Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity is a major health problem that contributes to the development of type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease. The current pharmacological therapies for obesity are limited and may have significant side effects. Leptin therapy was shown to effectively cause weight loss in obese rats, however its effectiveness in humans is still under investigation. Obese humans have significantly elevated plasma leptin concentrations compared with lean individuals. Plasma leptin concentrations strongly correlated with percentage of body fat. Leptin concentration in the cerebrospinal fluid (CSF) is correlated, in a nonlinear manner, with plasma leptin levels and body mass index (BMI). The ratio of CSF leptin levels to serum leptin levels was 4 times greater in lean individuals than in obese individuals. One interpretation of this finding is that human obesity could be secondary to a central resistance to leptin action, causing a relative leptin deficiency in the CNS. Six years after the discovery of leptin we still do not have a clear understanding of how leptin accesses its targets in the brain, or whether there is defect in this process in the brain of obese individuals. In this manuscript we will review the different leptin gateways to the brain and the potential sites where a defect in leptin action may be present, as well as some potential clinical implications of leptin. A better understanding of how leptin reaches the brain and how it modulates the release of hypothalamic neuropeptides will be important in understanding the role that leptin plays in the pathophysiology of obesity.
Pituitary
PMID:Limited brain access for leptin in obesity. 1182 2

Chronic cortisol hypersecretion causes central obesity, hypertension, insulin resistance, dyslipidemia, protrombotic state, manifestations which form a metabolic syndrome in all patients with Cushing's syndrome. These associated abnormalities determine an increased cardiovascular risk not only during the active phase of the disease but also long after the "biomedical remission". Clinical management of these patients should be particularly careful in identifying global cardiovascular risk. Considering that remission from hypercortisolism is often difficult to achieve care and control of all cardiovascular risk factors should be one of the primary goals during the follow up of these patients. Extending the indications of the recent consensus on Cushing's syndrome, we suggest to carry out an OGTT to avoid underestimation of diabetes mellitus, an echocardiography and Doppler ultrasonography of the epiaortic vessels in all patients at diagnosis and during follow-up.
Pituitary 2004
PMID:Cardiovascular risk in Cushing's syndrome. 1641 38

Approximately half of patients with HIV-infection develop abnormal body fat distribution, characterized by increased abdominal, breast, and dorsocervical adiposity and decreased fat in the limbs and face in association with antiretroviral therapy. Changes in fat distribution are associated with dyslipidemia, insulin resistance, and increased cardiovascular risk in patients with HIV lipodystrophy. Growth hormone secretion is reduced and responses to standardized stimulation testing altered, suggesting relative growth hormone deficiency in this population. Growth hormone secretion is characterized by normal pulse frequency, but decreased pulse amplitude, pulse width, and trough GH levels compared to weight matched, non-HIV-infected patients. Abnormalities in GH secretion are strongly associated with body composition and metabolic abnormalities in patients with HIV lipodystrophy, particularly with increased visceral fat and elevated free fatty acids. Increased somatostatin tone and decreased ghrelin concentrations may also contribute to reduced GH levels. Administration of exogenous GH or growth hormone releasing hormone (GHRH) to normalize growth hormone concentrations is effective to reduce visceral fat and improve lipid parameters in HIV-infected patients. Treatment with supraphysiologic GH is limited by side effects and exacerbation of insulin resistance, whereas administration of physiologic doses of GH demonstrates more modest treatment effects but fewer adverse effects. Initial studies of GHRH also show significant reductions in visceral adipose tissue (VAT) with potentially fewer adverse effects. GHRH may be particularly useful to normalize GH dynamics in patients with HIV lipodystrophy by increasing endogenous GH pulse height, GH pulse width, and trough GH levels, while preserving the negative feedback of IGF-I on pituitary GH secretion.
Pituitary 2009
PMID:GH/GHRH axis in HIV lipodystrophy. 1827 Aug 41

Recent evidence suggests that correction of hypercortisolism in Cushing's syndrome (CS) may not lead to complete remission of the clinical abnormalities associated with this condition. In particular, elevated cardiovascular risk may persist in "cured" CS patients long-term after eucortisolism has been reached. This is believed to be related with the maintenance of visceral obesity and altered adipokine secretory pattern which perpetuate features of metabolic syndrome, including impaired glucose tolerance, hypertension, dyslipidemia, atherosclerosis and hypercoagulability. Nephrolithiasis and incomplete recovery of bone mineral density have also been described in "cured" CS patients. Moreover, previous exposure to excess cortisol may have irreversible effects on the structures of the central nervous system controlling cognitive function and mood. Thus, sustained deterioration of the cardiovascular system, bone remodelling and cognitive function may be associated with high morbidity and poor quality of life in CS patients in remission for many years. Although mortality in "cured" CS patients may not differ from that in the general population, data beyond 20 years follow-up are very scarce, so further studies evaluating larger cohorts for longer follow-up periods are needed to draw definitive conclusions on longevity. Life-long monitoring is mandatory in CS patients in order to control long term complications of previous cortisol excess and, possibly, normalize life expectancy.
Pituitary 2012 Sep
PMID:Clinical consequences of Cushing's syndrome. 2252 17

A silent pituitary adenoma (SPA) is characterized by the expression of pituitary hormones, detected by immunohistochemical staining, in the absence of clinical signs or symptoms of hormonal excess. Compared with functional pituitary adenomas, little is known regarding the involvement of SPAs in metabolic disorders. This study aimed to examine the correlations between SPAs and metabolic disorders, including obesity, abnormal glucose tolerance, hypertension and dyslipidemia. Seventy-four patients with nonfunctional pituitary adenomas who underwent a pituitary adenomectomy in Hokkaido University Hospital from 2008 to 2016 were retrospectively examined. Pituitary adenomas were immunohistochemically classified into pituitary hormone positive or negative groups. Twenty whole hormone-negative pituitary adenomas were excluded because we couldn't identify pituitary transcription factors which is necessary for the diagnosis of a null cell adenoma. The preoperative rates of obesity, abnormal glucose tolerance, hypertension and dyslipidemia were compared between each group. Twenty-seven GH positive adenomas (50.0%), 32 gonadotroph positive adenomas (59.3%), 28 TSH positive adenomas (51.9%) and 21 ACTH positive adenomas (38.9%) were identified. Evaluation of the preoperative clinical data showed 25 cases of obesity (46.2%), 16 cases of abnormal glucose tolerance (29.6%), 29 cases of hypertension (53.7%) and 35 cases of dyslipidemia (64.8%). The rate of hypertension was significantly lower in the GH positive group (37.0%) than the GH negative group (70.4%) (p = 0.0140). In the GH negative group, postoperative systolic and diastolic blood pressure levels were significantly lower than preoperative values. GH positive SPAs may affect the homeostasis of blood pressure.
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PMID:Silent pituitary adenoma and metabolic disorders: obesity, abnormal glucose tolerance, hypertension and dyslipidemia. 3302 57