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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
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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