Publications
932 results found
Ratner LD, Stevens G, Marta Bonaventura M, et al., 2016, Hyperprolactinemia induced by hCG leads to metabolic disturbances in female mice, JOURNAL OF ENDOCRINOLOGY, Vol: 230, Pages: 157-169, ISSN: 0022-0795
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- Citations: 14
Ponikwicka-Tyszko D, Chrusciel M, Stelmaszewska J, et al., 2016, Functional Expression of FSH Receptor in Endometriotic Lesions, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 101, Pages: 2905-2914, ISSN: 0021-972X
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- Citations: 28
Antonio L, Wu FCW, O'Neill TW, et al., 2016, Low Free Testosterone Is Associated with Hypogonadal Signs and Symptoms in Men with Normal Total Testosterone, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 101, Pages: 2647-2657, ISSN: 0021-972X
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- Citations: 105
Alviggi C, Conforti A, Cariati F, et al., 2016, Impact of polymorphisms of gonadotropins and their receptors on controlled ovarian stimulation: a prospective observational study, Publisher: OXFORD UNIV PRESS, Pages: 443-443, ISSN: 0268-1161
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- Citations: 4
Bjorkgren I, Alvarez L, Blank N, et al., 2016, Targeted inactivation of the mouse epididymal beta-defensin 41 alters sperm flagellar beat pattern and zona pellucida binding, MOLECULAR AND CELLULAR ENDOCRINOLOGY, Vol: 427, Pages: 143-154, ISSN: 0303-7207
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- Citations: 23
Oduwole O, Poliandri A, Rawson P, et al., 2016, FSH supplementation increases the growth of PC-3 human prostate cancer cell xenograft in gonadotropin-suppressed nude mice, 18th European Congress of Endocrinology
Laurent MR, Cook MJ, Gielen E, et al., 2016, LOWER BONE TURNOVER AND RELATIVE CORTICAL BONE DEFICITS IN MEN WITH METABOLIC SYNDROME: A MATTER OF INSULIN RESISTANCE? THE EUROPEAN MALE AGEING STUDY, WCO-IOF-ESCEO World Congress on Osteoporosis, Osteoarthritis and Musculoskeletal Diseases, Publisher: SPRINGER LONDON LTD, Pages: S93-S94, ISSN: 0937-941X
Huhtaniemi I, 2016, Male late-onset hypogonadism: current concepts and controversies, Unit-for-Multidisciplinary-Research-in-Biomedicine Summit, Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0025-7974
McCabe PS, Pye SR, Mc Beth J, et al., 2016, Low vitamin D and the risk of developing chronic widespread pain: results from the European male ageing study, BMC Musculoskeletal Disorders, Vol: 17, ISSN: 1471-2474
Pesonen E, Pussinen P, Huhtaniemi I, 2016, Adaptation to acute coronary syndrome-induced stress with lowering of testosterone: a possible survival factor, European Journal of Endocrinology, Vol: 174, Pages: 481-489, ISSN: 1479-683X
Objective The objective of this study was to explore whether circulating testosterone (T) concentration is associated with the occurrence and risk for acute coronary syndromes (ACS).Method This case–control study included male patients with acute myocardial infarction (AMI) (n=174) or unstable angina pectoris (UAP) (n=90) and healthy controls (n=238). Patients gave serum samples during the acute (n=264) and recovery (n=132) phases after a median of 10.5 months after the incident event. Secondary events (ACS or cardiovascular death) were registered during the following 6 years.Results During the acute phase, AMI and UAP patients had similar significantly reduced concentrations of serum testosterone in comparison to controls. Testosterone associated inversely with weight, the degree of inflammation (i.e. C-reactive protein concentration) and signs of a chronic infection. In a multiadjusted Cox regression, when compared to testosterone concentrations considered high-normal (14.91–34.0 nmol/l), low-normal testosterone (9.26–14.90 nmol/l) in the acute phase predicted better prognosis for cardiovascular death rate with a hazard ratio (HR) of 0.17 (0.04–0.68, P=0.012). The increased testosterone concentrations after the recovery period did not associate with future cardiovascular disease events.Conclusion Low-normal testosterone levels in the acute phase of ACS predicted better survival. The observation may indicate better adaptation to stress in survivors and warrants further study.
Trehan A, Kielbus M, Czapinski J, et al., 2016, REPLACR-mutagenesis, a one-step method for site-directed mutagenesis by recombineering, Scientific Reports, Vol: 6, ISSN: 2045-2322
Oduwole O, Rawson P, Rahman N, et al., 2016, Effect of FSH supplementation on the GnRH antagonist suppressed growth of PC-3 cell xenografts in nude mice., Genitourinary Cancers Symposium, Publisher: AMER SOC CLINICAL ONCOLOGY, ISSN: 0732-183X
Jonas KC, Huhtaniemi I, Hanyaloglu AC, 2016, Single-molecule resolution of G protein-coupled receptor (GPCR) complexes, G PROTEIN-COUPLED RECEPTORS: SIGNALING, TRAFFICKING AND REGULATION, Editors: Shukla, Publisher: ELSEVIER ACADEMIC PRESS INC, Pages: 55-72, ISBN: 978-0-12-803595-5
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- Citations: 29
Wade KF, Lee DM, McBeth J, et al., 2015, Chronic widespread pain is associated with worsening frailty in European men, Age and Ageing, Vol: 45, Pages: 268-274, ISSN: 1468-2834
Background: we hypothesised that chronic widespread pain (CWP), by acting as a potential stressor, may predispose to the development of, or worsening, frailty.Setting: longitudinal analysis within the European Male Ageing Study (EMAS).Participants: a total of 2,736 community-dwelling men aged 40–79.Methods: subjects completed a pain questionnaire and shaded a manikin, with the presence of CWP defined using the American College of Rheumatology criteria. Physical activity, smoking, alcohol consumption and depression were measured. Repeat assessments took place a median of 4.3 years later. A frailty index (FI) was used, with frail defined as an FI >0.35. The association between CWP at baseline and the new occurrence of frailty was examined using logistic regression; the association between CWP at baseline and change in FI was examined using negative binomial regression.Results: at baseline, 218 (8.3%) men reported CWP. Of the 2,631 men who were defined as non-frail at baseline, 112 (4.3%) were frail at follow-up; their mean FI was 0.12 (SD 0.1) at baseline and 0.15 (SD 0.1) at follow-up, with a mean change of 0.03 (SD 0.08) P ≤ 0.001. Among men who were non-frail at baseline, those with CWP were significantly more likely to develop frailty. After adjustment for age and centre, compared with those with no pain, those with CWP at baseline had a 70% higher FI at follow-up; these associations remained significant after further adjustment for smoking, body mass index, depression, physical activity and FI at baseline.Conclusion: the presence of CWP is associated with an increased risk of frailty in older European men.
Wade K, Lee D, Pendleton N, et al., 2015, Chronic widespread pain is associated with worsening frailty in European men, Age and Ageing, Vol: 45, Pages: 268-274, ISSN: 1468-2834
Huhtaniemi IT, 2015, Editorial comment on “use of hormone testing for the diagnosis and evaluation of male hypogonadism and monitoring of testosterone therapy: application of hormone testing guideline recommendations in clinical practice”, Journal of Sexual Medicine, Vol: 12, Pages: 1895-1896, ISSN: 1743-6109
Shima Y, Matsuzaki S, Miyabayashi K, et al., 2015, Fetal Leydig Cells Persist as an Androgen-Independent Subpopulation in the Postnatal Testis, MOLECULAR ENDOCRINOLOGY, Vol: 29, Pages: 1581-1593, ISSN: 0888-8809
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- Citations: 50
Huhtaniemi I, 2015, A short evolutionary history of FSH-stimulated spermatogenesis, Hormones, Vol: 14, Pages: 468-478, ISSN: 0018-5051
It is well established in various experimental models that luteinizing hormone (LH) stimulated testosterone (T) production of Leydig cells is the key endocrine stimulus of spermatogenesis. The role of the other gonadotrophin, follicle-stimulating hormone (FSH), is as yet somewhat unclear given that several clinical conditions and experimental models, including men with inactivating FSH receptor (R) mutation and male Fshb and Fshrknockout mice, maintain fairly normal spermatogenesis and fertility. Furthermore, FSH treatment of male infertility has produced at best modest results. On the other hand, there are animal species (e.g. teleost fishes and the Djungarian hamster) where spermatogenesis is primarily FSH-dependent. The purpose of this article is to briefly review the gonadotrophin dependence of spermatogenesis in several model species and examine how it has shifted during evolution from FSH to LH dominance. The information may provide new insight into the role of FSH treatment of male infertility.
Ahtiainen JP, Nyman K, Huhtaniemi I, et al., 2015, Effects of resistance training on testosterone metabolism in younger and older men, EXPERIMENTAL GERONTOLOGY, Vol: 69, Pages: 148-158, ISSN: 0531-5565
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- Citations: 18
Manna PR, Stetson CL, Daugherty C, et al., 2015, Up-regulation of steroid biosynthesis by retinoid signaling: Implications for aging, Mechanisms of Ageing and Development, Vol: 150, Pages: 74-82, ISSN: 1872-6216
Retinoids (vitamin A and its derivatives) are critical for a spectrum of developmental and physiological processes, in which steroid hormones also play indispensable roles. The StAR protein predominantly regulates steroid biosynthesis in steroidogenic tissues. We have reported that regulation of retinoid, especially atRA and 9-cis RA, responsive StAR transcription is largely mediated by an LXR–RXR/RAR heterodimeric motif in the mouse StAR promoter. Herein we demonstrate that retinoids are capable of enhancing StAR protein, P-StAR, and steroid production in granulosa, adrenocortical, glial, and epidermal cells. Whereas transient expression of RARα and RXRα enhanced 9-cis RA induced StAR gene transcription, silencing of RXRα with siRNA, decreased StAR and steroid levels. An oligonucleotide probe encompassing an LXR–RXR/RAR motif bound to adrenocortical and epidermal keratinocyte nuclear proteins in EMSAs. ChIP studies revealed association of RARα and RXRα with the StAR proximal promoter. Further studies demonstrated that StAR mRNA levels decreased in diseased and elderly men and women skin tissues and that atRA could restore steroidogenesis in epidermal keratinocytes of aged individuals. These findings provide novel insights into the relevance of retinoid signaling in the up-regulation of steroid biosynthesis in various target tissues, and indicate that retinoid therapy may have important implications in age-related complications and diseases.
Giwercman A, Goulis DG, Huhtaniemi I, et al., 2015, Untitled, HORMONES-INTERNATIONAL JOURNAL OF ENDOCRINOLOGY AND METABOLISM, Vol: 14, Pages: 467-467, ISSN: 1109-3099
Taylor AE, Keevil B, Huhtaniemi IT, 2015, Mass spectrometry and immunoassay: how to measure steroid hormones today and tomorrow, EUROPEAN JOURNAL OF ENDOCRINOLOGY, Vol: 173, Pages: D1-D12, ISSN: 0804-4643
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- Citations: 181
Pye SR, Vanderschueren D, Boonen S, et al., 2015, Low heel ultrasound parameters predict mortality in men: results from the European Male Ageing Study (EMAS), Age and Ageing, Vol: 44, Pages: 801-807, ISSN: 1468-2834
Guillermet-Guibert J, Smith LB, Halet G, et al., 2015, Novel role for p110β PI 3-Kinase in male fertility through regulation of androgen receptor activity in sertoli cells, Plos Genetics, Vol: 11, ISSN: 1553-7404
Rivero-Muller A, Potorac I, Pintiaux A, et al., 2015, A novel inactivating mutation of the LH/chorionic gonadotrophin receptor with impaired membrane trafficking leading to Leydig cell hypoplasia type 1, EUROPEAN JOURNAL OF ENDOCRINOLOGY, Vol: 172, Pages: K27-K36, ISSN: 0804-4643
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- Citations: 12
Rastrelli G, Carter EL, Ahern T, et al., 2015, Development of and recovery from secondary hypogonadism in aging men: prospective results from the EMAS, Journal of Clinical Endocrinology & Metabolism, Vol: 100, Pages: 3172-3182, ISSN: 1945-7197
Oduwole O, Peltoketo H, Poliandri A, et al., 2015, Restoration of fertility in hypogonadal LH receptor null background male mice by a constitutive active mutant FSH receptor, 17th European Congress of Endocrinology
Rastrelli G, Carter E, Finn J, et al., 2015, DEVELOPMENT AND RECOVERY FROM SECONDARY HYPOGONADISM IN AGING MEN: RISK FACTORS AND CLINICAL FEATURES. PROSPECTIVE RESULTS FROM THE EUROPEAN MALE AGING STUDY (EMAS), Publisher: WILEY-BLACKWELL, Pages: 254-254, ISSN: 1743-6095
Antonio L, Wu FCW, O'Neill TW, et al., 2015, Associations Between Sex Steroids and the Development of Metabolic Syndrome: A Longitudinal Study in European Men, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 100, Pages: 1396-1404, ISSN: 0021-972X
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- Citations: 76
Ratner LD, Stevens G, Marcia C, et al., 2015, DOES IN UTERO EXPOSURE TO HUMAN CHORIONIC GONADOTROPIN (HCG) HAVE A PROTECTIVE EFFECT ON HORMONAL IMBALANCES IN TRANSGENIC MICE?, 6th Latin American Symposium on Maternal-Fetal Interaction and Placenta / 5th Latin American Symposium on Reproductive Immunology, Publisher: W B SAUNDERS CO LTD, Pages: 519-519, ISSN: 0143-4004
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