Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new cytomel research articles will be listed here shortly after becoming available to us.
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Br J Nutr. 2008 Jul 10; 1-10
Papadopoulos GA, Maes DG, Van Weyenberg S, van Kempen TA, Buyse J, Janssens GP
The present study aimed to investigate the effects of two lactation sow feeds, differing in n-6:n-3 ratio, given to sows before parturition on body condition and feed intake, periparturient metabolism (leptin, insulin, triiodothyronine (T3) and thyroxine (T4)), inflammatory parameters (TNFalpha, IL-6, serum amyloid A (SAA)) and on piglet performance (birth weight, survivability). The feed contained either a low (supplemented with fish oil; f groups) or high (supplemented with sunflower-seed oil; s groups) n-6:n-3 ratio and was administered from 8 d (f8, s8) or 3 d (f3, s3) before parturition until weaning. The level of inclusion of the oil sources was 2 %. Seventy-two sows were randomly allocated 8 d before expected farrowing into four groups: f3, f8, s3, s8. Type of feed had a significant influence on the sows' feed intake during the first 2 d of lactation (s < f), leptin on days 4, 3 and 2 before parturition (f < s), insulin on day 1 after parturition (f < s), T4 on the day before parturition (s < f) and rectal temperature on the day after parturition (f < s). Onset of administration of the feed (3 v. 8 d) had significant effects on leptin on day 2 before parturition (8 < 3), insulin on day 4 before parturition (3 < 8), T3 on day 4 before parturition and on the day after parturition (3 < 8), SAA on day 3 after parturition (8 < 3) and piglet weight during the first days postpartum (3 < 8). In conclusion, under the present conditions, a lactation feed low in n-6:n-3 ratio administered from 8 d before farrowing ensures improved feed intake during the first days postpartum and was associated with a better metabolic change and inflammatory profile in sows in the periparturient period.
Postnatal Administration of Dexamethasone for Weaning off the Ventilator Affects Thyroid Function.
Neonatology. 2008 Jul 9; 94(3): 164-169
Buimer M, van Wassenaer AG, Kok JH
Background: Very preterm neonates are at risk of hypothyroxinemia because of prematurity as well as because of neonatal disease. Hypothyroxinemia is associated with impaired developmental outcome. Preterm infants who cannot be weaned from the ventilator can be treated with dexamethasone. Glucocorticoid administration has been found to alter thyroid hormone parameters. Therefore, dexamethasone treatment in these infants might additionally impair their thyroid function, which could have consequences for developmental outcome. Objective: To assess what changes in thyroid function occur in the first hours after initiating dexamethasone treatment in ventilated preterm infants. Methods: Preterm infants, in whom the decision was taken to start dexamethasone treatment, were included. Thyroxine (T(4)), 3,5,3'-triiodothyronine (T(3)), reverse T(3) (rT(3)), thyroid-stimulating hormone (TSH) and cortisol were determined before and 6-9 h after administration of the first dose of a postnatal dexamethasone course. Details of clinical condition were recorded at both time points. Results: Sixteen very preterm infants were included at a median age of 20 days. While clinical condition was stable between start of dexamethasone and 6-9 h thereafter, TSH and T(3) levels decreased significantly. rT(3) levels significantly increased, resulting in a decrease in the T(3)/rT(3) ratio. There was no statistically significant effect on the levels of T(4). Conclusion: Postnatal dexamethasone administration negatively affects thyroid functionin the preterm infant with severe chronic lung disease.
Scand J Clin Lab Invest. 2008 Feb 5; 1-5
Asadi BA, Torjesen PA, Haug E, Berg JP
In resistance to thyroid hormone (RTH), decreased tissue responsiveness to thyroid hormones is usually caused by mutations in the thyroid hormone receptor beta (THRB) gene. Subsequently, in serum the level of thyroid stimulating hormone (TSH) is not suppressed despite increased concentrations of thyroxine (T(4)) and triiodothyronine (T(3)). In our laboratory, DNA sequences of exon 7 to 10 in the THRB gene have been analysed in individuals with biochemical signs of RTH. Four novel point mutations were identified (I250T, A279E, T327A and L440P) and their effects on T(3) binding activity characterized. The mutations were introduced into a vector carrying the wild-type THRB cDNA by in vitro mutagenesis. T(3)-binding activity was measured by a filter-binding assay procedure in receptors generated from the vector by in vitro transcription and translation. Specific binding was calculated as total activity subtracted by non-specific activity. The association constants (Ka) of the wild-type (WT) and mutant receptors were determined by Scatchard analysis. No specific T(3)-binding was observed for the receptor with the A279E mutation. The binding affinity was reduced by 74 % in the T327A mutant and by about 50 % in the I250T and L440P mutants compared to the WT receptor (Ka = 4.2x10(10) L/mol). The reduction of T(3)-binding affinity caused by the four mutations in our study is comparable to the effects of THRB gene mutations found in other patients with RTH and supports the assumption that the signs of RTH observed in our patients are caused by the mutations.
Kathmandu Univ Med J (KUMJ). 2007 Jul-Sep; 5(3): 330-4
Das BK, Baral N, Shyangwa PM, Toora BD, Lamsal M
Objective: To assess serum level of Thyroxine (T4), Triiodothyronine(T3) and thyroid stimulating hormone(TSH) in patient with depression. Methods: Thirty one clinically diagnosed depressed patients and equal number of healthy, age and sex matched control subjects were included in this study. Ham-D scale was used to classify the degree of depression into mild, moderate and severe grades. The biochemical parameters (T3, T4 and TSH) were estimated using commercially available kits. The data were analyzed by using (SPSS-10 software), one way ANOVA and chi2 test. Result: Female depressed (n = 17) cases outnumber the male depressed cases. The distributions of patients in mild, moderate and severe categories were similar. The T3 and T4 level were found to be significantly raised in the moderate depression as compared to the healthy controls. ANOVA with multiple comparisons testing among the patient group showed a significant high TSH level (F> 3.17) at 5% level of significance. A total of six depressive patients were found to have thyroid abnormalities. Conclusion: This study therefore points towards presence of thyroid dysfunction among the depressive which most often characterized as a "Lower Thyroid Syndrome". Thus inclusion of thyroid screening test among depressive patients may be helpful in proper management of cases.
Thyrotoxicosis outbreak linked to consumption of minced beef and chorizo: Minas, Uruguay, 2003-2004.
Public Health. 2008 Jul 3;
Conrey EJ, Lindner C, Estivariz C, Pereira M, Welsh J, Vignolo J, Fishbein D, Kettel Khan L, Grummer-Strawn L
OBJECTIVES: Thyrotoxicosis is produced by excessive quantities of thyroid hormone. Its most common causes involve inflammation of the thyroid gland. Much more rarely, thyrotoxicosis is due to exogenous intake of thyroid hormones or iodide compounds. Few outbreaks are documented. In 2003 to early 2004, doctors in Minas, Uruguay noted a sharp increase in the incidence of thyrotoxicosis in a neighbourhood, with multiple cases within families. The objective of this study was to identify the source of the outbreak. STUDY DESIGN: A case-control study was conducted following surveillance and environmental inspection. METHODS: Case patients were symptomatic residents of Minas with documented thyroid-stimulating hormone concentrations
J Med Food. 2008 Jun; 11(2): 376-81
Parmar HS, Kar A
ABSTRACT Peel extracts from Citrus sinensis, Punica granatum, and Musa paradisiaca were investigated for their effects on tissue lipid peroxidation (LPO) and on the concentration of thyroid hormones, insulin, and glucose in male rats. In vitro inhibition of H(2)O(2)-induced LPO in red blood cells of rats by 0.25, 0.50, 1.0, and 2.0 mug/mL C. sinensis, P. granatum, and M. paradisiaca peel extracts was observed in a dose-specific manner. Maximum inhibition was observed at 0.50 mug/mL C. sinensis, 2.0 mug/mL P. granatum, and 1.0 mug/mL M. paradisiaca. In the in vivo investigation, out of four different concentrations of each peel extract, 25, 200, and 100 mg/kg C. sinensis, P. granatum, and M. paradisiaca, respectively, were found to maximally inhibit hepatic LPO. The most effective doses were further evaluated for effects on serum triiodothyronine (T(3)), thyroxine (T(4)), insulin, and glucose concentrations. C. sinensis exhibited antithyroidal, hypoglycemic, and insulin stimulatory activities, in addition to inhibition of LPO, as it significantly decreased the serum T(4) (P < .05) and glucose (P < .001) concentrations with a concomitant increase in insulin levels (P < .05). P. granatum decreased LPO in hepatic, cardiac, and renal tissues (P < .01, P < .001, and P < .05, respectively) and serum glucose concentration (P < .01). M. paradisiaca strongly inhibited the serum level of thyroid hormones (P < .01 for both T(3) and T(4)) but increased the level of glucose (P < .05). These findings reveal the hitherto unknown potential of the tested peel extracts in the regulation of thyroid function and glucose metabolism. Besides antiperoxidative activity, C. sinensis extract has antithyroidal, hypoglycemic, and insulin stimulatory properties, which suggest its potential to ameliorate both hyperthyroidism and diabetes mellitus.
Functional central hypothyroidism in the elderly.
Aging Clin Exp Res. 2008 Jun; 20(3): 207-10
Sell MA, Schott M, Tharandt L, Cissewski K, Scherbaum WA, Willenberg HS
BACKGROUND AND AIMS: Previous studies have shown that blood concentrations of free thyroxin and basal thyroid-stimulating hormone (TSH) decrease during adult life. Suggested mechanisms include reduced thyroid activity resulting from decreased serum TSH concentrations, impairment of peripheral 5'-deiodinase, and an increase in reverse 3,5,3'-triiodothyronine due to non-thyroidal illness. However, testing of pituitary reserves leads to contradictory results and has infrequently been evaluated in studies. METHODS: We investigated whether the response of TSH to thyrotropin-releasing hormone (TRH) is preserved during aging. This was tested in a cohort of 387 subjects aged 13 to 100 years in whom thyroid disease was excluded by normal thyroid ultrasound, normal values for free thyroxin, free triiodothyronin, TSH, and negative thyroid peroxidase antibodies. RESULTS: Serum concentrations of free thyroxin remained almost unchanged, whereas free triiodothyronin and TSH levels were lower in older subjects. In addition, the TSH response to TRH was blunted in older subjects, especially in male individuals. CONCLUSIONS: There is evidence that the decreased thyroid hormone levels observed in aging are due to lower TSH concentrations, and that lower TSH concentrations may be linked to an impaired pituitary activity.
Rejuvenation Res. 2008 Jun; 11(3): 605-9
Weiss EP, Villareal DT, Racette SB, Steger-May K, Premachandra BN, Klein S, Fontana L
Abstract Caloric restriction (CR) decreases circulating triiodothyronine (T(3)) concentration. However, it is not known if this effect is due to body fat mass reductions or due to CR, per se. The purpose of this study was to test the hypothesis that plasma T(3) concentration decreases with CR-induced reductions in fat mass but not in response to similar decreases in fat mass that are induced by exercise. Sedentary, nonobese 50- to 60-year-old men and women with no clinical evidence of cardiovascular or metabolic disease and not taking thyroid medications were randomly assigned to 12 months of caloric restriction (n = 18) or exercise-induced weight loss (n = 17) or to a control group (n = 9). Body weight and composition and plasma concentrations of the thyroid hormones T(3), thyrotropin (TSH), thyroxine (T(4)), and free thyroxine (FT(4)) were measured at baseline and 12 months. Fat mass changed significantly in the CR (-6.3 +/- 1.0 kg) and exercise (-5.5 +/- 1.0 kg) groups but not in the control group (-0.6 +/- 1.4 kg). The changes were not significantly different between the CR and exercise groups. Plasma T(3) concentration decreased in the CR group (-9.8 +/- 2.0 ng/dL, p < 0.0001) but not in the exercise (-3.8 +/- 2.1 ng/dL, p = 0.07) or control (-1.3 +/- 2.8 ng/dL, p = 0.65) groups. TSH, T(4), and FT(4) did not change in any of the study groups. Twelve months of CR decreased circulating T(3) concentrations in middle-aged adults. This effect does not appear to be attributable to changes in body fat mass because a comparable decrease in T(3) concentration was not observed in response to an exercise-induced fat mass reduction.
Amiodarone increases the accumulation of DEA in a human alveolar epithelium-derived cell line.
Biol Pharm Bull. 2008 Jul; 31(7): 1449-52
Seki S, Itagaki S, Kobayashi M, Hirano T, Iseki K
Amiodarone (AMD)-induced pulmonary toxicity (AIPT) is the most life-threatening side-effect of AMD treatment. N-Monodesethylamiodarone (DEA), an active metabolite of AMD, also exhibits cytotoxicity and tends to accumulate in the lung more intensively than AMD. In this study, we characterized the mechanism of DEA accumulation using A549 cells as a model of the alveolar epithelium. Typical ATP-depletion compounds caused an approximately 30% increase in the accumulation of DEA in A549 cells, although these effects were less than those in Caco-2 cells. Triiodothyronine (T(3)), which exhibited an inhibitory effect on DEA efflux in Caco-2 cells, did not affect the accumulation of DEA in A549 cells. On the other hand, 100 microM AMD caused an approximately 200% increase in DEA content in A549 cells, although AMD accumulation was not affected by 100 microM DEA. Since the reducing effect of AMD on cellular ATP levels and that of FCCP were similar, the mechanism by which DEA accumulation is increased by AMD might be different from the ATP-dependent DEA efflux mechanism. The decrease in cell viability by DEA in the presence of AMD (IC(50) value of DEA for A549 cell viability: 25.4+/-2.4 microM) was more pronounced than that by DEA alone (IC(50) value: 11.5+/-3.0 microM). This further DEA accumulation by AMD might be a factor responsible for the greater accumulation of DEA than that of AMD in the lung in long-term AMD-treated patients.
Neurobiol Dis. 2008 Jun 4;
Vallortigara J, Alfos S, Micheau J, Higueret P, Enderlin V
Adult-onset hypothyroidism is associated with neurological changes such as cognitive dysfunction and impaired learning, which may be related to alterations of synaptic plasticity. We investigate the consequence of adult-onset hypothyroidism on thyroid-mediated transcription events in striatal synaptic plasticity, and the effect of triiodothyronine (T3) replacement. We used hypothyroid mice, treated with propylthiouracil (PTU) and methimazole (MMI), with or without subsequent administration of T3. We evaluated the amount of T3 nuclear receptors (TRalpha1, TRbeta) and striatal plasticity indicators: neurogranin (RC3), Ras homolog enriched in striatum (Rhes), Ca2+/calmodulin-dependent protein kinase (CaMKII), and dopamine- and cAMP-regulated phosphoprotein (DARPP-32). In addition, we assessed hypothyroid mice motor behavior as related to striatum synaptic functions. Hypothyroid mice exhibited significantly reduced TRbeta, RC3 and Rhes expression. T3 administration reversed the expression of TRbeta, RC3, and up-regulated CaMKII levels as well as motor behavior, and decreased DARPP-32 protein phosphorylation. We suggest that thyroid hormone modulation had a major impact on striatal synaptic plasticity of adult mice which produced in turn motor behavior modifications.