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Fig. 10.4
Protein expression. (
a
) Ratio of pIRS-1 by IRS-1 total content [pIRS-1/IRS-1]; (
b
) ratio
of pAKT by AKT total content [pAKT/AKT]. Data represents protein expression in the hypothala-
mus of animals C, CH, CHT, R, RH, and RHT.
Bars
represent means ± SEM. *
p
< 0.05 compared
to C.
N
= 4-8
Here, we also show that TAU supplementation prevented body fat accumulation,
hypercholesterolemia, and hyperglycemia caused by HFD in normal-protein mice
(Table
10.1
and Fig.
10.1
). Nardelli et al. (
2011
) also showed reduction in body
adiposity as well as lower lipids in plasma and liver of obese rats supplemented
with TAU. Thus, lower lipid storage may contribute to the improved plasma lipid
profile observed in our study.
In addition, TAU improved glucose tolerance in obese normal-protein mice
(Fig.
10.2
). This effect may be due to a possible interaction of TAU with the IR
(Maturo and Kulakowski,
1988
; Carneiro et al.
2009
). Also, TAU treatment nor-
malizes islet-cell proliferation and insulin secretion in fetal protein-restricted
rodents (Kalbe et al.
2005
). Restoration of insulin secretory capacity was observed
in rats submitted to protein restriction started at weaning and treated with TAU
(Batista et al.
2012
) .
Recently, Solon et al. (
2012
) showed that TAU dose dependently had an anorexi-
genic effect upon hypothalamus. Intracerebroventricular (icv) administration of
TAU reduces NPY expression without modifying the amount of POMC, decreasing
food intake in rats. This TAU effect was accompanied by enhanced hypothalamic
content of pAkt. In addition, TAU increases insulin hypothalamic sensitivity via
Akt/FOXO1, JAK2, STAT3, and mTOR activation (Solon et al.
2012
) , suggesting a
direct interaction of the amino acid with this pathway in CNS as already described
in peripheral tissues (Carneiro et al.
2009
). Our study is in accordance with the
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