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Featured researches published by Ethel Codner.


The Journal of Clinical Endocrinology and Metabolism | 2010

Metabolic and Reproductive Features before and during Puberty in Daughters of Women with Polycystic Ovary Syndrome

Teresa Sir-Petermann; Ethel Codner; Virginia Pérez; Bárbara Echiburú; Manuel Maliqueo; Amanda Ladrón de Guevara; Jessica Preisler; Nicolás Crisosto; Fernando Sánchez; Fernando Cassorla; Shalender Bhasin

CONTEXT A significant proportion of the first-degree female relatives of women with polycystic ovary syndrome (PCOS) may be at risk for developing PCOS. However, it is not known at which stage of pubertal development the hormonal and metabolic abnormalities ensue in PCOS. OBJECTIVE The aim of the study was to assess the reproductive and metabolic profiles of daughters of women with PCOS (PCOSd) during the peripubertal period, a stage during which the gonadal axis is activated and PCOS may become clinically manifest. DESIGN Ninety-nine PCOSd [30 prepubertal and 69 pubertal (Tanner II-V)] and 84 daughters of control women (Cd) (20 prepubertal and 64 pubertal) were studied. An oral glucose tolerance test, a GnRH agonist test (leuprolide acetate, 10 microg/kg sc), and a transabdominal ultrasound were performed. Gonadotropins, sex steroids, SHBG, glucose, insulin, and lipids were determined. RESULTS Both groups had similar chronological ages and body mass index sd scores according to Tanner stage distribution. Ovarian volume and 2-h insulin were significantly higher in PCOSd compared to Cd at all Tanner stages. In Tanner stages IV and V, basal testosterone and poststimulated LH, testosterone, and 17-hydroxyprogesterone concentrations were significantly higher in PCOSd compared to Cd. CONCLUSIONS Hyperinsulinemia and an increased ovarian volume are present in PCOSd before the onset of puberty and persist during pubertal development. The biochemical abnormalities of PCOS appear during late puberty. Considering the early onset and the nature of the alterations, PCOSd constitute a high-risk group for metabolic and reproductive derangements.


Diabetes | 2011

Permanent Neonatal Diabetes and Enteric Anendocrinosis Associated With Biallelic Mutations in NEUROG3

Oscar Rubio-Cabezas; Jan Jensen; Maria I. Hodgson; Ethel Codner; Sian Ellard; Palle Serup; Andrew T. Hattersley

OBJECTIVE NEUROG3 plays a central role in the development of both pancreatic islets and enteroendocrine cells. Homozygous hypomorphic missense mutations in NEUROG3 have been recently associated with a rare form of congenital malabsorptive diarrhea secondary to enteroendocrine cell dysgenesis. Interestingly, the patients did not develop neonatal diabetes but childhood-onset diabetes. We hypothesized that null mutations in NEUROG3 might be responsible for the disease in a patient with permanent neonatal diabetes and severe congenital malabsorptive diarrhea. RESEARCH DESIGN AND METHODS The single coding exon of NEUROG3 was amplified and sequenced from genomic DNA. The mutant protein isoforms were functionally characterized by measuring their ability to bind to an E-box element in the NEUROD1 promoter in vitro and to induce ectopic endocrine cell formation and cell delamination after in ovo chicken endoderm electroporation. RESULTS Two different heterozygous point mutations in NEUROG3 were identified in the proband [c.82G>T (p.E28X) and c.404T>C (p.L135P)], each being inherited from an unaffected parent. Both in vitro and in vivo functional studies indicated that the mutant isoforms are biologically inactive. In keeping with this, no enteroendocrine cells were detected in intestinal biopsy samples from the patient. CONCLUSIONS Severe deficiency of neurogenin 3 causes a rare novel subtype of permanent neonatal diabetes. This finding confirms the essential role of NEUROG3 in islet development and function in humans.


Human Reproduction Update | 2012

Female reproduction and type 1 diabetes: from mechanisms to clinical findings

Ethel Codner; P.M. Merino; Manuel Tena-Sempere

BACKGROUND The functional reproductive alterations seen in women with type 1 diabetes (T1D) have changed as therapy has improved. Historically, patients with T1D and insufficient metabolic control exhibited a high prevalence of amenorrhea, hypogonadism and infertility. This paper reviews the impact of diabetes on the reproductive axis of female T1D patients treated with modern insulin therapy, with special attention to the mechanisms by which diabetes disrupts hypothalamic-pituitary-ovarian function, as documented mainly by animal model studies. METHODS A comprehensive MEDLINE search of articles published from 1966 to 2012 was performed. Animal model studies on experimental diabetes and human studies on T1D were examined and cross-referenced with terms that referred to different aspects of the gonadotropic axis, gonadotrophins and gonadal steroids. RESULTS Recent studies have shown that women with T1D still display delayed puberty and menarche, menstrual irregularities (especially oligomenorrhoea), mild hyperandrogenism, polycystic ovarian syndrome, fewer live born children and possibly earlier menopause. Animal models have helped us to decipher the underlying basis of these conditions and have highlighted the variable contributions of defective leptin, insulin and kisspeptin signalling to the mechanisms of perturbed reproduction in T1D. CONCLUSIONS Despite improvements in insulin therapy, T1D patients still suffer many reproductive problems that warrant specific diagnoses and therapeutic management. Similar to other states of metabolic stress, T1D represents a challenge to the correct functioning of the reproductive axis.


Hormone Research in Paediatrics | 2015

The Diagnosis of Polycystic Ovary Syndrome during Adolescence

Selma F. Witchel; Sharon E. Oberfield; Robert L. Rosenfield; Ethel Codner; Andrea E. Bonny; Lourdes Ibáñez; Alexia S Peña; Reiko Horikawa; Veronica Gomez-Lobo; Dipesalema Joel; Hala Tfayli; Silva Arslanian; Preeti Dabadghao; Cecilia Garcia Rudaz; Peter A. Lee

Background/Aims: The diagnostic criteria for polycystic ovary syndrome (PCOS) in adolescence are controversial, primarily because the diagnostic pathological features used in adult women may be normal pubertal physiological events. Hence, international pediatric and adolescent specialty societies have defined criteria that have sufficient evidence to be used for the diagnosis of PCOS in adolescents. Methods: The literature has been reviewed and evidence graded to address a series of questions regarding the diagnosis of PCOS during adolescence including the following: clinical and biochemical evidence of hyperandrogenism, criteria for oligo-anovulation and polycystic ovary morphology, diagnostic criteria to exclude other causes of hyperandrogenism and amenorrhea, role of insulin resistance, and intervention. Results and Conclusion: Features of PCOS overlap normal pubertal development. Hence, caution should be taken before diagnosing PCOS without longitudinal evaluation. However, treatment may be indicated even in the absence of a definitive diagnosis. While obesity, insulin resistance, and hyperinsulinemia are common findings in adolescents with hyperandrogenism, these features should not be used to diagnose PCOS among adolescent girls.


Immunobiology | 2013

MicroRNAs miR-21a and miR-93 are down regulated in peripheral blood mononuclear cells (PBMCs) from patients with type 1 diabetes

Francisca Salas-Pérez; Ethel Codner; Elizabeth Valencia; Carolina Pizarro; Elena Carrasco; Francisco Pérez-Bravo

INTRODUCTION It is well established that type 1 diabetes (T1D) is an autoimmune disease. Controversial data exists regarding the differential control of the immune system in T1D patients compared to unaffected individuals. MicroRNAs (miRNAs) are involved in the control of gene expression (by negative regulation of gene expression at post-transcriptional level, by mediating translational repression or degradation of the mRNA targets). Their potential role in T cell activation and autoimmunity is controversial. AIM We investigated the expression profile of miR-21a and miR-93 in PMC samples of 20 T1D patients and 20 healthy controls by means of qPCR in different glucose concentrations (basal, 11 nM and 25 mM), and we analyzed the possible relationship of this expression pattern with autoimmunity. RESULTS MiR-21a was significantly underexpressed in T1D samples (media values expression 0.23 ± 0.05, p < 0.01) compared to controls (values less than 1 indicate a decrease in gene expression). When the PMCs were incubated with glucose 11 mM and 25 mM, miR-21a expression decreased in controls and increased in T1D samples (0.506 ± 0.05, p < 0.04). MiR-93 was underexpressed in T1D patients (0.331 ± 0.05, p < 0.02) compared to control samples. However, when the PBMCs were incubated with glucose, no changes were observed. No association with autoimmunity was observed. CONCLUSION We demonstrated that miRNAs have a differential expression in PBMCs from T1D patients compared to controls, suggesting that these miRNAs or others could be involved in T cell regulation.


Human Reproduction | 2009

Anti-Müllerian hormone and inhibin B levels as markers of premature ovarian aging and transition to menopause in type 1 diabetes mellitus

Néstor Soto; Germán Iñiguez; Patricia López; Gladys Larenas; Verónica Mujica; Rodolfo Rey; Ethel Codner

BACKGROUND Serum anti-Müllerian hormone (AMH) levels decrease early during the transition to menopause and women with type 1 diabetes mellitus (DM1) experience menopause at a younger age. We hypothesized that older women with DM1 will have lower AMH levels than controls. METHODS We studied ovarian function in women with DM1 (n = 66) and healthy controls (n = 58), all <45 years old. Steroids, gonadotrophins, AMH and inhibin B levels were measured during the follicular phase. RESULTS Piece-wise regression analysis demonstrated that AMH levels begin to decrease at 33 years of age in both groups. This age limit was used to compare data in both groups. AMH levels were lower in DM1 women than in controls >33 years (4.1 +/- 4.2 versus 9.5 +/- 7.9 pmol/l, mean +/- SD, P = 0.006). A higher proportion of women with DM1 showed AMH levels in the menopausal range compared with controls (16.7% versus 3.4%, respectively, P = 0.02). For all patients, those with DM1 exhibited lower inhibin B levels than controls (89.3 +/- 51.7 versus 113.2 +/- 76.0 ng/ml, P < 0.05). FSH and estradiol were similar in both groups. Regression analysis showed an earlier decline in AMH levels in women with DM1 than controls. Even after age adjustment, DM1 was a significant factor for the determination of inhibin B and AMH levels. CONCLUSIONS Lower AMH levels in women with DM1 during the fourth decade of life suggest the presence of an earlier decline in the ovarian follicle pool in these women. Further studies are needed to evaluate the mechanism of this complication.


The Journal of Clinical Endocrinology and Metabolism | 2008

Metabolic Profile in Sons of Women with Polycystic Ovary Syndrome

Sergio E. Recabarren; Rosita Smith; Rafael Ríos; Manuel Maliqueo; Bárbara Echiburú; Ethel Codner; Fernando Cassorla; Pedro Rojas; Teresa Sir-Petermann

CONTEXT Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder with strong familial aggregation. It has been demonstrated that parents and brothers of PCOS women exhibit insulin resistance and related metabolic defects. However, metabolic phenotypes in sons of PCOS women have not been described. OBJECTIVE Our objective was to assess the metabolic profiles in sons of women with PCOS during different stages of life: early infancy, childhood, and adulthood. DESIGN Eighty sons of women with PCOS (PCOS(S)) and 56 sons of control women without hyperandrogenism (C(S)), matched for age, were studied. In early infancy, glucose and insulin were determined in the basal sample. In children and adults, a 2-h oral glucose tolerance test was performed with measurements of glucose and insulin. Adiponectin, leptin, C-reactive protein, SHBG, and serum lipids were determined in the basal sample during the three periods. RESULTS During early infancy, PCOS(S) showed higher weight (P = 0.038) and weight sd score (P = 0.031) than C(S). During childhood, weight (P = 0.003), body mass index (BMI) (P < 0.001), BMI sd score (P < 0.001), waist circumference (P = 0.001), total cholesterol (P = 0.007), and low-density lipoprotein cholesterol (P = 0.022) were higher in PCOS(S) compared with C(S), but after adjusting for BMI, these differences were nonsignificant. During adulthood, PCOS(S) exhibited higher weight (P = 0.022), BMI (P = 0.046), and waist circumference (P = 0.028) than C(S). Fasting insulin (P = 0.030), homeostasis model assessment for insulin resistance (P = 0.034), total cholesterol (P = 0.043), low-density lipoprotein cholesterol (P = 0.034), and 2-h insulin (P = 0.006) were also significantly higher and insulin sensitivity index composite significantly lower in PCOS(S) than in C(S) (P = 0.003). After adjusting for BMI, only 2-h insulin and insulin sensitivity index composite remained significantly different. CONCLUSIONS This study indicates that sons of PCOS women exhibit higher body weight from early infancy. In addition, insulin resistance became evident as the subjects got older, which may place them at risk for the development of type 2 diabetes and cardiovascular disease.


Hormone Research in Paediatrics | 2009

Puberty and Ovarian Function in Girls with Type 1 Diabetes Mellitus

Ethel Codner; Fernando Cassorla

Insulin is well known for its effects on carbohydrate metabolism, but this hormone also plays an important role in regulating ovarian function. Granulosa, theca and stromal ovarian cells may be affected by insulin deficiency or excess, which may be present in women with type 1 diabetes mellitus (T1D). Recent publications have shown that in spite of intensive insulin therapy, some delay in the age of thelarche, pubarche and menarche is still observed in girls with T1D. In addition, ovarian hyperandrogenism may be observed during late adolescence and an increased prevalence of hirsutism and polycystic ovarian syndrome (PCOS) has been described in adult women with T1D. These endocrine abnormalities may be related to nonphysiologic insulin replacement therapy and to hyperglycemia. This paper reviews the pubertal development and the clinical reproductive abnormalities observed in girls with type 1 diabetes mellitus, and shows that several significant clinical problems, such as pubertal delay, menstrual disturbances and hyperandrogenism which may ultimately lead to the development of PCOS in adulthood, may be observed in some of these patients.


Pediatric Diabetes | 2007

Tobacco, alcohol, and illicit drug use in adolescents with diabetes mellitus.

Alejandro Martínez-Aguayo; Juan Carlos Araneda; Daniela Fernandez; Andrea Gleisner; Virginia Pérez; Ethel Codner

Background:  Substance abuse in adolescents with diabetes mellitus (DM) is associated with the development of acute and chronic complications.


Human Reproduction | 2011

Polycystic ovarian morphology in adolescents with regular menstrual cycles is associated with elevated anti-Müllerian hormone

C. Villarroel; P.M. Merino; Patricia López; F.C. Eyzaguirre; A. Van Velzën; Germán Iñiguez; Ethel Codner

BACKGROUND The significance of polycystic ovarian morphology (PCOM) during adolescence is not clear. The aim of this study was to determine the relationship between PCOM and anti-Müllerian hormone (AMH), inhibin B, testosterone and insulin levels in healthy girls during the second decade of life. We also determined whether AMH could be used as a surrogate marker of PCOM during adolescence. METHODS Seventy-four non-obese adolescents (age range: 13.5-19.75 years old) with regular menstrual cycles participated in this study. Transabdominal ultrasound and blood samples were obtained during the follicular phase. RESULTS PCOM was present in 33.8% of the subjects. Girls with PCOM had higher AMH levels than girls without PCOM (72.5 ± 6.1 versus 33.4 ± 2.6 pmol/l; P < 0.0001) and lower FSH levels (5.4 ± 0.3 versus 6.2 ± 0.2 mUI/ml; P < 0.036). Similar levels of inhibin B, androgens and LH were observed in girls with and without PCOM. PCOM prevalence and AMH levels were not associated with age (P = 0.745 and 0.2, respectively) or BMI-SDS (P = 0.951 and 0.096, respectively). AMH levels positively correlated with the of 2-5 mm follicle number. AMH levels ≥ 60.15 pmol/l had a sensitivity and specificity of 64.0 and 89.8%, respectively, to diagnose PCOM (area under the curve = 0.873). CONCLUSIONS These data confirm that PCOM in healthy non-hyperandrogenic girls with regular menstrual cycles is prevalent and is not associated with hyperandrogenism. The elevated AMH and lower FSH levels observed in healthy girls with regular menses and PCOM suggest that this ovarian pattern is secondary to a larger number of 2-5 mm follicles. An elevated AMH level is suggestive of the presence of PCOM during adolescence.

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