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Conditions Causing Type 2 Diabetes And High BP : Study - 0 views

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    A study by scientists in a UK university has shown the scale of the prevalence of a condition that can lead to various cardiometabolic diseases. The study published in the Annals of Internal Medicine journal on Tuesday (January 4) has prompted calls for changes to healthcare policy after researchers revealed, for the first time, the scale of the impact of the condition associated with benign tumours that can lead to type 2 diabetes and high blood pressure. Up to 10 per cent of adults have a benign tumour, or lump, known as an 'adrenal incidentaloma' in their adrenal glands which can be associated with the overproduction of hormones including the stress steroid hormone cortisol that can lead to type 2 diabetes and high blood pressure. Previous small studies suggested that one in three adrenal incidentalomas produce excess cortisol, a condition called mild autonomous cortisol secretion (MACS). An international research team led by the University of Birmingham carried out the largest ever prospective study of over 1,305 patients with adrenal incidentalomas to assess their risk of high blood pressure and type 2 diabetes and their cortisol production by comparing patients with and without MACS.
Nathan Goodyear

Hypothalamo-Pituitary-Adrenal Axis Dysfunction in Chronic Fatigue Syndrome, and the Eff... - 0 views

  • We conclude that the improvement in fatigue seen in some patients with chronic fatigue syndrome during hydrocortisone treatment is accompanied by a reversal of the blunted cortisol responses to human CRH
  • These data further suggest that the hypocortisolism found in chronic fatigue syndrome may be secondary to reduced adrenal gland output.
  • 5-mg replacement dose of hydrocortisone, and the remainder 10 mg
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    low dose hydrocortisone therapy (defined as 5-10 mg), in this study, was used to treat CFS.  This study found an improvement in symptoms in these patients.  Additionally, low cortisol was found in these patients with CFS.  Their conclusion, was that low adrenal function is a component of CFS and low dose hydrocortisone therapy is an effective treatment.   Now, is the low cortisol as the result of increased metabolism as well?
Nathan Goodyear

Expression of aromatase, androgen and estrogen receptors in peripheral target tissues i... - 0 views

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    Interesting animal study found that diabetic animals associated with increased aromatase expression in adrenal cortex, kidneys, and other tissue, androgen receptors were decreased in adrenal glands, and ER-alpha expression in the kidneys was increased by 159%.
Nathan Goodyear

Immunohistochemical localization of ... [J Clin Endocrinol Metab. 1998] - PubMed - NCBI - 0 views

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    11beta-HSD type I is highly expressed in liver, adrenal glands, ovaries, and adipose tissue in human immunohistochemical analysis.
Nathan Goodyear

Reliability of hypothalamic-pituitary-adrena... [Eur J Epidemiol. 2011] - PubMed - NCBI - 0 views

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    Study finds salivary cortisol testing is "reliable" measure of chronic cortisol production.  This study found similarity between diurnal cortisol and dexamethasone suppressed cortisol and adrenal gland volume based on literature review.
Nathan Goodyear

Cytokines and steroidogenesis. - PubMed - NCBI - 0 views

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    Inflammatory cytokines appear to inhibit hormone production at the levels of the adrenal glands, testes, and ovaries.  This is in addition to suppression at the level of the hypothalamus and pituitary.  One proposed mechanism is via a reduction of sensitivity of the testes to LH.
Nathan Goodyear

Renin-angiotensin system and cancer: A review - 0 views

  • crucial role of the RAS in the development and maintenance of cancer
  • kidneys, which produce renin in response to decreased arterial pressure, reduced sodium in the distal tubule, or sympathetic nervous system activity via the β-adrenergic receptors
  • Renin is secreted from the juxtaglomerular cells into the bloodstream where it encounters angiotensinogen (AGN), normally produced by the liver
  • ...22 more annotations...
  • Renin catalyses the conversion of AGN to angiotensin I (ATI), which is quickly cleaved by angiotensin converting enzyme (ACE) to form angiotensin II (ATII)
  • ATII triggers the release of aldosterone from the adrenal glands, which stimulates reabsorption of sodium and water and thereby increases blood volume and blood pressure
  • ATII also acts on smooth muscle to cause vasoconstriction of the arterioles
  • ATII promotes the release of antidiuretic hormone from the posterior pituitary gland, which results in water retention and triggers the thirst reflex
  • ability of non-CSCs to ‘de-differentiate’ into CSCs due to epigenetic or environmental factors, which further increases the complexity of tumour biology and treatment
  • efficacy of RAS modulators on cancer in both cancer models and cancer patients
  • A localised (‘paracrine’) RAS mechanism has been identified in many types of cancers, and interruption of the control of the RAS is thought to be the basis for its role in cancer
  • Components of the RAS are expressed by these CSCs, supporting the hypothesis of the presence of a ‘paracrine RAS’ in regulating these CSCs
  • Renin is an enzyme normally released by the kidneys in response to falling arterial pressure
  • a study of GBM demonstrating overexpression of PRR coupled with the observation that inhibition of renin reduces cellular proliferation and promotes apoptosis
  • PRR has been found to be vital for normal Wnt signalling
  • A major focus of PRR research is its relationship with Wnt signalling
  • suggest a crucial role for PRR activation on the proliferation of CSCs, possibly via Wnt/β-catenin signalling, leading to carcinogenesis.
  • Angiotensin converting enzyme (ACE), also known as CD143, is the endothelial-bound peptidase which physiologically converts ATI to ATII
  • ACE is crucial in the regulation of blood pressure, angiogenesis and inflammation
  • results suggest that an overactive ACE promotes cancer growth and progression, and an inhibited or low-activity ACE may have cancer-protective effects
  • When bound to ATII or ATIII it causes vasoconstriction by stimulating the release of vasopressin, reabsorption of water and sodium by promoting secretion of aldosterone and insulin, fibrosis, cellular growth and migration, pro-inflammation, glucose release from the liver, increased plasma triglyceride concentration, and reduced gluconeogenesis
  • ATIIR1 is a G-protein-coupled receptor, with downstream signalling involved in vasodilation, hypertrophy and NF-κB activation leading to TNF-α and PAI-1 expression
  • ATIIR1 has well-documented links with cancer, with one study demonstrating its overexpression in ~20% of breast cancer patients
  • the effect of RAS dysregulation has been associated with increased VEGF expression and angiogenesis in cancers
  • In ovarian and cervical cancer, ATIIR1 overexpression has been shown to be an indicator of tumour invasiveness
  • administration of ATIIR1 blockers (ARBs) have been associated with reduced tumour size, reduction in tumour vascularisation, lower occurrence of metastases, and lower VEGF levels
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    Great review on RAS in cancer.
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