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ACTA ENDOCRINOLOGICA (BUC)
The International Journal of Romanian Society of Endocrinology / Registered in 1938in Web of Science Master Journal List
Acta Endocrinologica(Bucharest) is live in PubMed Central
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Notes & Comments
Akbas A, Dagmura H, Gul S, Dasiran F, Daldal E, Okan I
Management Principles of Incidental Thyroid 18F-FDG Uptake Identified on 18F-FDG PET/CT ImagingActa Endo (Buc) 2022 18(2): 253-257 doi: 10.4183/aeb.2022.253
AbstractPurpose. The purpose of this study is to determine the clinical significance of incidental thyroid 18F-FDG PET/ CT uptake in oncology patients with the focus achieving the most appropriate management of this challenging situation. Materials and method. Two thousand five hundred and eighty 18F-FDG PET/CT studies performed at our institute in the past 4 years were retrospectively reviewed. Patients with incidental FDG uptake in the thyroid gland were further analysed. Results. The prevalence of incidental FDG uptake in thyroid gland was 7.6% (129 patients). 26 patients (20.1%) had diffuse 18F-FDG PET/CT uptake, 103 patients (79.1%) had nodular uptake in thyroid gland. All diffuse uptake patients who were further examined diagnosed to be a benign condition. 53 patients in the nodular uptake group were further examined and the final histopathology examinations revealed an 18.8% malignancy rate. SUV max values ranged from 2 to 21.8 with a significant highness in malignant lesions. Conclusion. 18F-FDG PET/CT uptake in the thyroid gland may be diffuse or nodular. Diffuse uptake needs no further examination as it usually accompanied by benign thyroid disorders. Patients with nodular uptake whose general condition is good should be further examined due to high rates of malignancy. -
Case Report
Goren TA, Kilimci DD, Yigit Y, Yildirim AT, Gulen H, Ersoy B
Episode of Acute Hemolysis Due to Undiagnosed Glucose-6-Phosphate Dehidrogenase Deficiency in an Adolescent with Newly Diagnosed Type 1 Diabetes Mellitus: Case Report and Review of LiteratureActa Endo (Buc) 2023 19(2): 256-259 doi: 10.4183/aeb.2023.256
AbstractGlucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is common in the community. The most important clinical manifestation of G6PD deficiency is acute hemolytic anemia due to oxidative stressors. Diabetes Mellitus (DM) can precipitate hemolysis in patients with G6PD deficiency. Here, we described a 15-year-old male with newly diagnosed type 1 DM (T1DM) and unknown G6PD deficiency who suffered from hemolytic anemia during normalization of blood glucose. On admission, the patient did not have ketoacidosis. After the patient's blood sugars were regulated with insulin therapy, he presented five days later with hemolytic anemia. The cause of hemolytic anemia was G6PD deficiency. The patient had no previous episodes of hemolysis and had no relevant family history. Hypoglycemia did not occur during blood glucose regulation. The return of blood sugar to normal after a long period of hyperglycemia was thought to be the possible cause of hemolysis. In conclusion, G6PD deficiency should be considered when there is an episode of hemolysis in newly diagnosed children and adolescents with T1DM, especially in the absence of ketoacidosis and hypoglycemia. -
Perspectives
Koseoglu D, Ozdemir Baser O, Berker D, Guler S
Exenatide Treatment Reduces Thyroid Gland Volume, but Has No Effect on the Size Of Thyroid NodulesActa Endo (Buc) 2020 16(3): 275-279 doi: 10.4183/aeb.2020.275
AbstractContext. Exenatide is a Glucagon-like Peptide-1 receptor agonist, which is widely used for type 2 diabetes mellitus (T2DM). Limited and conflicting results are present about the effect of exenatide on the thyroid gland. Objective. The aim of this study was to evaluate the effect of exenatide treatment on structural and functional features of the thyroid gland in patients with T2DM. Design. The study was a prospective study, performed between 2015 and 2017. The laboratory values and thyroid ultrasonography features were compared before and after exenatide treatment. Subjects and Methods. The study included 39 obese diabetic patients. After inclusion to the study exenatide was started and patients were followed up for 6 months. Total thyroid volume, thyroid function tests, serum carcinoembryonic antigen (CEA) and calcitonin levels, the size and appearance of thyroid nodules were compared between baseline and after 6 months of treatment. Results. Exenatide at a dose of 5μg bid was started, increased to 10 μg bid after 4 weeks. We found a statistically significant decrease in thyroid volume (p=0.043) and serum thyroid stimulating hormone (TSH) levels (p=0.007), whereas serum ATPO. ATGl, fT4, fT3, CEA and calcitonin levels did no change with 6 months of exenatide treatment. There were no significant differences in the size and appearance of the thyroid nodules with treatment. The thyroid volume decrease was not correlated with TSH, body mass index and HbA1c reduction. Conclusion. Exenatide treatment for 6 months decreased serum TSH levels and thyroid volume, but had no effect on thyroid nodules and serum CEA and calcitonin levels. -
General Endocrinology
Genes D, Pekkolay Z, Simsek M, Saracoglu H, Turgut M, Tekes S, Tuzcu AK
Comparison of C-Peptide Levels in Monogenic Forms of Diabetes with other Types of Diabetes: a Single-Center StudyActa Endo (Buc) 2023 19(3): 281-285 doi: 10.4183/aeb.2023.281
AbstractObjective. This study aimed to evaluate the utility of C-peptide levels in the differentiation of monogenic forms of diabetes from type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) in clinical practice. Subjects and Methods. A total of 104 patients aged >16 who visited the Dicle University’s Faculty of Medicine between April 2011 and December 2020 and were diagnosed with monogenic diabetes by genetic analysis or with T1DM and T2DM were randomly selected for retrospective evaluation. The C-peptide levels of these patients at the time of diagnosis of diabetes were compared. Results. Of the 104 patients, 24 (23%) were diagnosed with maturity-onset diabetes of the young (MODY), 40 (38.5%) with T1DM, and 40 (38.5%) with T2DM. Median C-peptide levels (ng/mL) (interquartile range) were 1.78 (1.24–2.88) in MODY group, 0.86 (0.34– 1.22) in T1DM group, and 2.38 (1.58–4.27) in T2DM group. Conclusions. There was a difference in C-peptide levels between MODY and T1DM groups but not between MODY and T2DM groups. As per clinical evaluations, although C-peptide levels of patients with MODY are similar to those of patients with T2DM patients, the possibility of C-peptide levels being similar to those required for T1DM diagnosis should also be considered. -
Endocrine Care
Gheorghiu ML, Gussi I, Lutescu I, Galoiu S, Hortopan D, Caragheorgheopol A, Coculescu M
Mantaining physiological levels of serum prolactin in prolactinomas treated with dopamine agonists throughout pregnancy prevents tumor growthActa Endo (Buc) 2005 1(3): 281-298 doi: 10.4183/aeb.2005.281
Abstract ReferencesIntroduction: Prolactinomas may grow during pregnancy. Dopamine agonists (DA) prevent tumor growth, but usually suppress prolactin (PRL) both in mother and fetus. Possible long-term consequences on fetal development remain unknown.\r\nAim: to assess whether DA treatment throughout pregnancy in a dosage able to maintain physiological gestational serum levels of prolactin (PRL) still prevents prolactinoma growth.\r\nPatients and methods: We evaluated 68 pregnancies in 49 women with prolactinoma (PRM) and 46 pregnancies in healthy women as controls. Thirty-three pregnancies were recorded in 27 women treated throughout pregnancy with bromocriptine (BRC) (n = 25) or cabergoline (CAB) (n = 2) divided in 2 groups: group A (22 pregnancies in 18 patients) had suppressed serum PRL (below the 5th percentile of the control group Z during the last trimester); group B (11 pregnancies in 10 patients) had physiological serum PRL levels. Other 26 pregnancies in 21 patients were incompletely evaluated and included only in the pregnancy outcome and cure rate analysis. Treated patients were compared with the control group Y 8 women with PRM who discontinued DA after pregnancy induction (9 pregnancies) and a control group Z of 46 healthy pregnant women, randomly selected from two departments of Obstetrics. Patients with multiple pregnancies were recorded in each corresponding study group.\r\nResults: In the control group Y, tumor size showed an increase in 2 (intrasellar macroPRM) out of 8 cases (25%). DA treatment throughout gestation in 27 women with PRM prevented the growth in all cases and induced a shrinkage of more than 30% of tumor mass in 8/14 macroPRM (57.1%), i.e., in 4/7 (57.1%) of macroPRM with physiological serum PRL levels during pregnancy, and in 5/8 (62.5%) of macroPRM with suppressed PRL levels (p = NS) (1 patient had pregnancies in both groups). Low dose DA (BRC 2.5 ? 5 mg/day or CAB 0.5 mg/week) maintains physiological PRL levels in 6/12 (50%) macroPRM, but suppressed PRL in 80% of microPRM. Cure was recorded in 6/49 (12.2%) of patients. Two patients with PRM-induced neuroophthalmic syndrome were successfully treated with DA throughout 1 and respectively 3 pregnancies.\r\nConclusions: Some women with prolactinomas showed a tumour size increase if they were not treated with dopamine agonists throughout pregnancy. Maintaining physiological serum PRL levels during pregnancy (frequently with low doses of DA) prevented tumor growth, avoiding a PRL suppression that may have subtle influence on long-term foetal development.1. Sobrinho LG, Nunes MC, Santos MA, Mauricio JC. Radiological evidence for regression of prolactinoma after treatment with bromocriptine. Lancet 1978; 2(8083):257-258. [CrossRef]2. McGregor AM, Scanlon MF, Hall R, Hall K. Effects of bromocriptine on pituitary tumour size. Br Med J 1979; 2(6192):700-703. [CrossRef]3. Colao A, Annunziato L, Lombardi G. Treatment of prolactinomas. Ann Med 1998; 30(5):452-459. [CrossRef]4. Coculescu M, Simionescu N, Oprescu M, Alessandrescu D. Bromocriptine treatment of pituitary adenomas. Evaluation of withdrawal effect. Endocrinologie 1983; 21(3):157-168.5. Schlechte JA. Clinical practice. Prolactinoma. N Engl J Med 2003; 349(21):2035-2041. [CrossRef]6. Passos VQ, Souza JJ, Musolino NR, Bronstein MD. Long-term follow-up of prolactinomas: normoprolactinemia after bromocriptine withdrawal. J Clin Endocrinol Metab 2002; 87(8):3578-3582. [CrossRef]7. Coculescu M, Anghel R, Badiu C, Caragheorgheopol A, Hortopan D, Dumitrascu A et al. Additional effects of radiotherapy to dopamine agonists in the treatment of macroprolactinomas. Acta Endocrinologica (Buc) 2005; 1(1):43-60. [CrossRef]8. Colao A, Di Sarno A, Cappabianca P, Di Somma C, Pivonello R, Lombardi G. Withdrawal of longterm cabergoline therapy for tumoral and nontumoral hyperprolactinemia. N Engl J Med 2003; 349(21):2023-2033. [CrossRef]9. Robert E, Musatti L, Piscitelli G, Ferrari CI. Pregnancy outcome after treatment with the ergot derivative, cabergoline. Reprod Toxicol 1996; 10(4):333-337. [CrossRef]10. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16(6):791-793. [CrossRef]11. Ricci E, Parazzini F, Motta T, Ferrari CI, Colao A, Clavenna A et al. Pregnancy outcome after cabergoline treatment in early weeks of gestation. Reprod Toxicol 2002; 16(6):791-793. [CrossRef]12. Alessandrescu D, Coculescu M, Oprescu M, Brotea G, Zagrean L, Petrenciuc O. Pregnancy induced and maintained under 2-Br-alfa-ergocryptin in a patient with evolutive prolactinoma (in Romanian). Obstetrica si Ginecologia 1981; 29:209-215.13. Briggs GG, Freeman RK, Yaffe SJ. Bromocriptine. Drugs in pregnancy and lactation. Philadelphia: Lippincott Williams & Wilkins, 2002: 143-145.14. Kletzky OA, Rossman F, Bertolli SI, Platt LD, Mishell DR, Jr. Dynamics of human chorionic gonadotropin, prolactin, and growth hormone in serum and amniotic fluid throughout normal human pregnancy. Am J Obstet Gynecol 1985; 151(7):878-884.15. Ben Jonathan N, Hnasko R. Dopamine as a prolactin (PRL) inhibitor. Endocr Rev 2001; 22(6):724-763. [CrossRef]16. Bigazzi M, Ronga R, Lancranjan I, Ferraro S, Branconi F, Buzzoni P et al. A pregnancy in an acromegalic woman during bromocriptine treatment: effects on growth hormone and prolactin in the maternal, fetal, and amniotic compartments. J Clin Endocrinol Me [CrossRef]17. Handwerger S, Freemark M. Role of placental lactogen and prolactin in human pregnancy. Adv Exp Med Biol 1987; 219:399-420.18. American College of Obstetricians and Gynecologists CoTB. Early pregnancy loss. ACOG Technical Bulletin 212. 1995.19. Elster AD, Sanders TG, Vines FS, Chen MY. Size and shape of the pituitary gland during pregnancy and post partum: measurement with MR imaging. Radiology 1991; 181(2):531-535.20. Gonzalez JG, Elizondo G, Saldivar D, Nanez H, Todd LE, Villarreal JZ. Pituitary gland growth during normal pregnancy: an in vivo study using magnetic resonance imaging. Am J Med 1988; 85(2):217-220. [CrossRef]21. Scheithauer BW, Sano T, Kovacs KT, Young WF, Jr., Ryan N, Randall RV. The pituitary gland in pregnancy: a clinicopathologic and immunohistochemical study of 69 cases. Mayo Clin Proc 1990; 65(4):461-474.22. Kupersmith MJ, Rosenberg C, Kleinberg D. Visual loss in pregnant women with pituitary adenomas. Ann Intern Med 1994; 121(7):473-477.23. Molitch ME. Pregnancy and the hyperprolactinemic woman. N Engl J Med 1985; 312(21):1364-1370. [CrossRef]24. Crosignani P, Ferrari C, Mattei AM. Visual field defects and reduced visual acuity during pregnancy in two patients with prolactinoma: rapid regression of symptoms under bromocriptine. Case reports. Br J Obstet Gynaecol 1984; 91(8):821-823.25. Konopka P, Raymond JP, Merceron RE, Seneze J. Continuous administration of bromocriptine in the prevention of neurological complications in pregnant women with prolactinomas. Am J Obstet Gynecol 1983; 146(8):935-938.26. Coculescu M, Hudita D, Gussi I, Gheorghiu M, Hortopan D, Caragheorgheopol A. Tumor size changes in prolactinomas treated with minimum bromocriptine throughout gestation . Gynecological Endocrinology 2000; 14(suppl 2):50.27. Canales ES, Garcia IC, Ruiz JE, Zarate A. Bromocriptine as prophylactic therapy in prolactinoma during pregnancy. Fertil Steril 1981; 36(4):524-526.28. Shanis BS, Check JH. Relative resistance of a macroprolactinoma to bromocriptine therapy during pregnancy. Gynecol Endocrinol 1996; 10(2):91-94. [CrossRef]29. Liu C, Tyrrell JB. Successful treatment of a large macroprolactinoma with cabergoline during pregnancy. Pituitary 2001; 4(3):179-185. [CrossRef]30. de Turris P, Venuti L, Zuppa AA. [Long-term treatment with cabergoline in pregnancy and neonatal outcome: report of a clinical case]. Pediatr Med Chir 2003; 25(3):178-180.31. Verhelst J, Abs R, Maiter D, van den BA, Vandeweghe M, Velkeniers B et al. Cabergoline in the treatment of hyperprolactinemia: a study in 455 patients. J Clin Endocrinol Metab 1999; 84(7):2518-2522. [CrossRef]32. Cannavo S, Curto L, Squadrito S, Almoto B, Vieni A, Trimarchi F. Cabergoline: a first-choice treatment in patients with previously untreated prolactin-secreting pituitary adenoma. J Endocrinol Invest 1999; 22(5):354-359.33. Ciccarelli E, Grottoli S, Razzore P, Gaia D, Bertagna A, Cirillo S et al. Long-term treatment with cabergoline, a new long-lasting ergoline derivate, in idiopathic or tumorous hyperprolactinaemia and outcome of drug-induced pregnancy. J Endocrinol Inves34. Jones J, Bashir T, Olney J, Wheatley T. Cabergoline treatment for a large macroprolactinoma throughout pregnancy. J Obstet Gynaecol 1997; 17(4):375-376.35. Divers WA, Jr., Yen SS. Prolactin-producing microadenomas in pregnancy. Obstet Gynecol 1983; 62(4):425-429.36. Luthman M, Bremme K, Eneroth P, Werner S. Women with prolactin-producing pituitary adenoma show decreased serum placental lactogen during pregnancy. Gynecol Obstet Invest 1993; 35(2):80-85. [CrossRef]37. Kubota T, Nagae M, Yaoi Y, Kumasaka T, Saito M. Prolactin-releasing system in maternal, fetal, and amniotic compartments during labor. Obstet Gynecol 1986; 68(1):80-85.38. Yuen BH, Moon YS, Shin DH. Inhibition of human chorionic gonadotropin production by prolactin from term human trophoblast. Am J Obstet Gynecol 1986; 154(2):336-340.39. Leav I, Merk FB, Lee KF, Loda M, Mandoki M, McNeal JE et al. Prolactin receptor expression in the developing human prostate and in hyperplastic, dysplastic, and neoplastic lesions. Am J Pathol 1999; 154(3):863-870. [CrossRef]40. Gussi I, Gheorghiu M, Lutescu I, Hortopan D, Caragheorgheopol A, Hudita D et al. Maintaining physiological profile of prolactin throughout pregnancy in women with prolactinomas on dopamine agonists. Rom J Endocrinol Metab 2002; 1(suppl 4):23.41. Molitch ME. Pituitary tumors and pregnancy. Growth Horm IGF Res 2003; 13 Suppl A:S38-S44.42. Ahmed M, al Dossary E, Woodhouse NJ. Macroprolactinomas with suprasellar extension: effect of bromocriptine withdrawal during one or more pregnancies. Fertil Steril 1992; 58(3):492-497.43. Daya S, Shewchuk AB, Bryceland N. The effect of multiparity on intrasellar prolactinomas. Am J Obstet Gynecol 1984; 148(5):512-515.44. Fujimoto M, Yoshino E, Mizukawa N, Hirakawa K. Spontaneous reduction in size of prolactinproducing adenoma after delivery. Case report. J Neurosurg 1985; 63(6):973-974. [CrossRef]45. Hammond CB, Haney AF, Land MR, van der Merwe JV, Ory SJ, Wiebe RH. The outcome of pregnancy in patients with treated and untreated prolactin-secreting pituitary tumors. Am J Obstet Gynecol 1983; 147(2):148-157.46. Yamada M, Miyake A, Koike K, Ikegami H, Aono T, Tanizawa O. Spontaneous pregnancy after a pregnancy induced by treatment in hyperprolactinemic women. Eur J Obstet Gynecol Reprod Biol 1990; 35(2-3):125-129. [CrossRef]47. Bergh T, Nillius SJ, Larsson SG, Wide L. Effects of bromocriptine-induced pregnancy on prolactin-secreting pituitary tumours. Acta Endocrinol (Copenh) 1981; 98(3):333-338. -
Case Report
Guney F, Gumus H, Emlik D, Kaya A
Diabetes Mellitus with Left Transverse and Sigmoid Sinus Thrombosis Extending into the Internal Jugular VeinActa Endo (Buc) 2011 7(2): 283-290 doi: 10.4183/aeb.2011.283
AbstractBackground. Cerebral vein and sinus thrombosis (CVT) is less encountered, compared to arterial stroke. Commonly witnessed symptoms are headache, nausea, vomiting, confusion, aphasia, seizures, cranial nerve dysfunction and motor or sensorial deficits. The diagnosis is accurately determined by the help of MRI and MR venography. Multiple risk factors associated with CVT are present. Venous thrombosis tends to occur when there is an imbalance between prothrombotic and thrombolytic processes.\r\nCase report. In this report, a patient with CVT extending from left transverse and sigmoid sinuses to jugular vein and diagnosed with diabetes mellitus (DM) during this period\r\nwas discussed in light of literature. The 55-year-old man was evaluated in the neurology clinic with the complaints of headache, nausea, vomiting and blurred speech. On neurologic examination, he was diagnosed with sensorial aphasia and consequently, with DM over the hospital stay. On the cranial MR venography, CVT thrombosis was detected, extending from transverse and sigmoid sinuses to internal jugular vein. Decreased level of protein C and shortage of aPTT were\r\nfound. Anticoagulant treatment was carried out. All complaints were improved.\r\nConclusion. In our subject, the existence of decreased protein C and shortage of APTT, along with DM, is a situation to increase hypercoagulability and the risk of cerebral vein and sinus thrombosis. -
General Endocrinology
Koc A, Guney I, Kizilarslanoglu MC, Gonulalan G, Deniz CD, Sackan F, Ergul F, Sozen M
Evaluation of the Association of Plasma Pentraxin-3 Levels with Carotid Intima-Media Thickness and High-Sensitive CRP in Patients with Subclinical HypothyroidismActa Endo (Buc) 2023 19(3): 286-291 doi: 10.4183/aeb.2023.286
AbstractContext. Inflammation-related markers may predict cardiovascular diseases. Objective. In this study, it was aimed to assess pentraxin-3 (PTX-3) levels and its relationship with carotid intima-media thickness (CIMT) and high-sensitive C-reactive protein (hsCRP) in patients with subclinical hypothyroidism. Design. Prospective cross-sectional study Methods. This study included 60 patients (aged 30-60 years) with subclinical hypothyroidism and 30 healthy volunteers as controls. The demographic characteristics and anthropometric measurements were performed in all patients and controls. In addition, sonographic carotid artery examination, thyroid functional tests, lipid profile, hsCRP, and PTX-3 levels of the participants were investigated. Results. The PTX-3, hsCRP levels and CIMT were higher in patients with subclinical hypothyroidism when compared to controls (p=0.008, p=0.001, p<0.001, respectively). The PTX-3 level was strongly correlated with hsCRP (r=0.865; p<0.001), but no such correlation was detected with CIMT (r=-0.255; p=0.50). In binominal logistic regression analysis, it was found that CIMT and serum uric acid levels were independent parameters associated with subclinical hypothyroidism. In ROC analysis, a cut-off value of >3.75 ng/mL for serum PTX-3 level predicted subclinical hypothyroidism with a sensitivity of 60% and specificity of 60.7% (AUC: 0.672, p=0.004). Conclusion. Showing inflammation and endothelial dysfunction, the PTX-3 may be a helpful marker in patients with subclinical hypothyroidism associated with increased risk for cardiovascular disease. -
Perspectives
Naraoka Y, Yamaguchi T, Hu A, Akimoto K, Kobayashi H
Short Chain Fatty Acids Upregulate Adipokine Production in Type 2 Diabetes Derived Human AdipocytesActa Endo (Buc) 2018 14(3): 287-293 doi: 10.4183/aeb.2018.287
AbstractPurpose. Short chain fatty acids (SCFAs) play a major regulatory role in adipocyte function and metabolism. The aim of this study was to investigate the effects of SCFAs on adiponectin and leptin expression in adipocytes, and also to determine whether the effects of SCFA treatment in visceral adipocytes obtained from healthy subjects are different relative to the effects in adipocytes from patients with type 2 diabetes. Materials and Methods. Human pericardiac preadipocytes and human pericardiac preadipocytes type 2 diabetes were differentiated into adipocytes for 21 days in 48-well plates. After differentiation, two kinds of mature adipocytes, human pericardiac adipocytes (HPAd) and human pericardiac adipocytes-type 2 diabetes (HPAd-T2D) were incubated with or without 1 mM of acetic acid (AA), butyrate acid (BA), and propionic acid (PA). After 48 hours of incubation, intracellular lipid accumulation was measured using oil red staining. In addition, mRNA levels of adiponectin, leptin and Peroxisome Proliferator-Activated Receptor γ (PPARγ) were determined by Real-Time PCR system. Results. In HPAd, SCFA supplementation did not inhibit lipid accumulation. By contrast, both AA (p<0.01) and PA (p<0.01) significantly inhibited lipid accumulation in HPAd-T2D. Regarding mRNA levels of adiponectin, no significant changes were found in HPAd, while all three types of SCFAs significantly increased (p<0.05) adiponectin expression in HPAd-T2D. Leptin mRNA expression levels were significantly increased by treatment with all three types of SCFAs in both HPAd (p<0.05) and HPAd-T2D (p<0.05). Conclusion. SCFAs inhibited lipid droplet accumulation and increased mRNA expression of adiponectin and leptin in T2D-derived adipocytes. -
General Endocrinology
Chen L, Gu T, Yang LZ
A Novel Intragenic Deletion Related to the Arginine Vasopressin V2 Receptor Causes Nephrogenic Diabetes InsipidusActa Endo (Buc) 2020 16(3): 295-297 doi: 10.4183/aeb.2020.295
AbstractBackground. Nephrogenic diabetes insipidus (NDI) is a disease characterized by a defective response to the antidiuretic hormone (ADH) of the renal collecting duct leading to a decline in the ability of the pro-urine concentration. Case presentation. A 23-year-old man presented with an over 20-year history of polyuria concomitant with hydronephrosis. The diagnosis of NDI was established by gene analysis as well as a water-deprivation and vasopressin test. All exons of arginine vasopressin V2 receptor (AVPR2) gene were amplified and sequenced. A novel hemizygous intragenic inframe deletion, cDNA 255th bp to 263th bp in exon 2 of AVPR2, was identified. These relevant translations from the 85th amino acid Asp to 88th amino acid Val were missed and replaced by amino acid Glu. After treating the patient with hydrochlorothiazide, his symptoms improved significantly. Conclusion. The genetic analysis revealed a novel X-linked intragenic inframe deletion, AVPR2 gene cDNA 255th bp to 263th bp, causing NDI. -
General Endocrinology
Vata L, DumitriuI, Gurzu M, Slatineanu S, Vata A, Gurzu B
Ghrelin effects on local renin angiotensin from pulmonary vesselsActa Endo (Buc) 2010 6(3): 295-304 doi: 10.4183/aeb.2010.295
AbstractBackground: Published data sustain the participation of vascular renin angiotensin system (RAS) on alteration of pulmonary vessels reactivity during the allergic airway inflammation. Ghrelin is a growth hormone-releasing peptide involved in modulation of immune function.\r\nObjective: This study aims to investigate the interaction between ghrelin and local RAS from rat pulmonary vessels during ovalbumin ? induced allergic airway disease. Methods: The angiotensinogen (AGT) ? induced contractions were assessed on isolated pulmonary artery and veins from ovalbumin sensitized rats receiving either saline (OSR) or ghrelin (OSG) by endotracheal instillation. Experiments were performed in the absence or the presence of losartan, D-ALA7, chymostatin and Nω-nitro-L-arginine methyl ester (L-NAME).\r\nResults: The AGT contractile effects mediated by AT1 receptors were lower with at least 25% on vessels from OSG than from OSR. The D-ALA7 and L-NAME significantly increases the AGT ? induced contraction on OSG. The amount of nitric oxide released after stimulation with AGT is higher on OSG and it is blocked by D-ALA7.\r\nConclusion: Our results suggested that pulmonary delivery of ghrelin could modulate the local RAS from pulmonary vessels by promoted the angiotensin 1-7 mediated effects. These data sustained the existence of another possible way for ghrelin?s beneficial effects on the lung.