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Copyright of Gazi Medical Journal is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Gazi Medical Journal is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: The aim of this study is to investigate the length of telomere and serum silent information regulator-1 levels in type 2 diabetic subjects as well as their associations with body composition, glycemic control, and diabetic complications. Methods: We enrolled 84 type 2 diabetic subjects and 40 controls. The length of telomere and serum silent information regulator-1 (Sirtuin-1) levels, body composition and diabetic complications were examined. Results: Median T/S ratio tended to be lower in type 2 diabetic subjects compared to the controls (1.03 (0.20-1.48) vs. 1.25 (0.80-1.69), P = .064); however, the percentage of having shorter telomere (T/S ratio < 1) was significantly higher in type 2 diabetic subjects than in the controls (47.6% vs. 27.5%, P = .035). Serum Sirtuin-1 level was lower in type 2 diabetic subjects than in controls (95.48 ± 29.9 vs. 138.40 ± 42.66 pg/mL, P < .001). There were no differences in the length of telomere and serum sirtuin-1 between the groups divided according to the presence of diabetic complications (P > .05). The percentage of having shorter telomere was higher in obese patients than in non-obese patients with DM (35.7% vs. 60%, P = .029). The T/S ratio was correlated with truncal fat in type 2 diabetic subjects (r = -0.250, P = .028). Conclusions: The length of telomere and silent information regulator-1 may have a role in cellular aging in type 2 diabetic subjects in relation to visceral obesity. [ABSTRACT FROM AUTHOR]

Beige adipocyte, the third and relatively new type of adipocyte, can emerge in white adipose tissue (WAT) under thermogenic stimulations that is termed as browning of WAT. Recent studies suggest that browning of WAT deserves more attention and therapies targeting browning of WAT can be helpful for reducing obesity. Beyond the major inducers of browning, namely cold and β3 -adrenergic stimulation, beige adipocytes are affected by several factors, and excess adiposity per se may also influence the browning process. The objective of the present review is to provide an overview of recent clinical and preclinical studies on the hormonal and nonhormonal factors that affect the browning of WAT. This review further focuses on the role of obesity per se on browning process. [ABSTRACT FROM AUTHOR]

Copyright of Gazi Medical Journal is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Journal of Endocrinology & Metabolism is the property of Aves Yayincilik Ltd. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Diabetes mellitus (DM) and osteoporosis are serious health problems that cause morbidity and mortality, especially in middle-aged and elderly population. An increased fracture risk has been reported in patients with DM. However, the complex mechanisms underlying the relationship between DM and osteoporosis are still unclear. In this article, coexistence of type 1 and type 2 diabetes and osteoporosis as well as the effects of diabetic complications and antidiabetic treatments on osteoporosis are discussed. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Osteoporosis / Turk Osteoporoz Dergisi is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aim: Macroprolactin is a high-molecular-weight form of prolactin. It has been suggested that macroprolactin has no clinical importance because of its decreased or limited bioactivity. Although screening for macroprolactinemia is recommended especially in patients with idiopathic hyperprolactinemia; recent studies reported that patients with macroprolactinemia may have some hyperprolactinemia symptoms. Currently, the causes of the symptoms as well as the treatment and follow-up of this group of patients are not clear. In our study, we aimed to retrospectively evaluate and compare the clinical characteristics and gonadal hormone levels of patients with macroprolactinemia and hyperprolactinemia. Materials and Methods: Forty patients with macroprolactinemia and 15 patients with hyperprolactinemia who referred to Obstetrics and Gynecology Hospital were examined. Results: We observed that the patients with macroprolactinemia had similar menstrual disturbances (oligomenorrhea/amenorrhea) to the patients with hyperprolactinemia. There was no statistically significant difference between the two groups with respect to FSH, LH and estradiol levels. The frequencies of galactorrhea (p=0.002), headache (p=0.04) and positive radiological finding (p=0.001) were higher in patients with hyperprolactinemia. Infertility rate was found to be increased in women with macroprolactinemia (p=0.02). Conclusion: Patients with macroprolactinemia may have very similar clinic symptoms to those with hyperprolactinemia. Therefore, macroprolactin levels should be measured regardless of the symptoms of hyperprolactinemia in patients with elevated prolactin levels. [ABSTRACT FROM AUTHOR]

Betatrophin and fibroblast growth factor-21 (FGF-21), as recently discovered members of hepatokine/adipokine family, have been proposed to be associated with some metabolic disorders in which insulin resistance plays a major role. We aimed to investigate serum betatrophin and FGF-21 concentrations in women with polycystic ovary syndrome (PCOS). In this cross-sectional study, we recruited 34 women with PCOS and 31 women as healthy controls. Serum betatrophin level and its relationship with serum FGF-21 level as well as other metabolic parameters were examined. Serum betatrophin level was significantly higher in women with PCOS than the control group (1.10 (0.20-4.20) vs 0.70 (0.20-3.50) ng/ml, p=0.004), whereas, FGF-21 did not differ between the groups (74.80 (7.80-435.90) vs 119.30 (10.50-443.40) pg/ml, p=0.13). Serum betatrophin correlated positively with LH levels (r=0.26, p=0.03). After controlling BMI, there was a significant positive correlation between betatrophin and FGF-21 (r=0.25, p=0.04). Multivariate regression analysis revealed that FGF-21 and presence of PCOS were the significant predictors of betatrophin concentrations (R²=0.22, F=2.56, p=0.03). Our results indicate that betatrophin levels are increased and associated with LH and FGF-21 levels, not insulin resistance, in women with PCOS. [ABSTRACT FROM AUTHOR]