The patient has a low libido and inability to maintain erections. Hypogonadotrophic hypogonadism (HH) is defined as subnormal free testosterone in the presence of inappropriately low gonadotrophins [4]. The clinical manifestations include low libido, erectile dysfunction, fatigue, loss of muscle mass, reduced bone density and depression [4].

About 25–40 % of men with type 2 diabetes mellitus (DM) have been found to have HH [5, 6]. The mechanism behind this is thought to be due to insulin resistance rather than hyperglycaemia itself [4]. Studies in mouse models have demonstrated that insulin facilitates secretion of gonadotrophin-releasing hormone (GnRH) from neuronal cells. Therefore insulin resistance would affect GnRH secretion, thus testosterone levels [7]. There have also been reports of raised inflammatory markers being associated with HH, suggesting an underlying inflammatory response [7].

Obesity is also associated with HH, with studies showing an inverse relationship between free testosterone and body mass index [8]. The proposed mechanism is related to an increase in adipose tissue which leads to increased oestradiol levels due to enhanced aromatase activity, thus leading to suppression of GnRH release [4]. Diabetes in conjunction contributes to low free testosterone levels, however studies have shown that low circulating testosterone levels are also observed in non-diabetic obese men [9].

Furthermore, low sex hormone binding globulin (SHBG) levels are observed in such patients [9]. Since a significant proportion of circulating testosterone is bound to SHBG, a low serum SHBG level will invariably result in lower total testosterone levels [9].

Another possible explanation for low free testosterone levels observed in obese diabetic and non-diabetic patients is an abnormal scrotal temperature [10]. Embryological descent of the testes outside the body aims to maintain scrotal temperatures at 2 °C less than core body temperature to facilitate adequate testosterone production [10]. In obese patients, an increase in abdominal fat envelopes the scrotum between the thighs and abdomen. This results in temperatures similar to that of core body temperature thus impeding testosterone production [10].

In summary, diabetes and obesity are independent factors for developing hypogonadotrophic hypogonadism. However, obesity in the presence of type 2 DM adds to that risk [4, 8]. This patient has two biological children so it is unlikely that he suffers from primary infertility.

Studies have shown a link between erectile dysfunction (ED), hypogonadotrophic hypogonadism, type 2 diabetes and obesity [11]. Both type 2 diabetes and obesity represent independent risk factors for development of ED [4]. The mechanisms involved are metabolic, neurogenic and vascular.

Hyperglycaemia, hyperlipidaemia and poor metabolic control give rise to biochemical perturbations that lead to microvascular changes [12].

In diabetic patients, there is impaired neurogenic and nitric oxide mediated endothelial relaxation of smooth muscle. As a result autonomic neuropathy and arterial disease lead to ED [12]. In obese patients, androgen deficiency due to increased aromatase action and microvascular changes are contributors [4].

In people with diabetes, it is also possible that use of beta-blockers might be contributing to ED. Furthermore an increase in nocturnal urinary frequency suggests benign prostatic hypertrophy.

This man is likely to have Obstructive sleep apnoea (OSA), which is usually underdiagnosed. OSA is defined as spectrum of breathing disorders which occur during sleep. This ranges from snoring to hypoapnoea and apnoea [13]. It results from collapse of the upper airways leading to upper airway resistance, airflow impedance and ultimately oxygen desaturation [13, 14].

The patient typically has interrupted sleep due to periods of apnoea and wakes up feeling unrefreshed in the morning; this leads to daytime somnolence [13, 14].

OSA has been linked to obesity, hypertension and diabetes. Risk factors for developing OSA include age, obesity and male sex. Also certain craniofacial characteristics such as changes associated with acromegaly increase the risk [13].

Other respiratory disorders that are associated with in obesity include obesity hypoventilation syndrome in which patients develop night time hypoxia and daytime hypercapnia [15].

It is likely that the patient has OSA, therefore a referral to the Respiratory physicians for further assessment and treatment will be necessary. Weight loss tends to alleviate symptoms.

This patient has been diagnosed with depression by his general practitioner which has resulted in a poor quality of life. Studies have shown that 55 % of obese patients have an increased risk of developing depression [16]. People who are depressed have a 58 % risk of becoming overweight [16]. Large epidemiological studies have found a relationship between socioeconomic factors, chronic disease and psychological stress [17]. Some alleviation might be achieved through management of each chronic disease; however in severe cases of depression management with pharmacological therapy might be necessary.

It is important to identify potential eating behaviour contributing to the maintenance of obesity. It is also crucial to consider diabetes management which may be more relevant than aiming to quantify calorie intake or specific meal composition. Below is a list of eating behaviours that can contribute weight gain [18].

It is recommended that patients have contact with a dietitian to provide a detailed assessment of dieting history so as to identify problem areas or misconceptions that can be rectified [2].

Evaluation of the amount of daily exercise and exercise tolerance is necessary. Some obese patients experience difficulty increasing physical activity level due to various co-morbidities such as the pain associated with osteoarthritis and fibromyalgia. They might also experience increased shortness of breath due to cardiac and respiratory disease.

It would also be important to determine the history of pack years in smoking. Some observational studies have shown an increase in abdominal and visceral obesity in overweight smokers [19]. Combining smoking and obesity increases the risk of developing cancer as well as a tenfold increase in premature death [20]. However cessation of smoking can increase appetite and therefore cause weight gain which may be moderate and temporary if appropriate management is pre-empted [20].

General examination of an obese patient should include height and weight to determine BMI [1, 2]. Also it is useful to measure waist circumference to determine the waist to hip ratio. Body composition analyser helps to determine general distribution of fat [2]. It is however important to note that waist circumference determination becomes unreliable when BMI exceeds 35 kg/m² due to the effects of gravity on central adiposity creating folds of fat across the abdomen [2]. Neck circumference evaluation is necessary for those who are likely to suffer from OSA.

Assessment should include a skin examination for signs of insulin resistance such as acanthosis nigricans, skin tags and intertrigo. Also signs of dyslipidaemia such as xanthalesma and eruptive xanthoma should be sought [3]. Assessment of cardiovascular status is necessary with blood pressure and an electrocardiogram.

Examination of the abdomen might reveal hepatomegaly caused by fatty liver disease. Finally assessment of the musculoskeletal system is important to determine the presence of gout or osteoarthritis as this can affect future ability to exercise and attend rehabilitation programmes [3]. With regards to diabetes it is important to assess whether the patient has established microvascular and macrovascular complications.

During the assessment it is also important to rule out secondary causes of obesity as treatment of the underlying condition is also necessary [3]. Table 23.1 presents a summary of potential secondary causes.

Summary of possible medical conditions this patient has: