Pub Date : 2023-02-01DOI: 10.1080/07435800.2022.2158338
Muhammet Cuneyt Bilginer, Abbas Ali Tam, Sevgul Faki, Nagihan Bestepe, Fatma Dilek Dellal, Didem Ozdemir, Oya Topaloglu, Reyhan Ersoy, Bekir Cakir
Background: Patients with differentiated thyroid cancer (DTC) are exposed to subclinical exogenous hyperthyroidism for the suppression of thyroid-stimulating hormone (TSH). In this study, we aimed to evaluate the adrenal reserve in DTC patients receiving suppression therapy.
Materials and methods: The study included 55 DTC patients on suppression therapy and 32 healthy volunteers. Basal serum cortisol of all participants and adrenocorticotropic hormone (ACTH) of the patient group were measured. A standard-dose ACTH test (0.25 mg) was performed in patients with a basal cortisol <14.5 mcg/dL.
Results: In the patient group, TSH was lower, free thyroxine (fT4) was higher, and free triiodothyronine (fT3) was similar to those of the control group (p < .01, p < .01, p = .140, respectively). The serum cortisol of the patient group was significantly lower than the control group (12.14 ± 5.12 mcg/dL vs 18.00 ± 5.56 mcg/dL, p < .001). A total of 34 (61.8%) patients with DTC had a basal cortisol <14.5 mcg/dL. Prolonged TSH suppression (≥5 years vs <5 years) was associated with lower basal cortisol (7.46 ± 2.63 mcg/dL vs 9.48 ± 2.65 mcg/dL, p = .022). The ACTH stimulation test showed that 2 (5.8%) patients had a cortisol response <18 mcg/dL. The rate of adrenal insufficiency was 3.6% in DTC patients. A moderate negative correlation was found between ACTH and fT3 of patients with low basal cortisol (r = -0.358, p = .038).
Conclusion: Patients with DTC receiving TSH suppression therapy are at risk for adrenal insufficiency. The duration and severity of suppression might increase this possibility. Dynamic testing with synthetic ACTH can be used to reveal insufficient cortisol response in case of clinical suspicion.
{"title":"Evaluation of Adrenal Reserve in Patients with Differentiated Thyroid Cancer Receiving Thyroid Hormone Suppression Therapy- case-control Comparative Study.","authors":"Muhammet Cuneyt Bilginer, Abbas Ali Tam, Sevgul Faki, Nagihan Bestepe, Fatma Dilek Dellal, Didem Ozdemir, Oya Topaloglu, Reyhan Ersoy, Bekir Cakir","doi":"10.1080/07435800.2022.2158338","DOIUrl":"https://doi.org/10.1080/07435800.2022.2158338","url":null,"abstract":"<p><strong>Background: </strong>Patients with differentiated thyroid cancer (DTC) are exposed to subclinical exogenous hyperthyroidism for the suppression of thyroid-stimulating hormone (TSH). In this study, we aimed to evaluate the adrenal reserve in DTC patients receiving suppression therapy.</p><p><strong>Materials and methods: </strong>The study included 55 DTC patients on suppression therapy and 32 healthy volunteers. Basal serum cortisol of all participants and adrenocorticotropic hormone (ACTH) of the patient group were measured. A standard-dose ACTH test (0.25 mg) was performed in patients with a basal cortisol <14.5 mcg/dL.</p><p><strong>Results: </strong>In the patient group, TSH was lower, free thyroxine (fT4) was higher, and free triiodothyronine (fT3) was similar to those of the control group (p < .01, p < .01, p = .140, respectively). The serum cortisol of the patient group was significantly lower than the control group (12.14 ± 5.12 mcg/dL vs 18.00 ± 5.56 mcg/dL, p < .001). A total of 34 (61.8%) patients with DTC had a basal cortisol <14.5 mcg/dL. Prolonged TSH suppression (≥5 years vs <5 years) was associated with lower basal cortisol (7.46 ± 2.63 mcg/dL vs 9.48 ± 2.65 mcg/dL, p = .022). The ACTH stimulation test showed that 2 (5.8%) patients had a cortisol response <18 mcg/dL. The rate of adrenal insufficiency was 3.6% in DTC patients. A moderate negative correlation was found between ACTH and fT3 of patients with low basal cortisol (r = -0.358, p = .038).</p><p><strong>Conclusion: </strong>Patients with DTC receiving TSH suppression therapy are at risk for adrenal insufficiency. The duration and severity of suppression might increase this possibility. Dynamic testing with synthetic ACTH can be used to reveal insufficient cortisol response in case of clinical suspicion.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10756664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-01DOI: 10.1080/07435800.2022.2142239
Jeong Min Seong, Mi Young Gi, Ju Ae Cha, Hyun Ho Sung, So Young Park, Cho Hee Park, Hyun Yoon
Aims: This study was conducted to assess the association of uric acid (UA) with the homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-B) by gender in nondiabetic Korean adults.
Materials and methods: The study was carried out using data from the 2019 Korean National Health and Nutrition Examination Survey and included nondiabetic Korean men, premenopausal women, and postmenopausal women aged 20 years or older.
Results: First, after adjusted for the related variables (excluding obesity), the prevalence of hyperuricemia (UA ≥ 7.0 mg/dL in men or UA ≥ 6.0 mg/dL in women) was positively associated with the quartiles of HOMA-IR and HOMA-B in men, premenopausal women, and postmenopausal women. Second, when further adjusted for obesity, hyperuricemia was positively associated with the quartiles of HOMA-IR and HOMA-B in men and postmenopausal women but not in premenopausal women. Third, after adjusted for the related variables (including obesity), UA level was positively associated with the quartiles of HOMA-IR and HOMA-B in men and postmenopausal women but not in premenopausal women.
Conclusions: hyperuricemia is positively associated with insulin resistance and beta-cell function in nondiabetic Korean men and postmenopausal women but not in premenopausal women.
{"title":"Gender Difference in the Association of Hyperuricemia with Insulin Resistance and beta-cell Function in Nondiabetic Korean Adults: The 2019 Korea National Health and Nutrition Examination Survey.","authors":"Jeong Min Seong, Mi Young Gi, Ju Ae Cha, Hyun Ho Sung, So Young Park, Cho Hee Park, Hyun Yoon","doi":"10.1080/07435800.2022.2142239","DOIUrl":"https://doi.org/10.1080/07435800.2022.2142239","url":null,"abstract":"<p><strong>Aims: </strong>This study was conducted to assess the association of uric acid (UA) with the homeostasis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-<i>B</i>) by gender in nondiabetic Korean adults.</p><p><strong>Materials and methods: </strong>The study was carried out using data from the 2019 Korean National Health and Nutrition Examination Survey and included nondiabetic Korean men, premenopausal women, and postmenopausal women aged 20 years or older.</p><p><strong>Results: </strong>First, after adjusted for the related variables (excluding obesity), the prevalence of hyperuricemia (UA ≥ 7.0 mg/dL in men or UA ≥ 6.0 mg/dL in women) was positively associated with the quartiles of HOMA-IR and HOMA-<i>B</i> in men, premenopausal women, and postmenopausal women. Second, when further adjusted for obesity, hyperuricemia was positively associated with the quartiles of HOMA-IR and HOMA-<i>B</i> in men and postmenopausal women but not in premenopausal women. Third, after adjusted for the related variables (including obesity), UA level was positively associated with the quartiles of HOMA-IR and HOMA-<i>B</i> in men and postmenopausal women but not in premenopausal women.</p><p><strong>Conclusions: </strong>hyperuricemia is positively associated with insulin resistance and beta-cell function in nondiabetic Korean men and postmenopausal women but not in premenopausal women.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10743424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: B cell activating factor (BAFF), a crucial factor for B cell survival and differentiation, has been linked to several autoimmune conditions. The aim of this study was to evaluate the association of BAFF gene's polymorphisms with its serum levels and to assess their effect on Graves' disease (GD) susceptibility and presentation.
Methods: Sixty-two GD patients and 152 healthy controls have been enrolled to investigate BAFF rs9514827 (-2841 T/C), rs1041569 (-2701 T/A) and rs9514828 (-871 C/T) gene's polymorphism by PCR-RFLP and serum BAFF level's kinetics under medical treatment by ELISA.
Results: Median serum BAFF level at baseline was significantly higher in GD patients (841.7 pg/ml [685.23-1058.32]) comparatively to controls (495.75 pg/ml [383.17-595.7]), p = 7.29 E-25. A ROC curve was used to assess BAFF performances in GD diagnosis and revealed an AUC of 94.9% [0.919-0.979], p = 7.29 E-25. At a cutoff value of 654.9 pg/ml of BAFF at baseline, the sensitivity and the specificity were, respectively, 83.9% and 90.8%. BAFF level was significantly increased in smoking patients (1079.55 pg/ml [875.35-1203]) comparatively to nonsmokers (746.95 pg/ml [643.2-915.7]), p = 3.1 E-5. While -2841 T/C and -2701 T/A genotypes and alleles frequencies were similar between patients and controls, the -871*T allele was significantly more prevalent in patients (0.613) than in controls (0.477); p = .01, OR [95% CI] = 1.73 [1.13-2.65]. The three studied polymorphisms were not associated with serum BAFF level at baseline.
Conclusion: Serum BAFF level is significantly increased in GD especially in smoking patients. rs9514828 - 871*T allele might be a susceptibility variant for GD.
{"title":"Pre- and Post-treatment Serum BAFF Levels and BAFF Gene Polymorphisms in Patients with Graves' Disease.","authors":"Tarak Dhaouadi, Imen Rojbi, Sameh Ghammouki, Ibtissem Ben Nacef, Meriem Adel, Sabrine Mekni, Karima Khiari, Taïeb Ben Abdallah, Imen Sfar, Yousr Gorgi","doi":"10.1080/07435800.2023.2167087","DOIUrl":"https://doi.org/10.1080/07435800.2023.2167087","url":null,"abstract":"<p><strong>Background: </strong>B cell activating factor (BAFF), a crucial factor for B cell survival and differentiation, has been linked to several autoimmune conditions. The aim of this study was to evaluate the association of BAFF gene's polymorphisms with its serum levels and to assess their effect on Graves' disease (GD) susceptibility and presentation.</p><p><strong>Methods: </strong>Sixty-two GD patients and 152 healthy controls have been enrolled to investigate BAFF rs9514827 (-2841 T/C), rs1041569 (-2701 T/A) and rs9514828 (-871 C/T) gene's polymorphism by PCR-RFLP and serum BAFF level's kinetics under medical treatment by ELISA.</p><p><strong>Results: </strong>Median serum BAFF level at baseline was significantly higher in GD patients (841.7 pg/ml [685.23-1058.32]) comparatively to controls (495.75 pg/ml [383.17-595.7]), <i>p</i> = 7.29 E-25. A ROC curve was used to assess BAFF performances in GD diagnosis and revealed an AUC of 94.9% [0.919-0.979], <i>p</i> = 7.29 E-25. At a cutoff value of 654.9 pg/ml of BAFF at baseline, the sensitivity and the specificity were, respectively, 83.9% and 90.8%. BAFF level was significantly increased in smoking patients (1079.55 pg/ml [875.35-1203]) comparatively to nonsmokers (746.95 pg/ml [643.2-915.7]), <i>p</i> = 3.1 E-5. While -2841 T/C and -2701 T/A genotypes and alleles frequencies were similar between patients and controls, the -871*T allele was significantly more prevalent in patients (0.613) than in controls (0.477); <i>p</i> = .01, OR [95% CI] = 1.73 [1.13-2.65]. The three studied polymorphisms were not associated with serum BAFF level at baseline.</p><p><strong>Conclusion: </strong>Serum BAFF level is significantly increased in GD especially in smoking patients. rs9514828 - 871*T allele might be a susceptibility variant for GD.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9073395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-02-01DOI: 10.1080/07435800.2023.2176869
Shehrban Sobeh Khalil, Mohammad Sheikh Ahmad, Talia Sarah-Hefer, Ekaterina Yovanovich, Maria Reut, Limor Chen-Konak, Nariman Saba-Khazen, Leonard Saiegh
Purpose: In Cushing's disease (CD) patients, the aim of the present study is to confirm sensitivity of several ACTH and cortisol concentration values in different time points, during corticotropin-releasing hormone (CRH) stimulation test and during CRH stimulation following dexamethasone suppression (DEX-CRH) test.
Methods: We retrospectively analyzed cortisol and ACTH concentration increment during CRH and DEX-CRH tests in 23 patients with confirmed CD. Cortisol and ACTH concentrations were determined immediately before, 15 min and 30 min after CRH stimulation. We evaluated the sensitivity of different cutoff values including those reported in previous studies, in the diagnosis of CD.
Results: During DEX-CRH test, 15 min serum cortisol concentration of 1.4 μg/dl (38 nmol/L) had a sensitivity of 90.9%, and serum cortisol concentration ≥1.27 μg/dl (35 nmol/L) had a sensitivity of 100%. For plasma ACTH, sensitivity of 100% was obtained using ACTH ≥3.5pmol/L (16 pg/ml) at 30 min. During CRH test, 35% increase from baseline in ACTH concentration had a sensitivity of 72.7%. Twenty percent increase in cortisol 30 minutes after stimulation yielded a sensitivity of 85.7%. The best sensitivity of ACTH and cortisol increment was obtained 15 min after stimulation, using 19% and 9% increase, respectively (sensitivity of 100% and 92.8%, respectively).
Conclusion: During CRH and DEX-CRH tests, the study findings agree with the good sensitivity of ACTH and cortisol cutoff values suggested in previous studies; yet, other cutoff values may give a higher diagnostic sensitivity.
{"title":"Sensitivity of Different ACTH and Cortisol Concentration Values in Corticotropin-Releasing Hormone Based Tests in Cushing's Disease.","authors":"Shehrban Sobeh Khalil, Mohammad Sheikh Ahmad, Talia Sarah-Hefer, Ekaterina Yovanovich, Maria Reut, Limor Chen-Konak, Nariman Saba-Khazen, Leonard Saiegh","doi":"10.1080/07435800.2023.2176869","DOIUrl":"https://doi.org/10.1080/07435800.2023.2176869","url":null,"abstract":"<p><strong>Purpose: </strong>In Cushing's disease (CD) patients, the aim of the present study is to confirm sensitivity of several ACTH and cortisol concentration values in different time points, during corticotropin-releasing hormone (CRH) stimulation test and during CRH stimulation following dexamethasone suppression (DEX-CRH) test.</p><p><strong>Methods: </strong>We retrospectively analyzed cortisol and ACTH concentration increment during CRH and DEX-CRH tests in 23 patients with confirmed CD. Cortisol and ACTH concentrations were determined immediately before, 15 min and 30 min after CRH stimulation. We evaluated the sensitivity of different cutoff values including those reported in previous studies, in the diagnosis of CD.</p><p><strong>Results: </strong>During DEX-CRH test, 15 min serum cortisol concentration of 1.4 μg/dl (38 nmol/L) had a sensitivity of 90.9%, and serum cortisol concentration ≥1.27 μg/dl (35 nmol/L) had a sensitivity of 100%. For plasma ACTH, sensitivity of 100% was obtained using ACTH ≥3.5pmol/L (16 pg/ml) at 30 min. During CRH test, 35% increase from baseline in ACTH concentration had a sensitivity of 72.7%. Twenty percent increase in cortisol 30 minutes after stimulation yielded a sensitivity of 85.7%. The best sensitivity of ACTH and cortisol increment was obtained 15 min after stimulation, using 19% and 9% increase, respectively (sensitivity of 100% and 92.8%, respectively).</p><p><strong>Conclusion: </strong>During CRH and DEX-CRH tests, the study findings agree with the good sensitivity of ACTH and cortisol cutoff values suggested in previous studies; yet, other cutoff values may give a higher diagnostic sensitivity.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9306759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01Epub Date: 2022-07-22DOI: 10.1080/07435800.2022.2102649
Hira Zubair, Shazia Shamas, Hamid Ullah, Ghulam Nabi, Tanzeel Huma, Rahim Ullah, Rashad Hussain, Muhammad Shahab
Introduction: Kisspeptin is involved in the hypothalamic pituitary gonadal-axis' seasonal regulation in rodents and sheep. Studies of kisspeptin signaling in regulating the transition between breeding and nonbreeding seasons have focused on kisspeptin expression, myelin basic protein (MBP) expression around kisspeptin-ir cells, and quantifying the synaptic connections between kisspeptin and gonadotropin-releasing hormone (GnRH) neurons in various animal models; however, the role of kisspeptin in regulating the seasonal breeding of primates has not been explored yet.
Objective: This study investigated changes in kisspeptin signaling during breeding and a non-breeding season in a non-human primate model, the rhesus monkey.
Methods: Three adult male monkeys (n = 3) from the breeding season and two monkeys (n = 2) from the non-breeding season were used in this study. After measuring the testicular volume and collecting a single blood sample, all animals were humanely euthanized under controlled conditions, and their hypothalami were collected and processed. Two 20 µm thick hypothalamic sections (mediobasal hypothalamus) from each animal were processed for kisspeptin-MBP and kisspeptin-GnRH immunohistochemistry (IHC). One section from each animal was used as a primary antibody omitted control to check the nonspecific binding in each IHC.
Results: Compared to the non-breeding season, plasma testosterone levels and testicular volumes were significantly higher in monkeys during the breeding season. Furthermore, compared to the non-breeding season, increased kisspeptin expression and a higher number of synaptic contacts between kisspeptin fibers and GnRH cell bodies were observed in the arcuate nucleus of the breeding season monkeys. In contrast, enlarged kisspeptin soma and higher MBP expression were observed in non-breeding monkeys.
Conclusion: Our results indicated enhanced kisspeptin signaling in primate hypothalamus during the breeding season. These findings support the idea that kisspeptin acts as a mediator for the seasonal regulation of the reproductive axis in higher primates.
{"title":"Morphometric and Myelin Basic Protein Expression Changes in Arcuate Nucleus Kisspeptin Neurons Underlie Activation of Hypothalamic Pituitary Gonadal-axis in Monkeys (<i>Macaca Mulatta</i>) during the Breeding Season.","authors":"Hira Zubair, Shazia Shamas, Hamid Ullah, Ghulam Nabi, Tanzeel Huma, Rahim Ullah, Rashad Hussain, Muhammad Shahab","doi":"10.1080/07435800.2022.2102649","DOIUrl":"https://doi.org/10.1080/07435800.2022.2102649","url":null,"abstract":"<p><strong>Introduction: </strong>Kisspeptin is involved in the hypothalamic pituitary gonadal-axis' seasonal regulation in rodents and sheep. Studies of kisspeptin signaling in regulating the transition between breeding and nonbreeding seasons have focused on kisspeptin expression, myelin basic protein (MBP) expression around kisspeptin-ir cells, and quantifying the synaptic connections between kisspeptin and gonadotropin-releasing hormone (GnRH) neurons in various animal models; however, the role of kisspeptin in regulating the seasonal breeding of primates has not been explored yet.</p><p><strong>Objective: </strong>This study investigated changes in kisspeptin signaling during breeding and a non-breeding season in a non-human primate model, the rhesus monkey.</p><p><strong>Methods: </strong>Three adult male monkeys (n = 3) from the breeding season and two monkeys (n = 2) from the non-breeding season were used in this study. After measuring the testicular volume and collecting a single blood sample, all animals were humanely euthanized under controlled conditions, and their hypothalami were collected and processed. Two 20 µm thick hypothalamic sections (mediobasal hypothalamus) from each animal were processed for kisspeptin-MBP and kisspeptin-GnRH immunohistochemistry (IHC). One section from each animal was used as a primary antibody omitted control to check the nonspecific binding in each IHC.</p><p><strong>Results: </strong>Compared to the non-breeding season, plasma testosterone levels and testicular volumes were significantly higher in monkeys during the breeding season. Furthermore, compared to the non-breeding season, increased kisspeptin expression and a higher number of synaptic contacts between kisspeptin fibers and GnRH cell bodies were observed in the arcuate nucleus of the breeding season monkeys. In contrast, enlarged kisspeptin soma and higher MBP expression were observed in non-breeding monkeys.</p><p><strong>Conclusion: </strong>Our results indicated enhanced kisspeptin signaling in primate hypothalamus during the breeding season. These findings support the idea that kisspeptin acts as a mediator for the seasonal regulation of the reproductive axis in higher primates.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40528518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01Epub Date: 2022-08-02DOI: 10.1080/07435800.2022.2108049
Fernando Guerrero-Romero, Luis E Simental-Mendía
Background: It is well-recognized that hyperuricemia is a common abnormality among individuals with metabolic syndrome.
Aims: The objective of this study was to determine whether hyperuricemia is associated with the metabolically obese normal-weight (MONW) and metabolically healthy obese (MHO) phenotypes.
Methods: Men and women equal or greater than 18 years of age were enrolled in a cross-sectional study. Normal-weight subjects were allocated into the MONW or healthy normal-weight (HNW) groups; while obese individuals were divided into the MHO and metabolically unhealthy obese (MUO) subgroups. MONW phenotype was defined by body mass index (BMI) <25.0 kg/m2 accompanied by at least one cardiovascular risk factor (hyperglycemia, elevated blood pressure, hypertriglyceridemia, and low high-density lipoprotein cholesterol), and MHO phenotype was considered in obese subjects (BMI ≥30 kg/m2) without metabolic abnormalities.
Results: A total of 567 individuals were enrolled; of them, normal-weight subjects were allocated into the MONW (n = 101) and control (n = 72) groups, whereas obese individuals into the MHO (n = 61) and MUO (n = 333) groups. The multiple logistic regression analysis adjusted by age, gender, and body mass index revealed that hyperuricemia is significantly associated with MONW (OR = 5.14; 95% CI: 1.37-19.29) and MHO (OR = 0.34; 95% CI: 0.14-0.82) phenotypes.
Conclusion: Results of our study showed that hyperuricemia is associated with both MONW and MHO phenotypes.
{"title":"Hyperuricemia is Associated with the Presence of Metabolically Obese Normal-Weight and Metabolically Healthy Obese Phenotypes.","authors":"Fernando Guerrero-Romero, Luis E Simental-Mendía","doi":"10.1080/07435800.2022.2108049","DOIUrl":"https://doi.org/10.1080/07435800.2022.2108049","url":null,"abstract":"<p><strong>Background: </strong>It is well-recognized that hyperuricemia is a common abnormality among individuals with metabolic syndrome.</p><p><strong>Aims: </strong>The objective of this study was to determine whether hyperuricemia is associated with the metabolically obese normal-weight (MONW) and metabolically healthy obese (MHO) phenotypes.</p><p><strong>Methods: </strong>Men and women equal or greater than 18 years of age were enrolled in a cross-sectional study. Normal-weight subjects were allocated into the MONW or healthy normal-weight (HNW) groups; while obese individuals were divided into the MHO and metabolically unhealthy obese (MUO) subgroups. MONW phenotype was defined by body mass index (BMI) <25.0 kg/m<sup>2</sup> accompanied by at least one cardiovascular risk factor (hyperglycemia, elevated blood pressure, hypertriglyceridemia, and low high-density lipoprotein cholesterol), and MHO phenotype was considered in obese subjects (BMI ≥30 kg/m<sup>2</sup>) without metabolic abnormalities.</p><p><strong>Results: </strong>A total of 567 individuals were enrolled; of them, normal-weight subjects were allocated into the MONW (n = 101) and control (n = 72) groups, whereas obese individuals into the MHO (n = 61) and MUO (n = 333) groups. The multiple logistic regression analysis adjusted by age, gender, and body mass index revealed that hyperuricemia is significantly associated with MONW (OR = 5.14; 95% CI: 1.37-19.29) and MHO (OR = 0.34; 95% CI: 0.14-0.82) phenotypes.</p><p><strong>Conclusion: </strong>Results of our study showed that hyperuricemia is associated with both MONW and MHO phenotypes.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40595574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Introduction: DNA methylation in the CpG sites of intron 1 of HIF3A is associated with body mass index (BMI). This cross-sectional study investigated correlations between DNA methylation of HIF3A and BMI or adiposity parameters in the Japanese population.
Method: DNA methylation of HIF3A was quantified via pyrosequencing.
Result: DNA methylation of HIF3A differed only in women; DNA methylation level at cg27146050 was associated with visceral adipose tissue thickness and correlated with BMI and percent (%) body fat after excluding smokers.
Conclusion: Peripheral blood DNA methylation at the CpG site (cg27146050) of HIF3A correlated with VAT thickness in Japanese women.
{"title":"Association between the Extent of Peripheral Blood DNA Methylation of <i>HIF3A</i> and Accumulation of Adiposity in community-dwelling Women: The Yakumo Study.","authors":"Genki Mizuno, Hiroya Yamada, Eiji Munetsuna, Mirai Yamazaki, Yoshitaka Ando, Ryosuke Fujii, Yoshiki Tsuboi, Atsushi Teshigawara, Itsuki Kageyama, Keisuke Osakabe, Keiko Sugimoto, Hiroaki Ishikawa, Naohiro Ichino, Yoshiji Ohta, Koji Ohashi, Shuji Hashimoto, Koji Suzuki","doi":"10.1080/07435800.2022.2121967","DOIUrl":"https://doi.org/10.1080/07435800.2022.2121967","url":null,"abstract":"<p><strong>Introduction: </strong>DNA methylation in the CpG sites of intron 1 of <i>HIF3A</i> is associated with body mass index (BMI). This cross-sectional study investigated correlations between DNA methylation of <i>HIF3A</i> and BMI or adiposity parameters in the Japanese population.</p><p><strong>Method: </strong>DNA methylation of <i>HIF3A</i> was quantified via pyrosequencing.</p><p><strong>Result: </strong>DNA methylation of <i>HIF3A</i> differed only in women; DNA methylation level at cg27146050 was associated with visceral adipose tissue thickness and correlated with BMI and percent (%) body fat after excluding smokers.</p><p><strong>Conclusion: </strong>Peripheral blood DNA methylation at the CpG site (cg27146050) of <i>HIF3A</i> correlated with VAT thickness in Japanese women.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40355471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01Epub Date: 2022-09-13DOI: 10.1080/07435800.2022.2120893
Michael S Katz, Paul J Davis
Robert I. Gregerman, MD, a luminary in endocrine research and a pioneering investigator of the metabolic aspects of aging, died October 6, 2021, in San Antonio, Texas, at age 91 years. At the time of his death, following a protracted illness, he was at home, with family and hospice care members by his side. Dr. Gregerman leaves behind a distinguished legacy of academic accomplishment embodied in 60 years of innovative contributions to the medical literature and in generations of trainees who have themselves become leaders in the fields of endocrinology and biomedical gerontology. Robert (Bob) Gregerman (Figure 1) will be remembered as among the inaugural group of gifted scientists presciently recruited by Nathan W. Shock, PhD (1907– 1989), to “grow” the first inter-disciplinary program on aging research at the National Institutes of Health (NIH). In 1956, as a newly minted commissioned officer in the United States Public Health Service (USPHS), Bob arrived at Dr. Shock’s brainchild, then known as the Gerontology Branch of the National Heart Institute and a uniquely creative hybrid of a research enterprise–operating administratively as a unit within the NIH, housed on the grounds of the Baltimore City Hospitals (BCH) and affiliated academically with the Johns Hopkins University School of Medicine several miles away. By 1961, Bob had become the founding chief of the Endocrine Section within the Gerontology Branch, which in 1968 moved into its own NIH-financed building, designated the Gerontology Research Center (GRC), on the BCH campus, and subsequently matured into the intramural research program of the National Institute on Aging (NIA) established in 1974. Bob Gregerman’s laboratory at the GRC remained at the forefront of investigations into the endocrinology of aging for another two decades, during which time he was promoted to Professor of Medicine at Johns Hopkins. Then, in 1994, following retirement from the USPHS he moved with his wife Marjorie to San Antonio, Texas (Figure 2), to direct the research programs of the San Antonio Geriatric Research, Education and Clinical Center (GRECC) at the Audie L. Murphy Memorial Veterans Hospital, and with an appointment as Professor of Medicine at the affiliated University of Texas Health Science Center at San Antonio (UTHSCSA). In San Antonio, he extended the research inquiries he had long pursued in Baltimore, until formal retirement in 2011 afforded him time and opportunity for his favored activities, namely, visiting the UTHSCSA medical library to keep abreast of the literature and conferring with former trainees and colleagues over advances in the biology and endocrinology of aging. Many years earlier, he had written, “my field always serves as a reminder of the finiteness of time.” In the last years of his life (Figure 3), then, when his scientific endeavors, and his delight in pursuing them, did recede under the assaults of time, it likely came to him with regret but as no great surprise. For tho
{"title":"Robert I. Gregerman, MD (1930-2021). An Editorial Reminiscence.","authors":"Michael S Katz, Paul J Davis","doi":"10.1080/07435800.2022.2120893","DOIUrl":"https://doi.org/10.1080/07435800.2022.2120893","url":null,"abstract":"Robert I. Gregerman, MD, a luminary in endocrine research and a pioneering investigator of the metabolic aspects of aging, died October 6, 2021, in San Antonio, Texas, at age 91 years. At the time of his death, following a protracted illness, he was at home, with family and hospice care members by his side. Dr. Gregerman leaves behind a distinguished legacy of academic accomplishment embodied in 60 years of innovative contributions to the medical literature and in generations of trainees who have themselves become leaders in the fields of endocrinology and biomedical gerontology. Robert (Bob) Gregerman (Figure 1) will be remembered as among the inaugural group of gifted scientists presciently recruited by Nathan W. Shock, PhD (1907– 1989), to “grow” the first inter-disciplinary program on aging research at the National Institutes of Health (NIH). In 1956, as a newly minted commissioned officer in the United States Public Health Service (USPHS), Bob arrived at Dr. Shock’s brainchild, then known as the Gerontology Branch of the National Heart Institute and a uniquely creative hybrid of a research enterprise–operating administratively as a unit within the NIH, housed on the grounds of the Baltimore City Hospitals (BCH) and affiliated academically with the Johns Hopkins University School of Medicine several miles away. By 1961, Bob had become the founding chief of the Endocrine Section within the Gerontology Branch, which in 1968 moved into its own NIH-financed building, designated the Gerontology Research Center (GRC), on the BCH campus, and subsequently matured into the intramural research program of the National Institute on Aging (NIA) established in 1974. Bob Gregerman’s laboratory at the GRC remained at the forefront of investigations into the endocrinology of aging for another two decades, during which time he was promoted to Professor of Medicine at Johns Hopkins. Then, in 1994, following retirement from the USPHS he moved with his wife Marjorie to San Antonio, Texas (Figure 2), to direct the research programs of the San Antonio Geriatric Research, Education and Clinical Center (GRECC) at the Audie L. Murphy Memorial Veterans Hospital, and with an appointment as Professor of Medicine at the affiliated University of Texas Health Science Center at San Antonio (UTHSCSA). In San Antonio, he extended the research inquiries he had long pursued in Baltimore, until formal retirement in 2011 afforded him time and opportunity for his favored activities, namely, visiting the UTHSCSA medical library to keep abreast of the literature and conferring with former trainees and colleagues over advances in the biology and endocrinology of aging. Many years earlier, he had written, “my field always serves as a reminder of the finiteness of time.” In the last years of his life (Figure 3), then, when his scientific endeavors, and his delight in pursuing them, did recede under the assaults of time, it likely came to him with regret but as no great surprise. For tho","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40356885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01Epub Date: 2022-09-26DOI: 10.1080/07435800.2022.2127757
Canjia Zhang, Huan Chen, Shangxin Cui, Yeli Lin, Yongqiang Liang, Ping Zhao, Changyi Wang, Shan Xu, Xiaolin Peng, Hongen Chen, Li Wang, Dan Zhao, Ming Zhang, Dongsheng Hu, Yanmei Lou, Fulan Hu
Background: This study aimed at investigating the relationships between Platelet-Lymphocyte ratio (PLR) and Neutrophil-Lymphocyte ratio (NLR) and their dynamic changes (∆PLR, ∆NLR) with type 2 diabetes mellitus (T2DM) in a Chinese cohort study.
Methods: This study recruited 41,439 individuals who were diagnosed without T2DM at first health examination and completed at least one follow-up. The relationships between NLR, PLR, ∆PLR, ∆NLR and T2DM risk were analyzed using the Cox regression model with corresponding Hazard Ratios (HRs) and 95% Confidence Intervals (CIs).
Results: PLR exhibited significant correlation with T2DM risk in a linear reverse dose-response pattern, the corresponding HRs and 95% CIs were 0.81 (0.72, 0.90), 0.71 (0.63, 0.80) and 0.56 (0.49, 0.64) respectively (Ptrend < 0.001) for Q2, Q3 and Q4 vs Q1 after adjusting for age, gender, BMI, TG, TC, HDL-C, FPG, ALT, AST, heart rate, smoking, family history of diabetes, and alcohol consumption at baseline in Model 3. The significance remained in subgroups of women, <45 years, ≥45 years, BMI ≥ 24, with fatty liver disease, without fatty liver disease and normotension. Comparing with the largest decrease group of NLR (∆NLR < -0.32), the risk of T2DM increased for -0.003 ≤ ∆NLR < 0.31 (HR 1.17, 95% CI 1.01-1.36) and ∆NLR ≥ 0.31 (HR 1.23, 95% CI 1.06-1.43).
Conclusions: Higher PLR could reduce the risk of T2DM. Larger increase of NLR could increase T2DM risk.
{"title":"Platelet-Lymphocyte Ratio, Neutrophil-Lymphocyte Ratio and Their Dynamic Changes with Type 2 Diabetes Mellitus: A Cohort Study in China.","authors":"Canjia Zhang, Huan Chen, Shangxin Cui, Yeli Lin, Yongqiang Liang, Ping Zhao, Changyi Wang, Shan Xu, Xiaolin Peng, Hongen Chen, Li Wang, Dan Zhao, Ming Zhang, Dongsheng Hu, Yanmei Lou, Fulan Hu","doi":"10.1080/07435800.2022.2127757","DOIUrl":"https://doi.org/10.1080/07435800.2022.2127757","url":null,"abstract":"<p><strong>Background: </strong>This study aimed at investigating the relationships between Platelet-Lymphocyte ratio (PLR) and Neutrophil-Lymphocyte ratio (NLR) and their dynamic changes (∆PLR, ∆NLR) with type 2 diabetes mellitus (T2DM) in a Chinese cohort study.</p><p><strong>Methods: </strong>This study recruited 41,439 individuals who were diagnosed without T2DM at first health examination and completed at least one follow-up. The relationships between NLR, PLR, ∆PLR, ∆NLR and T2DM risk were analyzed using the Cox regression model with corresponding Hazard Ratios (HRs) and 95% Confidence Intervals (CIs).</p><p><strong>Results: </strong>PLR exhibited significant correlation with T2DM risk in a linear reverse dose-response pattern, the corresponding HRs and 95% CIs were 0.81 (0.72, 0.90), 0.71 (0.63, 0.80) and 0.56 (0.49, 0.64) respectively (<i>P</i><sub>trend</sub> < 0.001) for Q2, Q3 and Q4 vs Q1 after adjusting for age, gender, BMI, TG, TC, HDL-C, FPG, ALT, AST, heart rate, smoking, family history of diabetes, and alcohol consumption at baseline in Model 3. The significance remained in subgroups of women, <45 years, ≥45 years, BMI ≥ 24, with fatty liver disease, without fatty liver disease and normotension. Comparing with the largest decrease group of NLR (∆NLR < -0.32), the risk of T2DM increased for -0.003 ≤ ∆NLR < 0.31 (HR 1.17, 95% CI 1.01-1.36) and ∆NLR ≥ 0.31 (HR 1.23, 95% CI 1.06-1.43).</p><p><strong>Conclusions: </strong>Higher PLR could reduce the risk of T2DM. Larger increase of NLR could increase T2DM risk.</p>","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40376328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-04-29DOI: 10.1080/07435800.2022.2068572
Hrafnhildur Gunnarsdóttir, G. Jónsdóttir, G. Birgisson, Jon Gudmundsson, H. Sigurjonsdottir
ABSTRACT Background Long-term follow-up studies on primary aldosteronism (PA) are lacking. Objective We aim to review results of diagnostic procedures and histopathology for patients diagnosed during 2012–2016 in Iceland, compare unilateral (UD) and bilateral disease (BD) and assess treatment response. Methods Thirty-two patients aged 28–88 were diagnosed and treated according to guidelines. Results The majority had BD. Everyone needed potassium supplementation at case detection. We saw a reduction in systolic blood pressure (p < .001, both groups), antihypertensive agents (p = .002 UD and p = .04 BD) and potassium supplementation (p < .001, both groups). Conclusion Similar treatment response was seen in both subgroups. Ratio of hypokalemia and number of cases indicates severe PA underdiagnosis in Iceland.
{"title":"Are We Only Detecting the Tip of the Iceberg? A Nationwide Study on Primary Aldosteronism with up to 8-Year Follow-up","authors":"Hrafnhildur Gunnarsdóttir, G. Jónsdóttir, G. Birgisson, Jon Gudmundsson, H. Sigurjonsdottir","doi":"10.1080/07435800.2022.2068572","DOIUrl":"https://doi.org/10.1080/07435800.2022.2068572","url":null,"abstract":"ABSTRACT Background Long-term follow-up studies on primary aldosteronism (PA) are lacking. Objective We aim to review results of diagnostic procedures and histopathology for patients diagnosed during 2012–2016 in Iceland, compare unilateral (UD) and bilateral disease (BD) and assess treatment response. Methods Thirty-two patients aged 28–88 were diagnosed and treated according to guidelines. Results The majority had BD. Everyone needed potassium supplementation at case detection. We saw a reduction in systolic blood pressure (p < .001, both groups), antihypertensive agents (p = .002 UD and p = .04 BD) and potassium supplementation (p < .001, both groups). Conclusion Similar treatment response was seen in both subgroups. Ratio of hypokalemia and number of cases indicates severe PA underdiagnosis in Iceland.","PeriodicalId":11601,"journal":{"name":"Endocrine Research","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2022-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44786403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}