ACTA ENDOCRINOLOGICA (BUC)

Sustained exposure to high serum insulin-like growth factor (IGF-1) levels is likely to play a role in the development of the thyroid tumor in acromegaly; however, there is no report that indicate a promoting effect on the secretion of hormones by the thyroid tumor. We report a case of acromegaly in a seventy-one-year-old female with primary subclinical hyperthyroidism. Autoantibodies including\r\nanti-thyroglobulin antibody, anti-thyroid peroxidase antibody and thyroid stimulating hormone (TSH) receptor antibody were all negative. Ultrasonography of the thyroid\r\ndemonstrated a solid adenoma in the left thyroid lobe and Technetium-99m thyroid scintigraphy showed a high level of\r\naccumulation into the same lesion, indicating that toxic nodular goiter (TNG) was the cause of hyperthyroidism. Despite serum thyroid hormones remaining at normal levels,\r\nserum TSH levels went on decreasing gradually until transsphenoidal surgery to treat a growth hormone (GH) secreting pituitary adenoma. Interestingly, as IGF-I\r\nand GH levels normalized after operation, the serum TSH level increased and finally reached the normal level without\r\nintervention to the thyroid. Additionally, accumulation of Technetium-99m seen with thyroid scintigraphy slightly decreased. The evidence obtained from this case may\r\nsuggest a novel mechanism whereby excessive secretion of thyroid hormones from TNG in an acromegalic patient is\r\nregulated by IGF-I.

Background. There is no immunohistochemical study to show luteinizing hormone receptor (LHR), estrogen receptor (ER) and progesterone receptor (PR) in the pregnant Fallopian tubes (FT). Objective. To study LHR, ER, PR expression in FT containing an ectopic pregnancy (EP) and during the menstrual phase. Design. Thirty FT were obtained from women diagnosed with EP and twenty FT collected by hysterectomy performed for benign diseases not affecting the tubes were included in this study. Assessment of immunohistochemical expression staining LHR, ER, PR in epithelium, smooth muscle cell and blood vessel endothelium in FT containing an EP and during the different phases of menstrual cycle. Results. In ectopic pregnancy group we found LHR expression in epithelium in 30 cases, muscle cell in 28 cases, and endothelium in 9 cases in FT. In menstrual cycle group we noted LHR expression in FT in epithelium in all cases, muscle cell in 4 cases. Conclusion. There is a significant difference in the proportions of the existence of LH receptor immunostaining in the muscle cells for ectopic pregnancy group as compared to the menstrual cycle groups (p < 0.001). Our findings may suggest that the women who have increased LH receptors on muscle cells in Fallopian tubes are at increased risk for having external pregnancy.

Purpose. 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.