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In neurons, as in a variety of other cell types, the enzyme phosphatidylinositol-3-kinase (PI3K) is a key intermediate that is common to the signaling pathways of a number of peripheral metabolic cues, including insulin and leptin, which are well known to regulate both metabolic and reproductive functions. The achievement of reproductive competence as well as the normal sustenance of adult reproductive activity is highly affected by the availability of nutrients.
The mechanisms by which metabolic information is relayed to the hypothalamic GnRH network are not entirely clear.
The PI3K signaling cascade is well known for its role in mediating insulin and leptin effects on cell and tissue metabolism.
To better understand the mechanisms by which negative energy balance disrupts reproductive function, a number of in vivo animal models have been developed. Conditions of energy deficit are associated with a drastic decrease in the levels of peripherally produced metabolic cues such as insulin and the adipocyte-derived cytokine leptin. In women, obesity is co-morbid with menstrual dysfunction, decreased fertility, and an increased risk of miscarriages (Pasquali et al., 2007).
The effects of eating and metabolic disorders on the reproductive axis are not limited to adults. As interest in the effects of obesity on child development has increased, so have studies investigating the effects of diet on puberty.
These findings indicate that alterations in the activity of the GnRH network underlie many of the detrimental effects that metabolic imbalances have on the HPG axis. Non-receptor tyrosine kinases such as the cytoplasmic Janus tyrosine kinase family (JAKs) as well as other adapter proteins like GRB-2 at the plasma membrane can also initiate PI3K signaling in response to insulin, leptin, and growth factors (Cantrell, 2001). Pharmacological and genetic studies have demonstrated a role of several members of the PI3K signaling pathway in reproductive function (Table 1).
The steroid hormone E2 is essential for the feedback regulation of gonadotropin release and female reproductive behavior. The PI3K signaling pathway participates in the E2 facilitation of lordosis behavior, a reflexive posture displayed by female rodents during mating.
Recent studies suggest that the IGF-1 effect on advancing pubertal onset is mediated through direct regulation of GnRH neurons, which are known to co-express IGF-1Rs.
Finally, central IGF-1Rs regulate adult LH release and sexual receptivity (lordosis) in female rats. It has been found to account for up to 48% of hospital admissions with heart failure in South Africa1. Impaired left ventricular function may lead to cardiogenic shock and present with signs of congestive cardiac failure; for example, hypotension, elevated JVP, pulsatile liver, displaced and diffuse apex beat, third and fourth heart sounds, and bibasal crepitations. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button.
This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. This is particularly evident in female mammals, where physiological processes such as gestation, parturition, lactation, and rearing of the young are energetically demanding.
However, various peripheral metabolic signals, such as leptin and insulin, act on specific neuronal populations that in turn affect GnRH neuronal function. This lipid enzyme is activated in classical metabolic tissues such as liver, pancreas, skeletal muscle, and adipose tissue, where it participates in the regulation of carbohydrate and lipid homeostasis (Foukas and Withers, 2010).
Then the hypothesis that PI3K is a key integrator of metabolic and neural signals regulating GnRH neurosecretion will be explored. In these women, hypothalamic amenorrhea and menstrual irregularities are associated with impairments in gonadotropins, specifically LH release (Attia and Roberto, 2009).
Diet-induced obesity (DIO) in rodents has been utilized to mimic the gradual increase in body fat and body weight observed in obese humans. In men, it can result in reduced testosterone (T) levels and erectile dysfunction (Lebinger, 2007). Nutritional disturbances during early developmental stages can have adverse consequences on the reproductive axis as well. In female rodents, states of negative energy balance delay puberty, whereas a HFD has the opposite effect, advancing pubertal onset. These metabolic challenges are also accompanied by profound alterations in the levels and sensitivity to peripheral hormones and metabolic signals, including IGF-1, E2, leptin, and insulin. Summary of studies on the role of upstream and downstream components of the PI3K signaling pathway in HPG axis function.
For example, in vitro PI3K signaling induces the phosphorylation of discrete residues of the endogenous ER, upregulating its transcriptional activity and stability (Campbell et al., 2001).
The PI3K inhibitors wortmannin and LY294002 partially suppressed lordosis when administered during E2 priming (Etgen and Acosta-Martinez, 2003). In addition to its prominent role in the regulation of somatic growth, the IGF-1R signaling pathway participates in the regulation of GnRH release, the progression of puberty, adult reproductive function, and sexual behavior (reviewed in Daftary and Gore, 2005). The history had been preceded by a brief upper respiratory tract infection with general malaise and headache, from which he had recovered fully. Diagnosis and treatment can be challenging as it frequently affects young patients and those without risk factors for cardiac disease. Pulmonary oedema and other acute signs mentioned are thought to be a result of increased hydrostatic pressure in the right side of the circulation as a result of the failing left ventricle.
Although the mechanisms mediating the influence of metabolism and nutrition on fertility are currently unclear, the strong association between metabolic disorders and infertility is undeniable.
Thus, the hypothalamic pituitary gonadal (HPG) axis limits fertility when nutrient availability is inadequate to support these events.
This is the case for multiple hypothalamic neuropeptide systems such as neuropeptide Y (NPY), products of pro-opiomelanocortin (POMC), and galanin-like peptide (GALP), among many others (Crown et al., 2007). For instance, malnutrition and sickness in children can cause delayed puberty (Euling et al., 2008). These hormones have in common the capacity to activate the PI3K pathway in various reproductive tissues including the hypothalamus.
Traditionally, E2 acts through its receptor to regulate the transcription of important genes for reproduction, such as the progesterone receptor. Likewise, E2, presumably acting on membrane ERs, induces PI3K activity, which results in activation of gene transcription in the target cell (Pasapera Limon et al., 2003).
Interestingly, when both wortmannin and the MAPK inhibitor PD98059 are simultaneously infused, lordosis behavior is completely abolished (Etgen and Acosta-Martinez, 2003). Although IGF-1 can regulate the HPG axis by acting at the pituitary and gonads, it also acts centrally to stimulate GnRH release and puberty.
However, peripheral oedema, which is seen frequently in chronic sufferers, is thought to be a result of increased salt and fluid retention due to neurohormonal stimulation7.
For example, women suffering from anorectic disorders experience amenorrhea as a consequence of malnutrition-induced impairment of LH release, and at the other extreme, obesity is also commonly co-morbid with menstrual dysfunction and infertility. Many studies suggest that negative energy balance inhibits reproduction through the alteration of gonadotropin releasing hormone (GnRH) secretion in the hypothalamus. When these neuronal populations are not able to appropriately respond to metabolic cues, for example in states of malnutrition, obesity, and diabetes, the repercussions are not limited to imbalanced metabolic homeostasis, but can include reproductive dysfunction. The critical role that PI3K plays in regulation of metabolism does not exclude the possibility that it also participates in the control of other physiological processes such as reproduction.
These negative metabolic challenges can affect the HPG axis at various levels including decreased gonadotropin secretion, slow follicular development, and inhibited synthesis of gonadal steroids (Schneider, 2004). In addition, leptin treatment improves mean LH pulse frequency and ovulation when administered to AN patients (Chan and Mantzoros, 2005).


In female mice, DIO causes infertility, the degree of which depends on the background strain, the duration, and the percentage of fat in the diet. Obesity can also exacerbate female reproductive disorders such as PCOS (Lebinger, 2007; Nestler, 2008).
On the other hand, the prevalence of obesity and other metabolic diseases in children and adolescents has increased at alarming rates in recent decades. In mice, the effect of a HFD on VO is associated with increased insulin levels (Brill and Moenter, 2009). In vivo, E2 treatment evokes rapid activation of Akt in the hypothalamus (Burt et al., 2011). Therefore, the complete inhibition of this E2-dependent behavior requires concurrent suppression of both central MAPK and PI3K signaling. The effect of JB-1 on LH release is not observed in ovariectomized rats given no hormone replacement, suggesting that JB-1 acts primarily to suppress E2-positive feedback (Quesada and Etgen, 2002). This physiological adaption takes time and may explain why the patient in this case had developed acute changes consistent with congestive cardiac failure but did not yet have any peripheral oedema.
Impaired hypothalamic insulin and leptin receptor signaling is thought to be at the core of reproductive disorders associated with metabolic dysfunction. Therefore, metabolic hormones have a pivotal role in the central regulation of the HPG axis. In fact, the PI3K signaling cascade is a common pathway activated by hormones and growth factors that are also critical for the normal function of the HPG axis, including insulin and leptin.
However, it is the inhibition of the GnRH pulse generator, and hence GnRH release, that is responsible for the dysfunction of the reproductive axis.
These studies emphasized the importance of leptin and insulin in the metabolic control of the HPG axis. Several studies suggest that this too represents a metabolic challenge for normal reproductive development. Furthermore, treatment with the insulin sensitizer metformin blocked advancement of VO induced by HFD (Brill and Moenter, 2009).
Class IA regulatory subunits bind to tyrosine-phosphorylated proteins through their SH2 (Src homology 2) domains, linking them to tyrosine kinase signaling pathways.
These enzymes and transcription factors regulate intracellular metabolic functions such as the generation of glucose and protein synthesis (for a review see Vanhaesebroeck et al., 2005).
Future studies should examine whether central inhibition of PI3K participates in E2-induced LH release.
No data exist to suggest that dilated cardiomyopathy is any more prevalent within rural areas.
Heart murmurs may occur as a result of a disruption of the normal architecture of the heart; for example, mitral regurgitation. While low levels of leptin and insulin characterize states of negative energy balance, prolonged nutrient excess is associated with insulin and leptin resistance. The intermittent discharge from these specialized neurons in the hypothalamus is in fact responsible for the pulsatile secretion of the gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). It remains to be determined whether this signaling pathway integrates the effects of these or other hormones and growth factors in the regulation of GnRH release. For instance, infusing GnRH in a pulsatile manner can yield close to normal onset of puberty in food-restricted female rats, even in the total absence of body growth (Bronson, 1986). However, a decrease in the levels of other peripherally produced signals such as insulin-like growth factor-1 (IGF-1), glucose, and lipids may also contribute to the suppression of GnRH activity produced by negative energy balance. In these mice, a diet containing 24% fat is sufficient to significantly decrease natural pregnancy rates and follicular activity (Tortoriello et al., 2004). In the same study, treatment with the androgen receptor antagonist flutamide blocked pubertal acceleration while delaying VO in the lean diet fed control group, suggesting that androgens are involved in the pubertal process. In contrast, the Class IB regulatory subunits p84 and p101 lack SH2 domains and instead couple the Class IB catalytic subunit p110γ to G protein-coupled receptors.
However, local factors such as high HIV prevalence, prevalent familial forms and exposure to toxins, including venom, may theoretically predispose individuals to developing the disease2.
Shortness of breath can develop throughout the course of the disease due to fluid overload and may be accompanied by a pronounced P2 component to the second heart sound. The variety and complexity of signaling networks that affect cell metabolism and neuronal activity make this a daunting task.
Furthermore, the brain sites and neuronal populations in which activation of this enzyme is necessary for the regulation of energy homeostasis might not be the same as those involved in the regulation of the HPG axis. Their fertility defect is likely of central origin, because normal ovulatory responses and pregnancy rates are restored after exogenous gonadotropin stimulation (Tortoriello et al., 2004).
Specifically, a decreased sensitivity of the HPG axis to insulin and leptin actions due to insulin and leptin resistance is suspected to be a major contributing factor. At the neuroendocrine level, puberty starts when GnRH neurons secrete GnRH in a pulsatile manner.
It is important to point out that VO is an external marker of puberty onset that reflects exposure to pubertal sex steroid levels, but it does not necessarily imply central activation of gonadotropin secretion. We will limit our discussion to Class IA PI3Ks, which are the major targets of insulin and leptin actions.
Diagnosis and treatment are often further hindered by limited resources and a small range of available investigations.The following case study is directed at junior medical staff currently working within rural settings. Arrhythmias are common and patients may present with palpitations, syncope or even cardiac arrest. However, a clear link between this signaling pathway and the control of GnRH release by peripheral metabolic cues has not been established. Within the brain, the actions of gonadal steroids are then manifested as both feedback regulation of GnRH secretion and the facilitation of sexual behavior. However, peripheral hormones and metabolic cues such as leptin and insulin share specific signal transduction pathways that in many cases act synergistically or in parallel to affect neuronal function.
These studies confirm that positive energy balance is crucial for normal reproductive function, whether the female is an adult or peripubertal, and that proper activity of the GnRH network is essential for this to occur. Additionally, prolonged hyperleptinemia and central leptin resistance are accompanied by reduced hypothalamic GnRH gene expression (Tortoriello et al., 2004). Other parameters, such as day of first estrus and measurement of gonadotropin levels, are needed to further characterize these models. However, some patients may only present with vague constitutional symptoms, weight loss and fatigue.Treatment in the acute setting is aimed at reducing the preload and afterload, and improving cardiac contractility. Investigating the role of the signaling pathways shared by metabolic cues that are critical for a normal reproductive state can help identify possible targets in the treatment of metabolic and reproductive disorders such as polycystic ovarian syndrome. Therefore, molecules that serve as central integrators of metabolism and reproductive function might be identified by determining which signaling pathways are shared by peripheral metabolic cues known to affect both physiological functions. A cardiac ultrasound ruled out pericardial effusion but did show a dilated and hypokinetic left ventricle.
It has approximately 200 beds and caters for male and female medical and surgical patients, obstetrics and paediatrics. These results also support a model where obesity alters the hypothalamic sensitivity to the restraining effects of steroid negative feedback on GnRH neuronal activity early in development. It has a catchment population of 90 000. Medical staffing is variable and the hospital frequently has a relatively high concentration of foreign doctors. Diuretics including furosemide and spironolactone, angiotensin converting enzyme inhibitors (ACE-i) and digoxin are currently the mainstay of long-term management8,9. In these mice, 60% fat content in the diet resulted in decreased fertility, lack of regular estrous cyclicity, and reduced follicular activity (Brothers et al., 2010). Although the permanent staff are very experienced, there is no specialist care and the nearest referral centre is over 4 hours drive away.


The use of isosorbide dinatrate in combination with hydralazine has been used in patients intolerant to ACE-I and there is some evidence that their addition on top of standard treatments in patients with severe symptoms of congestive cardiac failure may improve mortality10.
The elevated LH levels observed in this model of DIO suggest that obesity affects the ability of steroid hormones to exert negative feedback on GnRH secretion. Diagnostic tests are limited, although plain film radiology, routine blood tests and simple ultrasound are all possible. Amiodarone can be used in those who are prone to arrhythmias but consideration should be given to an implanted defibrillator.
Interestingly, although this diet resulted in peripheral insulin resistance, the pituitary remained responsive to insulin and exhibited a heightened pituitary response to GnRH due to an increase in GnRH receptors (Brothers et al., 2010). Current guidelines for management and treatment of the disease and the unique challenges it presents to those working in a rural setting are discussed. Betablockers should always be considered as they may counteract the affect of sympathetic activation on the remodelling of the heart. In addition, DIO on this genetic background resulted in elevated androgen levels, a characteristic of polycystic ovarian syndrome (PCOS). In doing so, it is hoped prompt diagnosis and efficacious treatment will be encouraged, and overall prognosis improved.IssueCaseA 17 year old African boy presented to the outpatient department of Mseleni Hospital in South Africa on 17 December 2011 with a 1 month history of shortness of breath.
However, they should only be initiated once the patient is stable due to their negative ionotropic effects8.Obstacles to treatment within a rural healthcare settingWithin a rural setting the problems of diagnosing and treating this condition are increased. Therefore, it is important to remember that the history and physical examination are paramount. In general, male mice are very resistant to the detrimental effects DIO on fertility, even though it also results in similar degrees of obesity, insulin resistance, and hyperleptinemia.
Exertion of any kind exacerbated his symptoms, as did lying down, and he had also developed a dull central chest pain. As mentioned, signs of heart failure will help to differentiate a cardiac from a respiratory cause for acute onset shortness of breath. In order to observe reduced fertility in males, both a diet with a high fat content (60%) and a prolonged exposure to it are needed (Ghanayem et al., 2010).
He denied any history of cough and also denied any illicit drug abuse, alcohol intake or exposure to toxins. If available, a simple ultrasound scan of the heart can be very useful where diagnostic uncertainty remains. He had no significant past medical or family history.On admission, he was clearly in respiratory distress. Ultrasound will also help to rule out a pericardial effusion, an important differential for a dilated cardiac shadow on a chest x-ray.Due to cultural factors and poor infrastructure, patients in a rural setting may present late.
Patients are frequently malnourished and suffer from other serious co-morbidities such as HIV, giving them limited physiological reserve to cope with acute cardiac problems. On auscultation of the chest, he had a loud P2, third heart sound and a pansystolic murmur heard loudest at the apex. Treatment in the acute phase is aimed at offloading the excess preload placed on the left ventricle.
Intravenous furosemide is commonplace and can be used in conjunction with nitrates and small doses of morphine to achieve this end. Although infusion pumps of nitrates may not be feasible, the use of readily available sublingual alternatives can be very effective11.
His calves were soft and non-tender and unusually he had no peripheral oedema.Bloods were unremarkable. Patients should also be anti-coagulated, especially during the acute stage when bed rest is advocated and at discharge due to the increased chance of thrombus formation in the poorly contractile ventricle12. His anti-streptolysin O (ASO) titre was negative and Enzyme-Linked Immunosrobant Assay (ELISA) for both HIV 1 and 2 were negative. Within a rural setting, warfarinisation may be challenging as poor compliance and limited follow up capacity may mean the risks of bleeds outweigh the benefits. A chest x-ray was performed, which showed a prominent pulmonary trunk and a grossly dilated cardiac shadow that prompted a cardiac ultrasound. In this case, regular aspirin was used as an alternative on the advice of the local cardiology team. This showed no pericardial effusion but did reveal a globally dilated and hypokinetic left ventricle.A diagnosis of dilated cardiomyopathy secondary to a viral infection was made on the basis of the history. Intravenous fluid should be avoided unless the patient is hypotensive and then only used as a small bolus13. At all times it is important to recognise local limitations and early consultation with a referral centre is essential, especially in those patients refractory to treatment.
He clinically improved and was then started on a low dose of carvediolol before being discharged for follow up with cardiology.DiscussionCardiomyopathies are diseases of the cardiac muscle that lead to a deterioration in its function. Early initiation of an ACE-i has been shown to be beneficial providing the patient’s systolic blood pressure is above 80 mmHg in the absence of any postural symptoms8.
The term encompasses a large number of conditions that have both intrinsic and extrinsic causes. This and other long-term treatments discussed should be started at a low dose and gradually titrated up.Primary health care provision, as well as poor patient understanding and attendance, may hamper long-term follow up and treatment. In dilated cardiomyopathy, a portion of the ventricle expands leading to impaired systolic function and, as a consequence, further enlargement and remodelling of the heart driven by the release of hormones including catecholamines and angiotensin II3. A dilated ventricle requires more energy for effective contraction, as can be shown by Laplace’s Law for the relationship between wall tension, pressure and radius of an expanding sphere4. Having a basic understanding of their diagnosis and key warning symptoms will aid follow up and ensure early re-presentation. Although an often overlooked diagnosis, it is relatively common within South Africa where it has been found in up to 10–17% of patients at post-mortem with cardiac-related causes of death, and makes up to 48% of admissions with heart failure1.
There are many different causes and it is thought to be a combination of several insults that cause the initial damage (Table 1)5.
Contributing factors include toxins and alcohol exposure, viral infections, pregnancy and genetic factors.
Regular weight and renal function monitoring in the community ensure optimal diuresis is achieved.Lessons learnedConclusionCardiomyopathy is a significant cause of morbidity and mortality throughout Africa. In HIV positive individuals, non-viral infections may predominate and HIV itself may directly damage cardiac tissue3,5,6. Focusing on history and examination and the use of simple, readily available treatments can help to overcome this. Individuals with the HLA-DR1 and Dw10 halotypes appear to be at increased risk of developing dilated cardiomyopathy, lending further evidence for an immunologically mediated pathway to cardiac damage5.
Prognosis in patients with dilated cardiomyopathy is variable and 5 year survival is estimated at 40%14.
Three-dimensional simultaneous strain volume analysis describes left ventricular remodelling and its progression: a pilot study.
Incidence of dilated cardiomyopathy and detection of HIV in myocardial cells of HIV-positive patients. Prevalance of left chamber thrombi in patients with dilated left ventricle at sinus rhythm: the role of transesophageal echocardiography.



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