Effect of iodine intake and methimazole on lymphocytic thyroiditis in the BB/W rat

1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S70-S76 ◽  
Author(s):  
Lewis E. Braverman ◽  
Terri Paul ◽  
Walter Reinhardt ◽  
Michael C. Appel ◽  
Elsie M. Allen
Keyword(s):  
Thyroid Function ◽  
Low Dose ◽  
Elevated Serum ◽  
Iodine Intake ◽  
Sprague Dawley ◽  
Lower Serum ◽  
Excess Iodine ◽  
Essentially Normal ◽  
Sprague Dawley Rats ◽  
Serum Tsh

Abstract. Spontaneous LT and elevated serum anti-Tg occur in the diabetes prone BB/W rat, but thyroid function is essentially normal in the rats with LT. Prolonged low dose MMI decreases the incidence of LT in BB/W rats. The administration of excess iodine beginning at 30 days of age markedly accelerates the occurrence of LT and anti-Tg at 90 days of age. Low iodine intake decreases the incidence of LT. Excess iodine intake did not induce LT in W-line, Wistar-Furth, and SpragueDawley rats. This suggests that iodine induced LT occurs only in genetically susceptible rats. Despite the increased incidence of LT during iodine administration, thyroid function remains essentially normal. This is in contrast to the frequent induction of hypothyroidism following iodine administration to euthyroid patients with Hashimoto's thyroiditis. In order to decrease thyroid reserve, rats were hemiTX at 30 days of age. The administration of iodine markedly increased the incidence of LT and serum anti-Tg, increased the weight of the remaining lobe, and induced hypothyroidism as determined by significantly lower serum T4 and T3 concentrations and elevated serum TSH concentrations. Excess iodine administration to hemi-TX W-line rats (genetically equivalent, non-diabetes, non-LT prone BB/W rats) did not induce LT but did induce hypothyroidism, suggesting that BB/W and W-line rats are susceptible to iodine induced hypothyroidism, perhaps unrelated to the induction of LT. Excess iodine did not induce LT or affect thyroid function in hemi-TX Wistar-Furth and Sprague-Dawley rats.

scholarly journals Differential Effects of Refeeding on Melanocortin-Responsive Neurons in the Hypothalamic Paraventricular Nucleus

Endocrinology ◽  
2008 ◽  
Vol 149 (9) ◽  
pp. 4329-4335 ◽  
Author(s):  
Edith Sánchez ◽  
Praful S. Singru ◽  
Runa Acharya ◽  
Monica Bodria ◽  
Csaba Fekete ◽  
...  
Keyword(s):  
Gene Expression ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Early Action ◽  
Sprague Dawley Rats ◽  
Melanocortin Signaling ◽  
Agouti Related Protein ◽  
Serum Tsh

To explore the effect of refeeding on recovery of TRH gene expression in the hypothalamic paraventricular nucleus (PVN) and its correlation with the feeding-related neuropeptides in the arcuate nucleus (ARC), c-fos immunoreactivity (IR) in the PVN and ARC 2 h after refeeding and hypothalamic TRH, neuropeptide Y (NPY) and agouti-related protein (AGRP) mRNA levels 4, 12, and 24 h after refeeding were studied in Sprague-Dawley rats subjected to prolonged fasting. Despite rapid reactivation of proopiomelanocortin neurons by refeeding as demonstrated by c-fos IR in ARC α-MSH-IR neurons and ventral parvocellular subdivision PVN neurons, c-fos IR was present in only 9.7 ± 1.1% hypophysiotropic TRH neurons. Serum TSH levels remained suppressed 4 and 12 h after the start of refeeding, returning to fed levels after 24 h. Fasting reduced TRH mRNA compared with fed animals, and similar to TSH, remained suppressed at 4 and 12 h after refeeding, returning toward normal at 24 h. AGRP and NPY gene expression in the ARC were markedly elevated in fasting rats, AGRP mRNA returning to baseline levels 12 h after refeeding and NPY mRNA remaining persistently elevated even at 24 h. These data raise the possibility that refeeding-induced activation of melanocortin signaling exerts differential actions on its target neurons in the PVN, an early action directed at neurons that may be involved in satiety, and a later action on hypophysiotropic TRH neurons involved in energy expenditure, potentially mediated by sustained elevations in AGRP and NPY. This response may be an important homeostatic mechanism to allow replenishment of depleted energy stores associated with fasting.

Subclinical hypothyroidism

2011 ◽  
pp. 543-547
Author(s):  
Jayne A. Franklyn
Keyword(s):  
Thyroid Function ◽  
Subclinical Hypothyroidism ◽  
Expert Panel ◽  
Elevated Serum ◽  
Thyroid Stimulating Hormone ◽  
Free Thyroxine ◽  
Thyroid Function Tests ◽  
Free Triiodothyronine ◽  
Function Tests ◽  
Serum Tsh

Subclinical hypothyroidism is defined biochemically as the association of a raised serum thyroid-stimulating hormone (TSH) concentration with normal circulating concentrations of free thyroxine (T4) and free triiodothyronine (T3). The term subclinical hypothyroidism implies that patients should be asymptomatic, although symptoms are difficult to assess, especially in patients in whom thyroid function tests have been checked because of nonspecific complaints such as tiredness. An expert panel has recently classified individuals with subclinical hypothyroidism into two groups (1): (1) those with mildly elevated serum TSH (typically TSH in the range 4.5–10.0 mU/l) and (2) those with more marked TSH elevation (serum TSH >10.0 mU/l).

Subchronic Toxicity of S-111-S-WB in Sprague Dawley Rats

2010 ◽  
Vol 29 (4) ◽  
pp. 358-371 ◽  
Author(s):  
Jozef J. W. M. Mertens ◽  
Daniel W. Sved ◽  
Gary B. Marit ◽  
Nichole R. Myers ◽  
Phil L. Stetson ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Steady State ◽  
Ammonium Salts ◽  
Serum Concentrations ◽  
Sprague Dawley ◽  
Subchronic Toxicity ◽  
Lower Serum ◽  
Sprague Dawley Rats ◽  
Steady State Serum ◽  
Effect Level

S-111-S-WB, a mixture of perfluoro fatty acid ammonium salts (C6-C13), was administered orally to Crl:CD (SD)IGS-BR rats. Higher hepatic β-oxidation and liver weights with hepatocellular hypertrophy were present at the 0.125 and 0.6 mg/kg/d dosage. The 0.6 mg/kg/d males developed hepatocellular degeneration and necrosis. Lower serum protein and higher bilirubin and BUN were seen in the 0.6 mg/kg/d males and lower globulin and higher alkaline phosphatase in the 0.125 mg/kg/d males and 0.6 mg/kg/d animals. After 2 weeks, serum concentrations of pentadecafluorooctanoic acid (C8), heptadecafluorononanoic acid (C9), perfluoroundecanoic acid (C11), and perfluorotridecanoic acid (C13) were constant for at least 8 hours. After 90 days, only C9 in the 0.025 mg/kg/d females had reached steady state. Serum C8 and C9 concentrations in the males were 10-fold higher than in the females, whereas C11 and C13 were similar for both genders. The main elimination was via the urine for C8 (males) and C9 (females), and via the feces for C11 and C13. The no-observed-effect level (NOEL) was 0.025 mg/kg/d for the males and 0.125 mg/kg/d for the females.

scholarly journals Chronic Microcystin-LR Exposure Induces Hepatocarcinogenesis via Increased Gankyrin in Vitro and in Vivo

2018 ◽  
Vol 49 (4) ◽  
pp. 1420-1430 ◽  
Author(s):  
Lixiong He ◽  
Yujing Huang ◽  
Qiaonan Guo ◽  
Hui Zeng ◽  
Chuanfen Zheng ◽  
...  
Keyword(s):  
Low Dose ◽  
Soft Agar ◽  
Tumor Formation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
L02 Cells ◽  
Insight Into

Background/Aims: Our recent study indicated that the serum microcystin-LR (MC-LR) level is positively linked to the risk of human hepatocellular carcinoma (HCC). Gankyrin is over-expressed in cancers and mediates oncogenesis; however, whether MC-LR induces tumor formation and the role of gankyrin in this process is unclear. Methods: We induced malignant transformation of L02 liver cells via 35 passages with exposure to 1, 10, or 100 nM MC-LR. Wound healing, plate and soft agar colony counts, and nude mice tumor formation were used to evaluate the tumorigenic phenotype of MC-LR-treated cells. Silencing gankyrin was used to confirm its function. We established a 35-week MC-LR exposure rat model by twice weekly intraperitoneal injection with 10 μg/kg body weight. In addition, 96 HCC patients were tested for tumor tissue gankyrin expression and serum MC-LR levels. Results: Chronic low-dose MC-LR exposure increased proliferation, mobility, clone and tumor formation abilities of L02 cells as a result of gankyrin activation, while silencing gankyrin inhibited the carcinogenic phenotype of MC-LR-treated cells. MC-LR also induced neoplastic liver lesions in Sprague-Dawley rats due to up-regulated gankyrin. Furthermore, a trend of increased gankyrin was observed in humans exposed to MC-LR. Conclusion: These results suggest that MC-LR induces hepatocarcinogenesis in vitro and in vivo by increasing gankyrin levels, providing new insight into MC-LR carcinogenicity studies.

scholarly journals Dose-dependent acceleration in the delayed effects of neonatal oral exposure to low-dose 17α-ethynylestradiol on reproductive functions in female Sprague-Dawley rats

2015 ◽  
Vol 40 (6) ◽  
pp. 727-738 ◽  
Author(s):  
Mariko Shirota ◽  
Jun Kawashima ◽  
Tomohiro Nakamura ◽  
Junichi Kamiie ◽  
Kinji Shirota ◽  
...  
Keyword(s):  
Low Dose ◽  
Oral Exposure ◽  
Sprague Dawley ◽  
Delayed Effects ◽  
Sprague Dawley Rats ◽  
Dose Dependent

Sympathetic and parasympathetic component of bradycardia triggered by stimulation of NTS P2X receptors

2006 ◽  
Vol 290 (2) ◽  
pp. H807-H812 ◽  
Author(s):  
Amy M. Kitchen ◽  
Donal S. O'Leary ◽  
Tadeusz J. Scislo
Keyword(s):  
Low Dose ◽  
Nucleus Tractus Solitarius ◽  
Receptor Activation ◽  
P2x Receptors ◽  
P2x Receptor ◽  
High Dose ◽  
Adrenergic Blockade ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Stimulation Of

We have previously shown that activation of P2X purinoceptors in the subpostremal nucleus tractus solitarius (NTS) produces a rapid bradycardia and hypotension. This bradycardia could occur via sympathetic withdrawal, parasympathetic activation, or a combination of both mechanisms. Thus we investigated the relative roles of parasympathetic activation and sympathetic withdrawal in mediating this bradycardia in chloralose-urethane anesthetized male Sprague-Dawley rats. Microinjections of the selective P2X purinoceptor agonist α,β-methylene ATP (25 pmol/50 nl and 100 pmol/50 nl) were made into the subpostremal NTS in control animals, after atenolol (2 mg/kg iv), a β1-selective antagonist, and after atropine methyl bromide (2 mg/kg iv), a muscarinic receptor antagonist. The bradycardia observed with activation of P2X receptors at the low dose of the agonist is mediated almost entirely by sympathetic withdrawal. After β1-adrenergic blockade, the bradycardia was reduced to just −5.1 ± 0.5 versus −28.8 ± 5.1 beats/min in intact animals. Muscarinic blockade did not produce any significant change in the bradycardic response at the low dose. At the high dose, both β1-adrenergic blockade and muscarinic blockade attenuated the bradycardia similarly, −37.4 ± 6.4 and −40.6 ± 3.7 beats/min, respectively, compared with −88.0 ± 11 beats/min in control animals. Double blockade of both β1-adrenergic and muscarinic receptors virtually abolished the response (−2.5 ± 0.8 beats/min). We conclude that the relative contributions of parasympathetic activation and sympathetic withdrawal are dependent on the extent of P2X receptor activation.

Excess Iodine Intake and Thyroid Function and Growth

Thyroid ◽  
1990 ◽  
Vol 1 (1) ◽  
pp. 69-72 ◽  
Author(s):  
ORLO H. CLARK
Keyword(s):  
Thyroid Function ◽  
Iodine Intake ◽  
Excess Iodine

PITUITARY-THYROID FUNCTION IN THYROTOXIC PATIENTS IN RELATION TO LONG-ACTING THYROID STIMULATOR (LATS) LEVELS

1970 ◽  
Vol 65 (4) ◽  
pp. 577-582 ◽  
Author(s):  
Minoru Fukuchi ◽  
Tohru Matsuoka ◽  
Tadashi Inoue ◽  
Kiyoshi Miyai ◽  
Yuichi Kumahara
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Function ◽  
Elevated Serum ◽  
Antithyroid Drug ◽  
Initial Values ◽  
Long Acting ◽  
Serum Tsh

ABSTRACT Serial changes in TSH, LATS, and thyroxine levels in the sera were studied following administration of an antithyroid drug or a thyroid hormone to thyrotoxic patients who became euthyroid after treatment. These changes were simultaneously determined by means of human TSH radioimmunoassay, McKenzie's bioassay. and the method of Murphy, respectively. Administration of 1-methyl-2-mercaptoimidazole (MMI) led to a decrease in thyroxine concentration and to a 6–10 times increase of the initial values in serum TSH concentration. Following administration of thyroxine at the end of the MMI treatment, the elevated serum TSH was rapidly decreased with an increase in thyroxine concentration. LATS activity, however, showed no significant changes throughout these experiments in which the reciprocal changes between TSH and thyroxine concentrations were observed.

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