ACTA ENDOCRINOLOGICA (BUC)

Background. The purpose of this study was to explore the influencing factors of serum uric acid (SUA) level and related gene polymorphisms in the healthy population. Methods. A total of 346 healthy individuals screened from different areas in Shenyang City and 195 patients with high SUA levels were included. Results. The levels of TC (total cholesterol), HDL-C (high-density lipoprotein cholesterol), LDL-C (lowdensity lipoprotein cholesterol), TG (triglycerides), GLU (blood glucose) ALT (alanine aminotransferase), TBA (total bile acid), TBIL (total bilirubin), CR (creatinine) and CYSC (Cystatin C) were statistically different between the healthy and hyperuricemia population (P<0.05). However, there was no statistical difference in the UA level between the two groups (P>0.05). After adjusting for UA, TC, HDL-C, LDL-C, GLU, TBIL and CYSC, the additive and recessive models of rs2231142 were statistically significant in females (P<0.05). For males, haplotypes of A-C-A-A-G-G, A-CG- C-G-G and A-T-G-A-A-G had significant difference between the healthy and hyperuricemia population (P<0.05). For females, the haplotypes of A-C-G-C-G-G and A-T-A-CA- T had significant differences (P<0.05). Conclusion. The distributions of SLC2A9 (solute carrier family 2 and facilitated glucose transporter member 9), ABCG2 (ATP-binding cassette G2), GCKR (glucokinase regulatory protein), KCNQ1, IGFIR (Insulin-like growth factor-I receptor) and VEGFR (Vascular Endothelial Growth Factor Receptor) were balanced in the population in Shenyang City. The haplotypes of A-C-A-A-G-G, A-CG- C-G-G and A-T-G-A-A-G were the influencing factors of high SUA in the population in Shenyang City.

Objective. To observe the impact of quercetin and isoquercitrin on gluconeogenesis in hepatocytes. Methods. Mouse primary hepatocytes were cultured with lactic acid and pyruvic acid. After treatment with quercetin and isoquercitrin for 24 hours, the glucose concentration in the culture supernatant was determined. RT-PCR was used to detect the mRNAs of PEPCK, G6Pase, LKB1, and AMPKα. Protein levels of LKB1, AMPKα, and Thr172 phosphorylation were evaluated by Western blot. Results. The glucose concentration in the gluconeogenesis group (GN) was significantly higher than in the control group (C), but the glucose concentrations in the high level quercetin(group 80Q) and high level isoquercitrin (group 80I) were significantly lower than in the group GN, P<0.01. In the group 80Q, and group 80I, the mRNA levels of PEPCK and LKB1were significantly lower than in the group GN (P<0.01), and the G6Pase mRNA were significantly lower than in the group GN (P<0.05). The protein levels of LKB1 and the phosphorylation of AMPKα Thr172 in the group 80Q, group 40I, and group 80I were higher than in the group GN. The effects of quercetin and isoquercitrin on LKB1 and AMPKα were similar to those of metformin. Conclusions. Quercetin and isoquercitrin inhibit gluconeogenesis in hepatocytes, which may be related to the LKB1 upregulation and phosphorylation of AMPKα.

Objective. The existing studies involving omentin-1 have mainly focused on relationships with single cardiovascular risk factor. Whether omentin-1 is associated with the aggregation of cardiovascular risk factors has not been reported. We investigate the relationship between the serum omentin-1 level and aggregation of cardiovascular risk factors in adolescents. Subjects and Methods. A total of 741 young students, 11–16 years of age, were enrolled using a stratified cluster sampling method. The participants were given a questionnaire survey and underwent a physical examination. The aggregation of cardiovascular risk factors was defined as two or more cardiovascular risk factors occurring simultaneously in the same individual. Results. Partial correlation analysis suggested that serum omentin-1 level was significantly correlated with waist circumference (R=-0.086, P=0.019) and Body Mass Index (R=-0.096, P=0.009). Logistic regression analysis showed that as the serum omentin-1 level increased, the risk of aggregation of cardiovascular risk factors decreased. Cardiovascular risk factors which were most closely associated with a decrease in the serum omentin-1 level were obesity calculated by Body Mass Index (OR=0.988, P=0.043) and central obesity calculated by waist circumference (OR=0.993, P=0.012). Conclusions. The serum omentin-1 level in adolescents is inversely associated with the aggregation of cardiovascular risk factors. Waist circumference and Body Mass Index are factors most closely associated with a decrease in the serum omentin-1 level.

Objective. In this study we investigated the effect of dorsomedial hypothalamus (DMH) neuropeptide Y (NPY) knock-down on hepatic insulin sensitivity in high-fat (HF) diet-fed rats. Methods. Forty-eight Sprague-Dawley rats were randomly assigned to receive bilateral DMH injections of adeno-associated virus AAVshNPY or AAVshCTL and then accessed to regular chow. Five weeks after viral injection, half rats in each group were given access to the HF diet. At 16 weeks, rat livers were collected. Insulin receptor substrate-1 (IRS-1) and phosphoinositide 3-kinase (PI3K) mRNA expression was measured by qRT-PCR. Blood glucose levels were measured by the oxidase method, serum insulin, triglyceride, and TC levels were measured by Elisa. Pathological changes in the liver were assessed by hematoxylin-eosin (HE) staining. AKT, p-AKT, and GSK-3 levels were measured by western blotting. Results. Compared with AAVshCTL-injected rats, AAVshNPY-injected rats showed a significant decrease in blood glucose concentrations; serum insulin, triglyceride, and TC; HOMA-IR; and IRS-1 and PI3K mRNA levels (P<0.05). ISI, GSK-3, and p-AKT levels were significantly increased (P<0.05). HE staining showed that AAVshNPYinjected rats fed the HF diet had mild fatty degeneration. Conclusion. These results suggest that DMH NPY knock-down improves hepatic insulin sensitivity in HF diet-fed rats by activating the hepatic PI3K/AKT insulin signalling pathway.

Radioactive iodine (RAI) therapy is a mainstay adjuvant treatment for thyroid cancer. Administration of RAI therapy after total or near-total thyroidectomy has shown a survival advantage in numerous properly selected patients. However, the role of RAI therapy after reoperation for persistent or recurrent differentiated thyroid carcinomas (DTCs) is unclear. One reason may be the possible downregulation of the I- transport system after primary surgery. RAI is transported by the sodium iodide symporter (NIS), PENDRIN, anoctamin 1 (ANO1) and cystic fibrosis transmembrane conductance regulator (CFTR) and emits β particles that destroy follicular cells. The identification of pathways of iodide (I-) transport has allowed use of the transport system to render tumours susceptible to RAI treatment via gene therapy. This review focuses on the effect of RAI therapy in follicular cell-derived thyroid cancers and offers potential novel targets that enable improved radioiodine uptake and thus an improved prognosis of thyroid cancer.

Introduction.Cardiomyopathy secondary to severe hypocalcaemia can lead to death when misdiagnosed. However, it can respond favorably to calcium and vitamin D as in this observation.\r\nCase report. SB, 50 years old, was hospitalized for heart failure. He was operated on for cataracts and treated for epilepsy, but was not known as having heart problems.\r\nClinical examination revealed global heart failure. Chest x ray showed cardiomegaly with bilateral pleural effusion. Echocardiography demonstrated myocardium dilatation with an\r\nimpaired systolic function (ejection fraction = 38%, N&#8805; 60). Heart screening did not find any cause, but laboratory investigation diagnosed severe hypocalcemia (mean value: 26mg/L (N=80-105) or 0.65 mmol/L), high phosphorus (61.5mg/L, N=25-45), and low parathormone (6.51 pg/mL, N=15-65 pg/mL). Corrected calcium according to protidemia\r\nwas 0.69 mmol/L. Magnesium was normal. Brain CT scan showed bilateral and symmetrical calcifications of basal ganglia\r\narguing for Fahr?s syndrome. After calcium (1g) and vitamin D (2, then 3 &#956;g/day) during one week, cardiac abnormalities improved promptly. Three months later seizures disappeared totally after stopping anti epileptic drugs.\r\nConclusion.The fast reversibility of heart failure and seizures under calcium suggests observed symptoms were due to hypocalcaemia, seemingly installed on a previously normal heart function. So, calcium assessment should be checked systematically in heart insufficiency.

Background. The implementation of assisted reproductive techniques (ART) is a complex treatment requiring both a good cooperation between various professional groups in the fertility centre, and the patient’s and her partner’s cooperation. Accordingly, there are many sources of failure, such as using the wrong medication or not considering optimal times. If there is an artificial application of the ovulation induction injection, the success of the treatment is endangered and in some cases the cycle is discontinued, if the patient failed to administer the drug correctly. An alternative to cycle cancellation might be the maturation of the oocytes in vitro. We report on a 31-year-old patient in whom we performed an oocyte retrieval procedure 24 hours after triggering ovulation followed by in vitro maturation of the immature oocytes over a period of more than 12 h. The treatment resulted in a healthy, ongoing pregnancy.

Introduction. Pituitary apoplexy is a rare, acute, and life threatening condition due to haemorrhage or necrosis within a pituitary adenoma. Its prognosis may be poor leading to a fatal issue, or be good inducing a decrease or cure of the pituitary adenoma as in the case presented.\r\nCase report. A man, aged 28 years, having a history of well proved acromegaly [Growth hormone =GH=205ng/mL (n<5),\r\nand pituitary adenoma measuring 19x16mm] with diabetes mellitus (Glycaemia 4g/L, glycosuria++++, with ketoacidosis) treated with insulin for one year, was referred for\r\nnumerous hypoglycaemias which obliged him to stop insulin and diet. Just before, he had an acute episode of headaches, nauseas and vomiting. Clinical exam showed typical\r\nacromegaly, but pituitary assessment demonstrated low GH=0.05ng/mL, normal IGF1, without pituitary deficits. Routine analyses were normal. Fasting glycaemias, and glycaemias after glucose loading were normal too. Cerebral MRI showed a significant decrease in pituitary tumour (10 x\r\n16mm). Ten years later, glycaemias, GH, IGF1, and other pituitary functions remained normal, the necrotic pituitary process decreased up to 4.5 mm in height.\r\nConclusion. This clinical history and outcome argued for a pituitary apoplexy secondary to apparently spontaneous\r\nnecrosis of a somatotrop adenoma that induced a total cure of acromegaly and diabetes mellitus.

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Context. The expression of TSHR-C on the serum tetraiodothyronine (T4) and TSH receptor antibody (TRAb) levels are rarely studied. Objective. The effect of TSHR-c on T4 and TRAb levels and concomitant thyroid histological changes in mice was investigated. Design. Animal experimental study. Subjects and methods. Female BALB/c mice at 6-8 weeks of age were immunized with the thyroid stimulating hormone receptor antigen C-terminus (TSHR-C), and randomly divided into control group (treated with the corresponding concentrations of normal saline) and four experimental subgroups: TSHR-c1 subgroup (4 μg), TSHR-c2 subgroup (6 μg), TSHR-c3 subgroup (8 μg) and TSHR-c4 subgroup (10 μg). Serum T4 and TRAb levels were determined. Results. The serum T4 level decreased significantly in the experimental mice as the concentration increased. All the experimental mice were positive for serum TRAb (experimental groups: 40 positive/40, 100% vs. control group: 3 positive/10, 30%) compared to the control group (P =0.000). HE staining showed that the follicles in the control mice were composed of small to medium-sized round follicles, whereas the follicles in the experimental mice were irregularly enlarged under light microscope. Conclusions. TSHR-c immunization resulted in thyroid hormone changes like those observed in hypothyroidism, probably due to the induction of TRAb generation.