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  • 1
    Online Resource
    Online Resource
    Influence of Smoking on Thyroid Function in Japanese Subjects: Longitudinal Study for One Year of On-Off Smoking
    The Endocrine Society ; 2019
    In:  Journal of the Endocrine Society Vol. 3, No. 12 ( 2019-12-01), p. 2385-2396
    Details
    In: Journal of the Endocrine Society, The Endocrine Society, Vol. 3, No. 12 ( 2019-12-01), p. 2385-2396
    Abstract: We previously identified factors affecting thyroid status, including sex, age, and smoking. Objective In the current study, we increased the number of subjects examined and investigated the effects of these factors, particularly smoking and the thyroid peroxidase antibody (TPO-Ab), in Japanese patients with euthyroxinemia and serum free T4 levels within the normal range. Participants A total of 12,289 subjects who underwent health checkups were analyzed in a cross-sectional and longitudinal study. Results The mean age of subjects was 50 ± 10 years (age range: 21 to 88 years). Serum TSH levels and the prevalence of positivity for TPO-Ab increased with age in Japanese subjects with euthyroxinemia. Mean serum TSH levels were significantly lower in the smoking group than in the nonsmoking group except for women older than 50 years. Serum TSH levels were significantly higher in subjects with positivity for TPO-Ab than in those with negativity at all ages and in both sexes; however, smoking did not affect free T4 levels or positivity for TPO-Ab. Among men, the rate of smokers was significantly higher in patients with subclinical hyperthyroidism (25%) than in those with subclinical hypothyroidism (10%; P 〈 0.05). Furthermore, the results of the longitudinal study revealed a significant decrease in serum TSH levels 1 year after the start of smoking in men (P 〈 0.05). Conclusion Because smoking appeared to lower serum TSH levels in Japanese subjects with euthyroxinemia, their smoking status warrants careful consideration when evaluating subclinical thyroid function.
    Type of Medium: Online Resource
    ISSN: 2472-1972
    URL: Article
    DOI: 10.1210/js.2019-00155
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2019
    detail.hit.zdb_id: 2881023-5
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  • 2
    Online Resource
    Online Resource
    THRAP3 Interacts with HELZ2 and Plays a Novel Role in Adipocyte Differentiation
    The Endocrine Society ; 2013
    In:  Molecular Endocrinology Vol. 27, No. 5 ( 2013-05-01), p. 769-780
    Details
    In: Molecular Endocrinology, The Endocrine Society, Vol. 27, No. 5 ( 2013-05-01), p. 769-780
    Abstract: Using yeast two-hybrid screen, we previously isolated HELZ2 (helicase with zinc finger 2, transcriptional coactivator) that functions as a coregulator of peroxisome proliferator-activated receptorγ (PPARγ). To further delineate its molecular function, we here identified thyroid hormone receptor-associated protein3 (THRAP3), a putative component of the Mediator complex, as a protein stably associating with HELZ2 using immunoprecipitation coupled with mass spectrometry analyses. In immunoprecipitation assays, Thrap3 could associate with endogenous Helz2 as well as Pparg in differentiated 3T3-L1 cells. HELZ2 interacts with the serine/arginine-rich domain and Bcl2 associated transcription factor1-homologous region in THRAP3, whereas THRAP3 directly binds 2 helicase motifs in HELZ2. HELZ2 and THRAP3 synergistically augment transcriptional activation mediated by PPARγ, whereas knockdown of endogenous THRAP3 abolished the enhancement by HELZ2 in reporter assays. Thrap3, similar to Helz2, is evenly expressed in the process of adipogenic differentiation in 3T3-L1 cells. Knockdown of Thrap3 in 3T3-L1 preadipocytes using short-interfering RNA did not influence the expression of Krox20, Klf5, Cebpb, or Cebpd during early stages of adipocyte differentiation, but significantly attenuated the expression of Pparg, Cebpa, and Fabp4/aP2 and accumulation of lipid droplets. Pharmacologic activation of Pparg by troglitazone could not fully restore the differentiation of Thrap3-knockdown adipocytes. In chromatin immunoprecipitation assays, endogenous Helz2 and Thrap3 could be co-recruited, in a ligand-dependent manner, to the PPARγ-response elements in Fabp4/aP2 and Adipoq gene enhancers in differentiated 3T3-L1 cells. These findings collectively suggest that Thrap3 could play indispensable roles in terminal differentiation of adipocytes by enhancing PPARγ-mediated gene activation cooperatively with Helz2.
    Type of Medium: Online Resource
    ISSN: 0888-8809 , 1944-9917
    URL: Article
    DOI: 10.1210/me.2012-1332
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2013
    detail.hit.zdb_id: 1492112-1
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  • 3
    Online Resource
    Online Resource
    Protection Against High-Fat Diet-Induced Obesity in Helz2-Deficient Male Mice Due to Enhanced Expression of Hepatic Leptin Receptor
    The Endocrine Society ; 2014
    In:  Endocrinology Vol. 155, No. 9 ( 2014-09-01), p. 3459-3472
    Details
    In: Endocrinology, The Endocrine Society, Vol. 155, No. 9 ( 2014-09-01), p. 3459-3472
    Abstract: Obesity arises from impaired energy balance, which is centrally coordinated by leptin through activation of the long form of leptin receptor (Leprb). Obesity causes central leptin resistance. However, whether enhanced peripheral leptin sensitivity could overcome central leptin resistance remains obscure. A peripheral metabolic organ targeted by leptin is the liver, with low Leprb expression. We here show that mice fed a high-fat diet (HFD) and obese patients with hepatosteatosis exhibit increased expression of hepatic helicase with zinc finger 2, a transcriptional coactivator (Helz2), which functions as a transcriptional coregulator of several nuclear receptors, including peroxisome proliferator-activated receptor γ in vitro. To explore the physiological importance of Helz2, we generated Helz2-deficient mice and analyzed their metabolic phenotypes. Helz2-deficient mice showing hyperleptinemia associated with central leptin resistance were protected against HFD-induced obesity and had significantly up-regulated hepatic Leprb expression. Helz2 deficiency and adenovirus-mediated liver-specific exogenous Leprb overexpression in wild-type mice significantly stimulated hepatic AMP-activated protein kinase on HFD, whereas Helz2-deficient db/db mice lacking functional Leprb did not. Fatty acid-β oxidation was increased in Helz2-deficeint hepatocytes, and Helz2-deficient mice revealed increased oxygen consumption and decreased respiratory quotient in calorimetry analyses. The enhanced hepatic AMP-activated protein kinase energy-sensing pathway in Helz2-deficient mice ameliorated hyperlipidemia, hepatosteatosis, and insulin resistance by reducing lipogenic gene expression and stimulating lipid-burning gene expression in the liver. These findings together demonstrate that Helz2 deficiency ameliorates HFD-induced metabolic abnormalities by stimulating endogenous hepatic Leprb expression, despite central leptin resistance. Hepatic HELZ2 might be a novel target molecule for the treatment of obesity with hepatosteatosis.
    Type of Medium: Online Resource
    ISSN: 0013-7227 , 1945-7170
    URL: Article
    DOI: 10.1210/en.2013-2160
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2014
    detail.hit.zdb_id: 2011695-0
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  • 4
    Online Resource
    Online Resource
    SAT-437 Influence of Smoking on Thyroid Function in Japanese Subjects: Longitudinal Study for One Year of On-Off Smoking
    The Endocrine Society ; 2020
    In:  Journal of the Endocrine Society Vol. 4, No. Supplement_1 ( 2020-05-08)
    Details
    In: Journal of the Endocrine Society, The Endocrine Society, Vol. 4, No. Supplement_1 ( 2020-05-08)
    Abstract: Recent studies showed that various factors, including age, gender, race, iodine intake, obesity, the thyroid peroxidase antibody (TPO-Ab), and/or smoking, influence the thyroid status. In the present study, we analyzed and investigated the effects of these factors, particularly smoking and the thyroid peroxidase antibody (TPO-Ab) in Japanese euthyroxinemia individuals with serum free T4 level within normal range. A total of 12,289 subjects who underwent health check-ups were analyzed in a cross-sectional and longitudinal study. The mean age of subjects was 50 ± 10 years (age range: 21–88 years). Serum TSH levels and the prevalence of positivity for TPO-Ab increased with age in Japanese euthyroxinemia subjects. Mean and median serum TSH levels increased with age in smokers and non-smokers, but were significantly lower in smokers than in non-smokers among men and women in most age groups; the median 97.5th percentiles of TSH levels were 1.2 mU/liter and 2.9 mU/liter in smokers, and 1.4 mU/liter and 3.9 mU/liter in non-smokers in 31- to 40-year-old men, p & lt;0.01, and 1.4mU/liter and 4.3 mU/liter, and 1.8mU/liter and 6.2 mU/liter in 61- to 70-year-old men, p & lt;0.01. However, smoking had a negligible effect on serum TSH levels in women older than 50 years; 1.3 mU/liter in smokers and 1.6 mU/liter in non-smokers in 31- to 40-year-old women, p & lt;0.01, and 1.5 mU/liter and 1.8 mU/liter in 51- to 60-year-old women, p=0.3. Furthermore, the present study confirmed that serum free T4 levels in men progressively decreased with age, whereas no significant change was observed in women. Smoking did not affect the relationship between age and serum free T4 levels in men or women, except for men in their 20s. Serum TSH levels were significantly higher in subjects with positivity for TPO-Ab than in those with negativity at all ages and in both genders; however, smoking did not affect free T4 levels or the positivity for TPO-Ab. The rate of smokers in men was significantly higher in patients with subclinical hyperthyroidism (25%) than in those with subclinical hypothyroidism (10%, p & lt;0.05). Furthermore, the results of the longitudinal study revealed a significant decrease in serum TSH levels one year after the start of smoking in men (p & lt;0.05). Since smoking appears to lower serum TSH levels in Japanese euthyroxinemia subjects careful consideration of the smoking status is needed when evaluating subclinical thyroid function.
    Type of Medium: Online Resource
    ISSN: 2472-1972
    URL: Article
    DOI: 10.1210/jendso/bvaa046.1544
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2020
    detail.hit.zdb_id: 2881023-5
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  • 5
    Online Resource
    Online Resource
    A Case of Relapse of Lymphocytic Hypophysitis Triggered by the Pregnancy of the Second Child
    The Endocrine Society ; 2021
    In:  Journal of the Endocrine Society Vol. 5, No. Supplement_1 ( 2021-05-03), p. A562-A563
    Details
    In: Journal of the Endocrine Society, The Endocrine Society, Vol. 5, No. Supplement_1 ( 2021-05-03), p. A562-A563
    Abstract: Lymphocytic hypophysitis is a rare immune-mediated inflammatory disorder that causes pituitary dysfunction. It has been reported that lymphocytic hypophysitis onset during pregnancy rarely relapses or exacerbates in subsequent pregnancies. We herein report a patient with relapse of lymphocytic hypophysitis triggered by the pregnancy of the second child. Case Presentation: At the age of 34, at 28 weeks of gestation of the first child, she became aware of left visual field disorder and was diagnosed as an upper left visual field defect. An MRI scan revealed an enlargement of the pituitary gland and the thickening of the stalk. She was referred to our hospital for diagnosis and treatment. Laboratory data showed central adrenocortical dysfunction and central hypothyroidism. Based on the course of the disease, MRI findings and laboratory data, we diagnosed her as lymphocytic hypophysitis occurred during pregnancy. With a replacement dose of hydrocortisone and levothyroxine, she gave birth by cesarean section at 38 weeks of gestation. We performed detailed assessment of anterior pituitary functions with hypothalamic hormone challenges after giving birth. It showed panhypopituitarism without diabetes insipidus. An MRI scan found the compression of the optic chiasm remained after childbirth, the patient underwent steroid pulse therapy. After that, visual field defect improved rapidly, and the patient continued to receive oral prednisolone with gradually reduced amount. An MRI scan performed over time and found the pituitary swelling gradually improved. The pituitary was completely intact 3 years after the onset of disease. At the age of 38, the patient became pregnant with her second child, showed no signs of hypopituitarism at the time of pregnancy. She still had been administrated with 3.5mg/day prednisolone. At the 21 weeks of pregnancy, she became aware of blurred vision and was diagnosed as a left paracenter scotoma. Laboratory data showed a decrease in blood glucose and neutrophil count, suggesting the occurrence of central adrenocortical insufficiency. Therefore, we suspected the relapse of hypophysitis due to second pregnancy. We started hydrocortisone supplementation in addition to prednisolone. No MRI scan was performed during pregnancy, since no progression of visual impairment was observed. She gave birth at 37 weeks of gestation, and postpartum MRI scan showed mild thickening of the stalk. Steroid pulse therapy was not performed because the visual field abnormality was spontaneously improved. Lymphocytic hypophysitis has a diverse course, and there is currently no confirmed risk factor for recurrence. In this case, hypophysitis recurred due to pregnancy despite the continuation of prednisolone administration, and the pathogenic mechanism may be different from the previously reported cases of recurrence of hypophysitis.
    Type of Medium: Online Resource
    ISSN: 2472-1972
    URL: Article
    DOI: 10.1210/jendso/bvab048.1146
    Language: English
    Publisher: The Endocrine Society
    Publication Date: 2021
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