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enzyme of gluconeogenesis, phosphoenol pyruvate carboxykinase (PCK1), but
found no difference in mRNA levels between groups (Table
5.1
).
5.3.3
Lipid Parameters
Fructose caused a significant decrease in hepatic triglyceride content, with taurine
supplementation rescuing this effect. No effect of taurine alone on hepatic triglycer-
ide content was observed (Table
5.1
). No difference between groups was observed
with regard to plasma triglycerides, nonesterified free fatty acids, HDL, LDL, or
total cholesterol (Table
5.1
).
5.4
Discussion
The current study set out to examine the effect of long-term taurine supplementation
in rats receiving a high-fructose diet. Surprisingly we saw both beneficial and detri-
mental effects of taurine upon glucose metabolism.
5.4.1
Taurine and Glucose Metabolism
Taurine has in studies from two different laboratories been shown to counteract the
effects of a high-fructose diet on glucose metabolism in Wistar rats, with no observ-
able negative side effects of taurine supplementation (El Mesallamy et al.
2010
;
Nandhini et al.
2004,
2005
; Nandhini and Anuradha
2002
) .
In the current study, taurine seems to have a beneficial effect on glucose toler-
ance in fructose-fed rats, but not when given together with a control diet. As taurine
has previously been shown to improve insulin signaling (Nakaya et al.
2000
;
Nandhini et al.
2005
) we examined whether or not this could be due to increased
insulin-induced skeletal muscle signaling through AKT. However, although we did
see an increase in AKT phosphorylation in the group receiving fructose and taurine,
the increase was not significant compared to the other groups, ruling out this mecha-
nism of action as an explanation of the improvement in glucose tolerance, although
further studies are needed to confirm this. Taurine has been shown to potentiate
insulin release (Carneiro et al.
2009
), and although some disagree (Kulakowski and
Maturo
1984
), one might speculate that this could be one possible explanation for
the improved glucose tolerance. Unfortunately we did not measure insulin levels
during the glucose tolerance tests and although we found no difference in fasting
insulin levels, this question remains unanswered.
We examined whether or not the increase in fasting glucose could be due to an
increase in hepatic gluconeogenesis by measuring the mRNA level of the rate-deter-
mining gluconeogenic enzyme PCK1 (Pilkis and Granner
1992
), but found no evi-
dence of PCK1 being increased. Increased glycogenolysis could also explain the
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