RESUMO
We reviewed emerging evidence linking serum levels and adipose tissue expression of leptin and adiponectin in women with polycystic ovary syndrome (PCOS). Previous data obtained by our group from a sample of overweight/obese PCOS women and a control sample of normal weight controls, both stratified by BMI, were reanalyzed. Circulating levels of leptin and adiponectin were determined by commercially available enzyme-linked immunosorbent assays. Adipose tissue total RNA was reserve-transcripted into complementary DNA samples, which were used as templates for quantitative real-time PCR amplification. Positive correlations were found between serum and mRNA levels for both leptin (r = 0.321; P = 0.005) and adiponectin (r = 0.266; P = 0.024). Determination of leptin and adiponectin serum levels could serve as an indirect method to assess adipocyte production, since leptin and adiponectin are predominantly produced by subcutaneous adipocytes in women.
Assuntos
Adiponectina/sangue , Leptina/sangue , Síndrome do Ovário Policístico/sangue , Gordura Subcutânea/metabolismo , Estudos de Casos e Controles , Feminino , Humanos , Obesidade/sangueRESUMO
Adipose tissue secretes a variety of adipokines, including leptin and adiponectin, which are involved in endocrine processes regulating glucose and fatty metabolism, energy expenditure, inflammatory response, immunity, cardiovascular function, and reproduction. The present article describes the fluctuations in circulating leptin and adiponectin as well as their patterns of secretion in women from birth to menopause. During pregnancy, leptin and adiponectin seem to act in an autocrine/paracrine fashion in the placenta and adipose tissue, playing a role in the maternal-fetal interface and contributing to glucose metabolism and fetal development. In newborns, adiponectin levels are two to three times higher than in adults. Full-term newborns have significantly higher leptin and adiponectin levels than preterms, whereas small-for-gestational-age infants have lower levels of these adipokines than adequate-for-gestational-age newborns. However, with weight gain, leptin concentrations increase significantly. Children between 5 and 8 years of age experience an increase in leptin and a decrease in adiponectin regardless of body mass index, with a reversal of the newborn pattern for adiponectin: plasma adiponectin levels at age five are inversely correlated with percentage of body fat. In puberty, leptin plays a role in the regulation of menstrual cycles. In adults, it has been suggested that obese individuals exhibit both leptin resistance and decreased serum adiponectin levels. In conclusion, a progressive increase in adiposity throughout life seems to influence the relationship between leptin and adiponectin in women.
Assuntos
Adolescente , Adulto , Idoso , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Recém-Nascido , Pessoa de Meia-Idade , Gravidez , Adulto Jovem , Adiponectina/sangue , Adiposidade/fisiologia , Leptina/sangue , Aumento de Peso/fisiologia , Fatores Etários , Desenvolvimento Infantil , Pós-Menopausa/sangue , Puberdade/sangueRESUMO
Adipose tissue secretes a variety of adipokines, including leptin and adiponectin, which are involved in endocrine processes regulating glucose and fatty metabolism, energy expenditure, inflammatory response, immunity, cardiovascular function, and reproduction. The present article describes the fluctuations in circulating leptin and adiponectin as well as their patterns of secretion in women from birth to menopause. During pregnancy, leptin and adiponectin seem to act in an autocrine/paracrine fashion in the placenta and adipose tissue, playing a role in the maternal-fetal interface and contributing to glucose metabolism and fetal development. In newborns, adiponectin levels are two to three times higher than in adults. Full-term newborns have significantly higher leptin and adiponectin levels than preterms, whereas small-for-gestational-age infants have lower levels of these adipokines than adequate-for-gestational-age newborns. However, with weight gain, leptin concentrations increase significantly. Children between 5 and 8 years of age experience an increase in leptin and a decrease in adiponectin regardless of body mass index, with a reversal of the newborn pattern for adiponectin: plasma adiponectin levels at age five are inversely correlated with percentage of body fat. In puberty, leptin plays a role in the regulation of menstrual cycles. In adults, it has been suggested that obese individuals exhibit both leptin resistance and decreased serum adiponectin levels. In conclusion, a progressive increase in adiposity throughout life seems to influence the relationship between leptin and adiponectin in women.
Assuntos
Adiponectina/sangue , Adiposidade/fisiologia , Leptina/sangue , Aumento de Peso/fisiologia , Adolescente , Adulto , Fatores Etários , Idoso , Criança , Desenvolvimento Infantil , Pré-Escolar , Feminino , Humanos , Lactente , Recém-Nascido , Pessoa de Meia-Idade , Pós-Menopausa/sangue , Gravidez , Puberdade/sangue , Adulto JovemRESUMO
The aim of this study was to evaluate whether androgen receptor (AR) and the enzymes that convert testosterone into the more potent androgen dihydrotestosterone, 5alpha-reductases (5alpha-R1 and 5alpha-R2) are expressed in pelvic endometriosis. The study involved 21 infertile women who underwent laparoscopy and were divided into two groups: control (n= 13) and endometriosis (n= 8) according to the histological and laparoscopic findings. Endometrial and endometriotic implant biopsies were performed. By reverse transcription polymerase chain reaction and immunohistochemistry, AR, 5alpha-R1 and 5alpha-R2 messenger RNA and protein were detected in biopsies of pelvic endometriosis, as well as in the eutopic endometrium of both groups. These findings suggest that active androgens may be formed within the endometriotic tissue and that both local and systemic androgens have the potential to act on endometriotic cells.
Assuntos
Colestenona 5 alfa-Redutase/metabolismo , Endometriose/metabolismo , Receptores Androgênicos/metabolismo , Adolescente , Adulto , Estudos de Casos e Controles , DNA Complementar/metabolismo , Di-Hidrotestosterona/metabolismo , Feminino , Humanos , Imuno-Histoquímica , Prognóstico , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
Fibroadenomas are the most common benign lump in females. The study of gene alterations and/or deregulation in reproductive years may help explain hormonal physiological processes involved in nodule development and evolution. The objective was to compare ER-alpha, c-myc, and bcl-2 gene expression in breast fibroadenomas and in normal tissue and evaluate menstrual cycle, parity, and oral contraceptive influences. Fifty-seven premenopausal women (14-49 years) undergoing surgical removal of fibroadenomas were selected. Samples from fibroadenomas and circumjacent normal tissue were obtained for RT-PCR paired analysis. Patients were divided in groups according to menstrual cycle, use of contraceptives and parity. Tissue from 32 patients was adequate for RT-PCR. Paired analysis showed higher expression of ER-alpha (P=0.012) and bcl-2 (P=0.001) in fibroadenomas than in normal breast, while c-myc presented a similar expression (P=0.655). ER-alpha was higher in fibroadenomas of patients in follicular phase versus contraceptive users and normal tissue (P=0.003); bcl-2 was higher in fibroadenomas of patients in luteal phase than in the normal samples from all groups (P=0.007). c-myc did not differ according to menstrual cycle, but was higher in fibroadenomas>3 cm versus<3 cm (P=0.015) and in nulliparous women (P=0.04). A positive correlation between c-myc levels and fibroadenoma diameter was demonstrated (r=0.536; P=0.007). Nulliparous mean nodule diameter was superior than parous women (P=0.008). In conclusion, the expression of ER-alpha, bcl-2 and c-myc depends on hormonal and reproductive factors, with a possible contribution to lump formation and evolution.
Assuntos
Neoplasias da Mama/metabolismo , Mama/metabolismo , Receptor alfa de Estrogênio/química , Fibroadenoma/metabolismo , Regulação Neoplásica da Expressão Gênica , Proteínas Proto-Oncogênicas c-bcl-2/química , Proteínas Proto-Oncogênicas c-myc/metabolismo , Adolescente , Adulto , Apoptose , DNA Complementar/metabolismo , Feminino , Humanos , Pessoa de Meia-Idade , Pré-Menopausa , Progesterona/metabolismo , RNA/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase ReversaRESUMO
We assessed androgen-induced cell growth and c-myc expression in human non-transformed epithelial prostatic (HNTEP) cells in primary culture. Prostatic tissue was obtained from 48 retropubic prostatectomy patients (age: 61-77years) with benign prostatic hyperplasia (malignant tumors excluded). HNTEP cells were treated with testosterone or DHT, alone or in association with hydroxyflutamide. DHT action on c-myc mRNA was examined using Northern blots and RT-PCR. RT-PCR also was used to verify if HNTEP cells expressed the androgen receptor gene. Cell proliferation was assessed on days 3 and 6. Testosterone (2 x 10(-11) M) and DHT (10(-13)M) caused a significant increase (P < 0.05) in cell proliferation on both days. Addition of hydroxyflutamide (10(-6) M) to DHT abolished cell proliferation. HNTEP cells expressed androgen receptor (AR) gene and the treatment with DHT increased AR mRNA levels. C-myc expression was maximal at 30 min and 1 h with DHT (10(-13) M). C-myc seems to play a key role in the control of hormone responsiveness and cell proliferation in epithelial prostatic cells. The detection of androgen receptor gene expression and the increase in this expression with the addition of androgen shows that the HTNEP cells maintain functional characteristics and hormone dependence, and that they are a fruitful in vitro model for studying steroid hormone action mechanisms.