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W
ater,po
d0
PD
X
150
m
g/d,po
d0
W
ater,po
d14
PD
X
150
m
g/d,po
d14
0
2
4
6
8
Totallipids(g/100g)
W
ater,po
d14
PD
X
150
m
g/d,po
d14
0
1
2
3
4
LDLrmRNA/RPLP0mRNA
Putaala H.1
, Raza G. S.2
, Tiihonen K.1
, Mäkelä K. A. 2
, Herzig K. H.2
BACKGROUND
METHODS
RESULTS
DISCUSSION
HYPOLIPIDEMIC EFFECTS
OF POLYDEXTROSE IN MOUSE
1
DuPont Nutrition & Health
Active Nutrition
Sokeritehtaantie 20
02460 KANTVIK, FINLAND
E-mail: heli.putaala@dupont.com
The information contained herein is based on data known to DuPont or its affiliates at the time of preparation of the information and believed by them to be reliable. This is business-to-business information intended for food, beverage and supplement producers, and is not intended for
the final consumer of a finished food, beverage or supplement product. The information is provided “as is” and its use is at the recipient’s sole discretion and risk. It is the recipient’s sole responsibility to determine the suitability and legality of its proposed use of DuPont products for its
specific purposes. Information and statements herein shall not be construed as licenses to practice, or recommendations to infringe, any patents or other intellectual property rights of DuPont or others. DUPONT HEREBY EXPRESSLY DISCLAIMS (I) ANY AND ALL LIABILITY IN
CONNECTION WITH SUCH INFORMATION, INCLUDING, BUT NOT LIMITED TO, ANY LIABILITY RELATING TO THE ACCURACY, COMPLETENESS, OR USEFULNESS OF SUCH INFORMATION, AND (II) ANY AND ALL REPRESENTATIONS OR WARRANTIES, EXPRESS OR
IMPLIED, WITH RESPECT TO SUCH INFORMATION, OR ANY PART THEREOF, INCLUDING ALL REPRESENTATIONS AND WARRANTIES OF TITLE, NONINFRINGEMENT OF COPYRIGHT OR PATENT RIGHTS OF OTHERS, MERCHANTABILITY, FITNESS OR SUITABILITY
FOR ANY PURPOSE, AND WARRANTIES ARISING BY LAW, STATUTE, USAGE OF TRADE OR COURSE OF DEALING.
Copyright © 2014 DuPont or its affiliates. All Rights
Reserved. The DuPont Oval Logo, DuPont™, The
miracles of science™ and all products denoted with
® or ™ are registered trademarks or trademarks of
E.I. du Pont de Nemours and Company or its
affiliated companies.
Hyperlipidemia is a risk factor for cardiovascular and metabolic diseases. It is established that elevated plasma triglyceride-rich lipoproteins and low levels of
HDL-cholesterol levels are directly related to the risk of cardiovascular disease [1].
Polydextrose (PDX, Litesse® Ultra™, DuPont) is soluble glucose polymer used as a fat and sugar replacer as well as dietary fibre. As PDX has potential to
improve hyperlipidemia [2-4] and satiety [5-7] we investigated effects of PDX on lipid profiles in mice fed with fiber-deficient and western diet with an attempt
to further characterize lipid-attenuating mechanisms.
Male C57BL/6 (n=36) mice were fed either fiber- deficient (<0.5% fibre 10%
kcal fat) or western- diet (5% fiber, 41% kcal fat) for 2 weeks. Animals were
gavaged twice a day either with water containing PDX 150 mg/day or water
alone as control. Body weight, food intake and indirect calorimetric measure-
ments were performed in a home cage- based monitoring system
(LabMaster®). Fasting blood samples and feces were collected for lipid
measurements. Gene expression for lipid metabolism was performed by
real–time PCR in liver.
In a recent meta-analysis, it was concluded that PDX can reduce voluntary energy intake at a subsequent meal [5]. The present study shows that longer-term
consumption of PDX might translate into a reduction of cumulative food intake and loss in body weight. Polydextrose has been shown to decrease postpran-
dial elevation of triglycerides [2]. The present study shows a longer-term effect of PDX on triglycerides and total cholesterol reduction, and is in accordance
with previous studies [3]. The upregulation of LDLreceptor gene in liver could increase LDL clearance by the liver which would then translate into reduction
of total cholesterol and triglycerides [1]. The binding of lipids to fiber and evacuation through feces may be additional mechanism.
2
Institute of Biomedicine,
Dept.of Physiology and Biocenter of Oulu,
Univ. of Oulu,
Medical Research Center Oulu and Oulu Univ. Hospital,
OULU, FINLAND
References:
[1] Miller, M., et al., Circulation, 2011. 123(20): p. 2292-2333. [2] Tiihonen, K., et al., Nutrition Journal, 2015. 14(1): p. 23. [3] Pronczuk, A. and K.C. Hayes, Nutrition Research, 2006. 26(1): p. 27-31. [4] Schwab, U., et al., European
Journal of Clinical Nutrition, 2006. 60(9): p. 1073-80. [5] Ibarra, A., et al., Appetite, 2014. 87C: p. 30-37. [6] Hull, S., et al., Appetite, 2012. 59(3): p. 706-712. [7] Ranawana, V., A. Muller, and C.J. Henry, European Journal of Nutri-
tion, 2013. 52(3): p. 885-93.
Cumulative body weight gain
Days
Cumulativebodyweight(g)
0 2 4 6 8 10 12 14
0.0
0.5
1.0
1.5
2.0
2.5
Water, po
PDX 150mg/day, po
Cumulative food intake
Days
Foodintake/bodyweight[g/g]
0 2 4 6 8 10 12 14
0.0
0.6
1.2
1.8
water, po
pdx 150mg/day, po
p<0,001
pd
Plasma triglyceride
Plasmatriglyceride(mg/dL)
W
ater,pox
150m
g/day,po
20
40
60
80
100
p<0,0005
pdx
1Plasma cholesterol
Plasmacholesterol(mg/dL)
W
ater,po
50m
g/day,po
100
120
140
160
180
p<0,019
Plasma triglyceride
Plasmatriglyceride(mg/dL)
W
ater,po
pdx
150m
g/day,po
0
20
40
60
80
100
Plasma cholesterol
Plasmacholesterol(mg/dL)
W
ater,po
pdx
150m
g/day,po
0
50
100
150
200
p<0,037
Figure 1. When fed with fiber-deficient diet, PDX reduced fasting plasma cholesterol
(p<0.05) (A), while the reduction in plasma triglycerides was not significant (B).
A B
Figure 2. When fed with western- diet, PDX significantly reduced food intake (p<0.001) (A), which
translated to a trend in body weight loss (p=0.074) (B). Both fasting plasma cholesterol (p<0.05)
(C) as well as triglycerides (p<0.001) (D) showed reduced values compared to control.
Figure 3. When fed with western- diet, the total fecal output of lipid increased numeri-
cally with PDX (A) and there was a trend for upregulation of LDLr gene expression in
liver by PDX (B).
A B
C D
A B

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Hypolipidemic effects of polydextrose in mouse

  • 1. W ater,po d0 PD X 150 m g/d,po d0 W ater,po d14 PD X 150 m g/d,po d14 0 2 4 6 8 Totallipids(g/100g) W ater,po d14 PD X 150 m g/d,po d14 0 1 2 3 4 LDLrmRNA/RPLP0mRNA Putaala H.1 , Raza G. S.2 , Tiihonen K.1 , Mäkelä K. A. 2 , Herzig K. H.2 BACKGROUND METHODS RESULTS DISCUSSION HYPOLIPIDEMIC EFFECTS OF POLYDEXTROSE IN MOUSE 1 DuPont Nutrition & Health Active Nutrition Sokeritehtaantie 20 02460 KANTVIK, FINLAND E-mail: heli.putaala@dupont.com The information contained herein is based on data known to DuPont or its affiliates at the time of preparation of the information and believed by them to be reliable. This is business-to-business information intended for food, beverage and supplement producers, and is not intended for the final consumer of a finished food, beverage or supplement product. The information is provided “as is” and its use is at the recipient’s sole discretion and risk. It is the recipient’s sole responsibility to determine the suitability and legality of its proposed use of DuPont products for its specific purposes. Information and statements herein shall not be construed as licenses to practice, or recommendations to infringe, any patents or other intellectual property rights of DuPont or others. DUPONT HEREBY EXPRESSLY DISCLAIMS (I) ANY AND ALL LIABILITY IN CONNECTION WITH SUCH INFORMATION, INCLUDING, BUT NOT LIMITED TO, ANY LIABILITY RELATING TO THE ACCURACY, COMPLETENESS, OR USEFULNESS OF SUCH INFORMATION, AND (II) ANY AND ALL REPRESENTATIONS OR WARRANTIES, EXPRESS OR IMPLIED, WITH RESPECT TO SUCH INFORMATION, OR ANY PART THEREOF, INCLUDING ALL REPRESENTATIONS AND WARRANTIES OF TITLE, NONINFRINGEMENT OF COPYRIGHT OR PATENT RIGHTS OF OTHERS, MERCHANTABILITY, FITNESS OR SUITABILITY FOR ANY PURPOSE, AND WARRANTIES ARISING BY LAW, STATUTE, USAGE OF TRADE OR COURSE OF DEALING. Copyright © 2014 DuPont or its affiliates. All Rights Reserved. The DuPont Oval Logo, DuPont™, The miracles of science™ and all products denoted with ® or ™ are registered trademarks or trademarks of E.I. du Pont de Nemours and Company or its affiliated companies. Hyperlipidemia is a risk factor for cardiovascular and metabolic diseases. It is established that elevated plasma triglyceride-rich lipoproteins and low levels of HDL-cholesterol levels are directly related to the risk of cardiovascular disease [1]. Polydextrose (PDX, Litesse® Ultra™, DuPont) is soluble glucose polymer used as a fat and sugar replacer as well as dietary fibre. As PDX has potential to improve hyperlipidemia [2-4] and satiety [5-7] we investigated effects of PDX on lipid profiles in mice fed with fiber-deficient and western diet with an attempt to further characterize lipid-attenuating mechanisms. Male C57BL/6 (n=36) mice were fed either fiber- deficient (<0.5% fibre 10% kcal fat) or western- diet (5% fiber, 41% kcal fat) for 2 weeks. Animals were gavaged twice a day either with water containing PDX 150 mg/day or water alone as control. Body weight, food intake and indirect calorimetric measure- ments were performed in a home cage- based monitoring system (LabMaster®). Fasting blood samples and feces were collected for lipid measurements. Gene expression for lipid metabolism was performed by real–time PCR in liver. In a recent meta-analysis, it was concluded that PDX can reduce voluntary energy intake at a subsequent meal [5]. The present study shows that longer-term consumption of PDX might translate into a reduction of cumulative food intake and loss in body weight. Polydextrose has been shown to decrease postpran- dial elevation of triglycerides [2]. The present study shows a longer-term effect of PDX on triglycerides and total cholesterol reduction, and is in accordance with previous studies [3]. The upregulation of LDLreceptor gene in liver could increase LDL clearance by the liver which would then translate into reduction of total cholesterol and triglycerides [1]. The binding of lipids to fiber and evacuation through feces may be additional mechanism. 2 Institute of Biomedicine, Dept.of Physiology and Biocenter of Oulu, Univ. of Oulu, Medical Research Center Oulu and Oulu Univ. Hospital, OULU, FINLAND References: [1] Miller, M., et al., Circulation, 2011. 123(20): p. 2292-2333. [2] Tiihonen, K., et al., Nutrition Journal, 2015. 14(1): p. 23. [3] Pronczuk, A. and K.C. Hayes, Nutrition Research, 2006. 26(1): p. 27-31. [4] Schwab, U., et al., European Journal of Clinical Nutrition, 2006. 60(9): p. 1073-80. [5] Ibarra, A., et al., Appetite, 2014. 87C: p. 30-37. [6] Hull, S., et al., Appetite, 2012. 59(3): p. 706-712. [7] Ranawana, V., A. Muller, and C.J. Henry, European Journal of Nutri- tion, 2013. 52(3): p. 885-93. Cumulative body weight gain Days Cumulativebodyweight(g) 0 2 4 6 8 10 12 14 0.0 0.5 1.0 1.5 2.0 2.5 Water, po PDX 150mg/day, po Cumulative food intake Days Foodintake/bodyweight[g/g] 0 2 4 6 8 10 12 14 0.0 0.6 1.2 1.8 water, po pdx 150mg/day, po p<0,001 pd Plasma triglyceride Plasmatriglyceride(mg/dL) W ater,pox 150m g/day,po 20 40 60 80 100 p<0,0005 pdx 1Plasma cholesterol Plasmacholesterol(mg/dL) W ater,po 50m g/day,po 100 120 140 160 180 p<0,019 Plasma triglyceride Plasmatriglyceride(mg/dL) W ater,po pdx 150m g/day,po 0 20 40 60 80 100 Plasma cholesterol Plasmacholesterol(mg/dL) W ater,po pdx 150m g/day,po 0 50 100 150 200 p<0,037 Figure 1. When fed with fiber-deficient diet, PDX reduced fasting plasma cholesterol (p<0.05) (A), while the reduction in plasma triglycerides was not significant (B). A B Figure 2. When fed with western- diet, PDX significantly reduced food intake (p<0.001) (A), which translated to a trend in body weight loss (p=0.074) (B). Both fasting plasma cholesterol (p<0.05) (C) as well as triglycerides (p<0.001) (D) showed reduced values compared to control. Figure 3. When fed with western- diet, the total fecal output of lipid increased numeri- cally with PDX (A) and there was a trend for upregulation of LDLr gene expression in liver by PDX (B). A B C D A B