The relationship between the thyroid gland and the liver

Malik, Raza; Hodgson, H. J. F.

doi:10.1093/qjmed/95.9.559

Cited by 302 publications

(273 citation statements)

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“…Since thyroid hormones influence the metabolic state of the liver (Malik & Hodgson 2002) and because we have recently demonstrated that SHBG gene expression in hepatocytes is dynamically regulated by changes in their metabolic state (Selva et al 2007), we set out to determine whether thyroid hormoneinduced changes in the metabolic state of HepG2 cells and the liver could account for changes in SHBG expression.…”

Section: Introductionmentioning

confidence: 99%

Thyroid hormones act indirectly to increase sex hormone-binding globulin production by liver via hepatocyte nuclear factor-4α

Selva¹,

Hammond²

2009

Journal of Molecular Endocrinology

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Thyroid hormones increase hepatic sex hormone-binding globulin (SHBG) production, which is also regulated by hepatocyte nuclear factor-4a (HNF-4a) in response to changes in the metabolic state of the liver. Since the human SHBG promoter lacks a typical thyroid hormone response element, and because thyroid hormones influence metabolic state, we set out to determine whether thyroid hormones mediate SHBG expression indirectly via changes in HNF-4a levels in HepG2 human hepatoblastoma cells, and in the livers of transgenic mice that express a 4 . 3 kb human SHBG transgene under the control of its own 0 . 8 kb promoter sequence. Thyroid hormones (triiodothyronine (T 3 ) and thyroxine (T 4 )) increase SHBG accumulation in HepG2 cell culture medium over 5 days, and increase cellular SHBG mRNA levels. In addition, T 4 treatment of HepG2 cells for 5 days increased HNF-4a mRNA and HNF-4a levels in concert with decreased cellular palmitate levels. Plasma SHBG levels were also increased in mice expressing a human SHBG transgene after 5 days treatment with T 3 along with increased hepatic HNF-4a levels. In HepG2 cells, the human SHBG promoter failed to respond acutely (within 24 h) to T 4 treatment, but a 4-day pre-treatment with T 4 resulted in a robust response that was prevented by co-treatment with HNF-4a siRNA, or by blocking the b-oxidation of palmitate through co-treatment with the carnitine palmitoyltransferase I inhibitor, etomoxir. These data lead us to conclude that thyroid hormones increase SHBG production indirectly by increasing HNF-4a gene expression, and by reducing cellular palmitate levels that further contribute to increased HNF-4a levels in hepatocytes.

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Section: Introductionmentioning

confidence: 99%

Thyroid hormones act indirectly to increase sex hormone-binding globulin production by liver via hepatocyte nuclear factor-4α

Selva¹,

Hammond²

2009

Journal of Molecular Endocrinology

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“…The thyroid gland is the body's primary regulator of metabolism through hormones such as triiodothyronine (T3) and thyroxine (T4), which are essential for the normal development of body organs (Malik & Hodgson, 2002;Peepre et al, 2014). Peepre et al (2014) found that vitamin C, VE, and turmeric extract increase the plasma T3 and T4 concentrations of Wistar rats.…”

Section: Discussionmentioning

confidence: 99%

Lipid Peroxidation in the Plasma, Lungs, Heart and Liver of Broilers Fed a Grape Seed Extract and Raised at 2278 m of Altitude

Rodríguez-Ortega

Juárez-Juárez

Pró-Martínez

et al. 2017

Rev. Bras. Cienc. Avic.

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Grape seed extract, high altitude, lipid peroxidation, vitamin E. ABSTRACTThe aim of this research was to evaluate the effect of partial substitution of vitamin E (VE) by grape seed extract (GSE) on glutathione peroxidase activity (GPxA), nitric oxide (NO) concentration and lipid peroxidation [malondialdehyde (MDA) concentration] in the plasma, lungs, heart and liver, and live performance of broilers raised at 2278 m of altitude. One-d-old Ross 308 male chickens (n = 420) were randomly distributed into three treatments: Control-AL (basal diet containing 40 IU of VE and fed ad libitum; AL), Control-FR (basal diet and feed restriction; FR) and GSE-AL [basal diet containing 10 mg of GSE (equivalent to 30 IU VE) plus 10 IU of VE and fed AL]. The data were analyzed using one-way analysis of variance. Glutathione peroxidase activity, and NO and MDA concentrations in the plasma were evaluated on d 46. On d 47, MDA was evaluated in the lungs, heart and liver. Live performance parameters were recorded weekly. There were no significant differences (p>0.05) in live performance and NO concentration among treatments. Birds from the GSE-AL treatment presented the lowest (p<0.05) GPxA, the highest (p<0.05) MDA concentration in the plasma, heart and liver, and intermediate MDA concentration in the lungs. Our results suggest that GSE may partially replace VE in broiler diets without impairment of live performance. However, further research is required to determine the optimal level of dietary GSE inclusion to reduce lipid peroxidation in the plasma, lungs, heart, and liver of broilers raised at 2278 m of altitude.

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“…The liver has a central role in de-iodination and also performs specific functions related to thyroid hormone transport and metabolism [17][18][19][20]. Normal functioning thyroid and liver axis are essential for normal growth and metabolism [21]. PSC in comparison with inflammatory bowel disease (IBD) was found to be more common with other autoimmune diseases like Hashimoto's thyroiditis, Graves's disease and Riedel's thyroiditis [2].…”

Section: Discussionmentioning

confidence: 99%