Complex relationship between sex hormones, insulin resistance and leptin in men with and without prostatic disease

Grosman, Halina; Fabre, Bibiana; López, Miguel; Scorticati, Carlos H.; Silva, Maximiliano López; Mesch, Viviana; Mazza, Osvaldo; Berg, Gabriela

doi:10.3109/13685538.2015.1100600

Cited by 29 publications

(15 citation statements)

References 47 publications

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“…Metabolic syndrome (Met S) is a complex pathology manifested through a host of interrelated factors, such as increased waist circumference (WC), elevated insulin resistance (IR), hyperglycemia, hypertension, visceral adiposity, dyslipidemia, endothelial dysfunction, and atherosclerotic disease concomitant with low-grade inflammation, as indicated by elevated non-specific inflammatory markers. The Met S components often exist concomitantly with a reduction in circulating serum testosterone (T) levels [2345678910111213]. Furthermore, Met S is thought to be associated with nephrolithiasis, BPH, LUTS, erectile dysfunction (ED), and infertility [14].…”

Section: Introductionmentioning

confidence: 99%

Impact of Testosterone Deficiency and Testosterone Therapy on Lower Urinary Tract Symptoms in Men with Metabolic Syndrome

Traish

Johansen

2018

World J Mens Health

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Lower urinary tract function is modulated by neural, vascular and urethral and bladder structural elements. The pathophysiological mechanisms of lower urinary tract symptoms (LUTS) encompass prostate enlargement, alterations in urethra histological structure bladder fibrosis and alterations in pelvic neuronal and vascular networks, The complex pathophysiological relationship between testosterone (T) deficiency (TD) and the constellations LUTS, and metabolic dysfunction manifested in the metabolic syndrome (Met S) remains poorly understood. TD has emerged as one the potential targets by which Met S may contribute to the onset and development as well as worsening of LUTS. Because it has been recognized that treatment of men with Met S with T therapy ameliorates Met S components, it is postulated that T therapy may represent a therapeutic target in improving LUTS. Furthermore, the effect of TD on the prostate remains unclear, and often debatable. It is believed that T exclusively promotes prostate growth, however recent evidence has strongly contradicted this belief. The true relationship between benign prostatic hyperplasia, TD, and LUTS remains elusive and further research will be required to clarify the role of T in both benign prostatic hypertrophy (BPH) and LUTS as a whole. Although there is conflicting evidence about the benefits of T therapy in men with BPH and LUTS, the current body of literature supports the safety of using this therapy in men with enlarged prostate. As the population afflicted with obesity epidemic continues to age, the number of men suffering from Met S and LUTS together is expected to increase.

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Section: Introductionmentioning

confidence: 99%

Impact of Testosterone Deficiency and Testosterone Therapy on Lower Urinary Tract Symptoms in Men with Metabolic Syndrome

Traish

Johansen

2018

World J Mens Health

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“…This pathologic process brings about a cell-senescence status with surreptitious but ongoing cellular oxidative stress, a doomed deviation of cell death from a neat, non-inflammatory one towards the gloomy, ruinous and pro-inflammatory cell destruction. This is the reasonable explanation for all those papers addressing the presence of marked inflammation in prostate gland in BPH [18][19][20][21][22][23][24][25][26][27][28]. With escalating pro-inflammatory condition and smoldering hypoxia and oxidative stress, the hypoxia-inducible factor-1 gene is also expressed which in due course results in tissue expression of a host of other abnormal local growth factors.…”

Section: Novel Perspectives With Regard To Bph Pathogenesismentioning

confidence: 99%

Management of Benign Prostatic Hyperplasia with Metformin, Letrozole and Scheduled Growth Hormone Injections: A Pathophysiology Oriented

Arjmand¹

2017

Epidemiology

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Benign prostatic hyperplasia (BPH) is a common and bothersome condition characterized by prostate overgrowth causing slowly progressive lower urinary tract symptoms. It is highly prevalent in old age, and somewhat inescapable stigma of senility. Due to its major urologic manifestations, BPH has been conventionally assigned as a urologic disorder. Hence, it has remained an orphan medical entity in terms of pathogenesis and management. In fact, BPH, as a true metabolo-proteomic disorder, demands some relevant management strategies. Despite the known impacts of age, inheritance, senile changes in androgen to estrogen ratio, obesity, and metabolic disorders on development of BPH, the core pathogenic mechanisms that logically link and reasonably bring all those scattered findings together has not yet been meaningfully addressed. We believe that almost all informative pieces of BPH pathogenesis have been identified already. Thus, to revolutionize our understanding and to pave a definitely novel path towards medical therapy of BPH with a protocol consisting of metformin, letrozole and scheduled growth hormone injections, we only need to sort the available data out into the jigsaw of BPH pathogenesis picture.Keywords Benign Prostatic Hyperplasia; Metabolic Syndrome; Metformin; Letrozole; Growth hormone Novel Perspectives with regard to BPH PathogenesisThe maintenance of anthropometric measures of human body in general and specific internal organs in particular, depends on an extraordinarily system that governs the balance between cell proliferation and programmed cell death, that is, apoptosis. Even subtle disorder in this complex equation leads to either hypoplasia or hyperplasia. A wide variety of systemic growth hormones and diverse tissue specific growth factors mediate, moderate and modulate the cellgrowth cycle, proliferation, discrimination and ongoing cell refreshment. On the other hand, an extremely delicate physiologic process controls the rate of programmed cell death or apoptosis; a neat and non-inflammatory cell autolysis. Superior to these two processes stands a hitherto unknown supervising system that constantly counts the number of proliferated cells, momently measures the anthropometric organ dimensions, meticulously processes the captured data and finally makes sound and sensible commandments to maintain the physiologic equilibrium between cell proliferation and apoptosis. Even a trivial aberration in this ongoing process leads to long-term ultra-structural changes in cell morphology and eventually gross dysmorphism [1,2]. Among the long list of growth factors, insulin and insulin-like growth factor 1 (IGF-1) are the most abundant and the most potent signals inducing protein synthesis and mitogenesis. It is actually very important to know, that the IGF-1 also serves as the major cell-apoptosis modulating factor. IGF-1 prevents premature apoptosis or pathologic cell death in damaged cells through a sophisticated cell-refreshing process. The dual function of IGF-1 in cell proliferation and progra...

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“…227 The source of inflammatory cytokines in adipose tissues is linked to androgen actions through stimulation of lipolysis 244 and inhibition of adipose tissue lipoprotein lipase activity. 245 Low T levels have been found to be associated with enhanced adipocytes-derived inflammatory markers such as leptin, 246,247 adiponectin. 104 The exogenous T suppressed serum leptin and adiponectin concentrations in young men.…”

Section: Inflammationmentioning

confidence: 99%

The Effects of Androgens on Cardiometabolic Syndrome: Current Therapeutic Concepts

et al. 2020

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Introduction: Cardiometabolic syndrome (CMS), as a bunch of metabolic disorders mainly characterized by type 2 diabetes mellitus (T2DM), hypertension, atherosclerosis, central adiposity, and abdominal obesity triggering androgen deficiency, is one of the most critical threats to men. Although many significant preclinical and clinical findings explain CMS, new approaches toward common pathophysiological mechanisms and reasonable therapeutic targets are lacking. Aim: To gain a further understanding of the role of androgen levels in various facets of CMS such as the constellation of cardiometabolic risk factors including central adiposity, dyslipidemia, insulin resistance, diabetes, and arterial hypertension and to define future directions for development of effective therapeutic modalities. Methods: Clinical and experimental data were searched through scientific literature databases (PubMed) from 2009 to October 2019. Main Outcome Measure: Evidence from basic and clinical research was gathered with regard to the causal impact and therapeutic roles of androgens on CMS. Results: There are important mechanisms implicated in androgen levels and the risk of CMS. Low testosterone levels have many signs and symptoms on cardiometabolic and glycometabolic risks as well as abdominal obesity in men. Clinical Implications: The implications of the findings can shed light on future improvements in androgen levels and add potentially predictive risk for CMS, as well as T2DM, abdominal obesity to guide clinical management in the early stage. Strengths & Limitations: This comprehensive review refers to the association between androgens and cardiovascular health. A limitation of this study is the lack of large, prospective population-based studies that analyze the effects of testosterone treatment on CMS or mortality. Conclusion: Low testosterone levels have several common features with metabolic syndrome. Thus, testosterone may have preventive role in the progress of metabolic syndrome and subsequent T2DM, abdominal obesity, and cardiovascular disease and likely affect aging men's health mainly through endocrine and vascular mechanisms. Further studies are necessary to evaluate the therapeutic interventions directed at preventing CMS in men. Kirlangic OF, Yilmaz-Oral D, Kaya-Sezginer E, et al. The Effects of Androgens on Cardiometabolic Syndrome: Current Therapeutic Concepts. Sex Med 2020;8:132e155.

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Complex relationship between sex hormones, insulin resistance and leptin in men with and without prostatic disease

Abstract: It was observed a coexistence of an altered hormone profile with increased sex hormones and leptin in PCa patients, in accordance with the new perspective of PCa pathogenesis.

Cited by 29 publications

References 47 publications

Impact of Testosterone Deficiency and Testosterone Therapy on Lower Urinary Tract Symptoms in Men with Metabolic Syndrome

Impact of Testosterone Deficiency and Testosterone Therapy on Lower Urinary Tract Symptoms in Men with Metabolic Syndrome

Management of Benign Prostatic Hyperplasia with Metformin, Letrozole and Scheduled Growth Hormone Injections: A Pathophysiology Oriented

The Effects of Androgens on Cardiometabolic Syndrome: Current Therapeutic Concepts

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