Male Obesity-related Secondary Hypogonadism – Pathophysiology, Clinical Implications and Management

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Abstract

The single most significant risk factor for testosterone deficiency in men is obesity. The pathophysiological mechanisms involved in male obesity-related secondary hypogonadism are highly complex. Obesity-induced increase in levels of leptin, insulin, proinflammatory cytokines and oestrogen can cause a functional hypogonadotrophic hypogonadism with the defect present at the level of the hypothalamic gonadotrophin-releasing hormone (GnRH) neurons. The resulting hypogonadism by itself can worsen obesity, creating a self-perpetuating cycle. Obesity-induced hypogonadism is reversible with substantial weight loss. Lifestyle-measures form the cornerstone of management as they can potentially improve androgen deficiency symptoms irrespective of their effect on testosterone levels. In selected patients, bariatric surgery can reverse the obesity-induced hypogonadism. If these measures fail to relieve symptoms and to normalise testosterone levels, in appropriately selected men, testosterone replacement therapy could be started. Aromatase inhibitors and selective oestrogen receptor modulators are not recommended due to lack of consistent clinical trial-based evidence.

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Identification of late-onset hypogonadism in middle-aged and elderly men.

Frederick C.W. Wu, Abdelouahid Tajar, Jennifer M. Beynon … (2010)

The association between aging-related testosterone deficiency and late-onset hypogonadism in men remains a controversial concept. We sought evidence-based criteria for identifying late-onset hypogonadism in the general population on the basis of an association between symptoms and a low testosterone level. We surveyed a random population sample of 3369 men between the ages of 40 and 79 years at eight European centers. Using questionnaires, we collected data with regard to the subjects' general, sexual, physical, and psychological health. Levels of total testosterone were measured in morning blood samples by mass spectrometry, and free testosterone levels were calculated with the use of Vermeulen's formula. Data were randomly split into separate training and validation sets for confirmatory analyses. In the training set, symptoms of poor morning erection, low sexual desire, erectile dysfunction, inability to perform vigorous activity, depression, and fatigue were significantly related to the testosterone level. Increased probabilities of the three sexual symptoms and limited physical vigor were discernible with decreased testosterone levels (ranges, 8.0 to 13.0 nmol per liter [2.3 to 3.7 ng per milliliter] for total testosterone and 160 to 280 pmol per liter [46 to 81 pg per milliliter] for free testosterone). However, only the three sexual symptoms had a syndromic association with decreased testosterone levels. An inverse relationship between an increasing number of sexual symptoms and a decreasing testosterone level was observed. These relationships were independently confirmed in the validation set, in which the strengths of the association between symptoms and low testosterone levels determined the minimum criteria necessary to identify late-onset hypogonadism. Late-onset hypogonadism can be defined by the presence of at least three sexual symptoms associated with a total testosterone level of less than 11 nmol per liter (3.2 ng per milliliter) and a free testosterone level of less than 220 pmol per liter (64 pg per milliliter). 2010 Massachusetts Medical Society

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Characteristics of secondary, primary, and compensated hypogonadism in aging men: evidence from the European Male Ageing Study.

Abdelouahid Tajar, Gianni Forti, Terence W O'Neill … (2010)

The diagnosis of late-onset hypogonadism (LOH) in older men with age-related declines in testosterone (T) is currently not well characterized. Our objective was to investigate whether different forms of hypogonadism can be distinguished among aging men. The study was a cross-sectional survey on 3369 community-dwelling men aged 40-79 yr in eight European centers. Four groups of subjects were defined: eugonadal (normal T and normal LH), secondary (low T and low/normal LH), primary (low T and elevated LH), and compensated (normal T and elevated LH) hypogonadism. Relationships between the defined gonadal status with potential risk factors and clinical symptoms were investigated by multilevel regression models. Among the men, 11.8, 2.0, and 9.5% were classified into the secondary, primary, and compensated hypogonadism categories, respectively. Older men were more likely to have primary [relative risk ratio (RRR) = 3.04; P < 0.001] and compensated (RRR = 2.41; P < 0.001) hypogonadism. Body mass index of 30 kg/m(2) or higher was associated with secondary hypogonadism (RRR = 8.74; P < 0.001). Comorbidity was associated with both secondary and primary hypogonadism. Sexual symptoms were more prevalent in secondary and primary hypogonadism, whereas physical symptoms were more likely in compensated hypogonadism. Symptomatic elderly men considered to have LOH can be differentiated on the basis of endocrine and clinical features and predisposing risk factors. Secondary hypogonadism is associated with obesity and primary hypogonadism predominately with age. Compensated hypogonadism can be considered a distinct clinical state associated with aging. Classification of LOH into different categories by combining LH with T may improve the diagnosis and management of LOH.

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Adipocytokines and the metabolic complications of obesity.

Philip A Kern, Neda Rasouli (2008)

Adipose tissue is increasingly recognized as an active endocrine organ with many secretory products and part of the innate immune system. With obesity, macrophages infiltrate adipose tissue, and numerous adipocytokines are released by both macrophages and adipocytes. Adipocytokines play important roles in the pathogenesis of insulin resistance and associated metabolic complications such as dyslipidemia, hypertension, and premature heart disease. Published literature was analyzed with the intent of addressing the role of the major adipose secretory proteins in human obesity, insulin resistance, and type 2 diabetes. This review analyzes the characteristics of different adipocytokines, including leptin, adiponectin, pro-inflammatory cytokines, resistin, retinol binding protein 4, visfatin, and others, and their roles in the pathogenesis of insulin resistance. Inflamed fat in obesity secretes an array of proteins implicated in the impairment of insulin signaling. Further studies are needed to understand the triggers that initiate inflammation in adipose tissue and the role of each adipokine in the pathogenesis of insulin resistance.

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Author and article information

Journal

Journal ID (nlm-ta): Eur Endocrinol

Journal ID (iso-abbrev): Eur Endocrinol

Journal ID (publisher-id): EE

Title: European Endocrinology

Publisher: Touch Medical Media

ISSN (Print): 1758-3772

ISSN (Electronic): 1758-3780

Publication date (Print): August 2019

Publication date (Electronic): 16 August 2019

Volume: 15

Issue: 2

Pages: 83-90

Affiliations

[1 ] Department of Endocrinology & Metabolism, Pilgrim Hospital, United Lincolnshire Hospitals NHS Trust, Boston, UK

[2 ] Department of Endocrinology, Jersey General Hospital, St Helier, Jersey

[3 ] Department of Endocrinology & Metabolism, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, UK

Author notes

Corresponding Author: Joseph M Pappachan, Department of Endocrinology & Metabolism, Lancashire Teaching Hospitals NHS Foundation Trust, Preston, PR2 9HT, United Kingdom. E: drpappachan@ 123456yahoo.co.in

Disclosure: Cornelius J Fernandez, Elias C Chacko and Joseph M Pappachan have nothing to declare in relation to this article.

Article

DOI: 10.17925/EE.2019.15.2.83

PMC ID: 6785957

PubMed ID: 31616498

SO-VID: 7f323140-2ba8-48be-97c8-b4458a4a2a42

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Review Process: Double-blind peer review.

Compliance with Ethics: This article involves a review of literature and does not report on new clinical data, or any studies with human or animal subjects performed by any of the authors.

Authorship: All named authors meet the criteria of the International Committee of Medical Journal Editors for authorship for this manuscript, take responsibility for the integrity of the work as a whole and have given final approval for the version to be published.

History

Date received : 25 June 2019

Date accepted : 04 July 2019

Page count

Pages: 8

Funding

Funding support: No funding was received in the publication of this article.

Male Obesity-related Secondary Hypogonadism – Pathophysiology, Clinical Implications and Management

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Most cited references 79

Identification of late-onset hypogonadism in middle-aged and elderly men.

Characteristics of secondary, primary, and compensated hypogonadism in aging men: evidence from the European Male Ageing Study.

Adipocytokines and the metabolic complications of obesity.

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