2010
DOI: 10.1016/j.jnutbio.2009.07.008
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Effects of dietary fish oil on thyroid hormone signaling in the liver

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Cited by 27 publications
(22 citation statements)
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“…In our present study, FO treatment led to a slight increase in serum T 4 , with no changes in serum T 3 or TSH, only in euthyroid status, due to an unknown mechanism. Because in our previous study animals fed a FO-enriched diet exhibited no alterations in serum TH levels, but still presented higher TRb1 and mGPD expression (Souza et al 2010), we believe that the induction of the enzyme, in euthyroid condition, was due to the increased availability of TRb1 caused by FO treatment, independent of serum TH. Liver mGPD is also a target of PPARa (Patsouris et al 2004), but hypothyroidism has been shown to attenuate the effect of a PPARa agonist on mGPD activity (Shoemaker & Yamazaki 1991, Pacot et al 1993.…”
Section: Discussionmentioning
confidence: 69%
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“…In our present study, FO treatment led to a slight increase in serum T 4 , with no changes in serum T 3 or TSH, only in euthyroid status, due to an unknown mechanism. Because in our previous study animals fed a FO-enriched diet exhibited no alterations in serum TH levels, but still presented higher TRb1 and mGPD expression (Souza et al 2010), we believe that the induction of the enzyme, in euthyroid condition, was due to the increased availability of TRb1 caused by FO treatment, independent of serum TH. Liver mGPD is also a target of PPARa (Patsouris et al 2004), but hypothyroidism has been shown to attenuate the effect of a PPARa agonist on mGPD activity (Shoemaker & Yamazaki 1991, Pacot et al 1993.…”
Section: Discussionmentioning
confidence: 69%
“…Previously, we had reported that rats fed an FO-enriched diet, from lactation to adulthood, exhibited higher hepatic TRb1 expression (Souza et al 2010) accompanied by higher enzymatic activity of the mGPD, a well-known target of TH, involved in glycerol metabolism and in the oxidative mitochondrial process. In this study, we observed that FO given to adult animals, as a supplement by oral administration, during a shorter period of treatment (3 weeks) also provoked the enhancement of not only TRb1 protein content and mGPD activity but also their respective mRNAs, suggesting the involvement of a transcriptional mechanism.…”
Section: Discussionmentioning
confidence: 98%
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“…These studies showed that decreased liver damage after n-3 PUFA supplementation and T 3 administration was accompanied by normalization of NF-κB signaling and TNF-α response, with values of NF-κB DNA binding activity, haptoglobin mRNA expression and content, and serum TNF-α levels and liver TNF-α mRNA content being similar to those of control sham-operated animals. Recent reports on the effects of long-term supplementation of dietary fish oil suggest enhancement of thyroid hormone action by fish oil supplementation, as shown by higher expression of liver thyroid hormone receptor β1 protein and enhanced activity of liver mitochondrial glycerophosphate dehydrogenase, the enzyme involved in thermogenesis and a well-characterized target of thyroid hormone, stimulated by T 3 via thyroid hormone receptor β1 [27]. Although the effects of short-term n-3 PUFA supplementation on thyroid signaling via thyroid hormone receptor β1 have not been assessed, the molecular mechanisms responsible for liver preconditioning after n-3 PUFA supplementation and T 3 administration may include enhancement of thyroid hormone action by fish oil supplementation.…”
Section: Discussionmentioning
confidence: 99%