin Nutr.
2014;68:575–80.

Rizkalla SW, et al. Health benefits of low glycaemic index foods, such as pulses, in diabetic patients and healthy
individuals. Br J Nutr. 2002 Dec;88 Suppl 3:S255-62. doi: 10.1079/BJN2002715. PMID: 12498625.

Sadler M, et al, Food, Glycaemic Response and Health. ILSI Europe Concise Monograph Series 2011:1-30.
Available from ILSI Europe.

Saeedi P, et al. IDF Diabetes Atlas Committee. Global and regional diabetes prevalence estimates for 2019 and
projections for 2030 and 2045: Results from the International Diabetes Federation Diabetes Atlas, 9th edition.
Diabetes Res Clin Pract. 2019 Nov;157:107843. doi: 10.1016/j.diabres.2019.107843. Epub 2019 Sep 10.
PMID: 31518657.

Shah P, et al. Comparison of the Acute Glycemic and Insulinemic Response of Fossence™, a Short Chain
Fructo-Oligosaccharide, Taken Alone, Added or Substituted into a Carbohydrate Load, Current Developments in
Nutrition, 4(S2): 774.

Vidya R, et al. Glycemic Index of Indian Cereal Staple Foods and their Relationship to Diabetes and Metabolic
Syndrome. InWheat and Rice in Disease Prevention and Health 2014 Jan 1 (pp. 333-346). Academic Press.

WHO Factsheet-Obesity and overweight. Updated April 2018.

Wolever TM, et al. The glycemic index: methodology and clinical implications. Am J Clin Nutr. 1991 Nov
1;54(5):846-54.

Page 13