Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

History of hypertension is a frequent finding in patients with acute myocardial infarction (AMI) and its recurring association with female sex, diabetes, older age, less frequent smoking and more frequent vascular comorbidities composes a risk profile quite distinctive from the normotensive ischemic counterpart.Antecedent hypertension associates with higher rates of death and morbid events both during the early and long-term course of AMI, particularly if complicated by left ventricular dysfunction and/or congestive heart failure. Renin-angiotensin-aldosterone system blockade, through either angiotensin-converting enzyme inhibition, angiotensin II receptor blockade or aldosterone antagonism, exerts particular benefits in that high-risk hypertensive subgroup.In contrast to the negative implications carried by antecedent hypertension, higher systolic pressure at the onset of chest pain associates with lower mortality within 1 year from coronary occlusion, whereas increased blood pressure recorded after hemodynamic stabilization from the acute ischemic event bears inconsistent relationships with recurring coronary events in the long-term follow-up.Whether antihypertensive treatment in post-AMI hypertensive patients prevents ischemic relapses is uncertain. As a matter of fact, excessive diastolic pressure drops may jeopardize coronary perfusion and predispose to new acute coronary events, although the precise cause-effect mechanisms underlying this phenomenon need further evaluation.
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PMID:Hypertension and acute myocardial infarction: an overview. 2231 27

Diabetic nephropathy is the leading cause of end-stage renal disease in the United States. Renin-angiotensin-aldosterone system (RAAS) blockers are thought to have a specific renoprotective effect in diabetes. Hirst et al. report the results of randomized clinical trials assessing the effects of RAAS inhibitors on urinary albumin excretion levels in diabetic patients. Although reductions in urinary albumin excretion were observed, whether RAAS inhibitors offer additional protection over other antihypertensive agents is unclear.
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PMID:Viper venom for diabetic nephropathy. 2218 41

We examined the effects of hyperglycemic conditions on liver metastasis of colorectal cancer (CRC). Angiotensin (A)-II increased growth, invasion, and anti-apoptotic survival in HT29 and CT26 cells. In contrast, angiotensinogen (ATG) increased these features in HT29 cells but not in CT26 cells. HT29 cells expressed A-II type 1 receptor, chymase, and rennin, whereas CT26 cells did not express renin. Renin expression and ATG-induced cell growth, invasion, and survival induced and increased as glucose concentration increased in HT29 cells and also CT26 cells. An inhibitor of renin or chymase abrogated A-II production in HT29 cells. Reduction of hepatic ATG production by cholesterol-conjugated antisense S-oligodeoxynucleotide suppressed liver metastasis of HT29 cells. An examination of 121 CRC patients showed that diabetes in CRC cases was associated with higher blood HbA1c, higher renin and A-II concentrations in the primary tumors, and higher incidence of liver metastasis than in nondiabetic cases. These results suggest that diabetes-associated angiotensin activation enhances liver metastasis of CRC and may therefore provide a possible target for antimetastatic therapy in CRC.
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PMID:Diabetes-associated angiotensin activation enhances liver metastasis of colon cancer. 2255 72

In this study, the anti-inflammatory and antioxidant known as lycopene was applied to rats with experimental diabetes with the aim of investigating the detection of diabetes-related complications, and to determine the possible role of lycopene in diabetes complications regarding the effects of ACE activity. In order to induce diabetes in rats in the diabetes (D) and diabetes+lycopene (DL) groups, rats were given 45 mg/kg single-dose streptozotocin (STZ) intraperitoneally (i.p.); lycopene (10 mg/kg/day dissolved in sunflower oil) was administered to the rats in the lycopene-only (L) and DL groups. Blood glucose levels and HbA1c% in diabetes+lycopene group and diabetes group increased (p <0.05) compared to control and only lycopene treated group. The highest level of ACE activity was observed in the (D) group (p < 0.05). Activity in the (L) group was also significantly greater than in the control group (p < 0.05). The (DL) group had lower (p < 0.05). ACE activity than the (D) group. Lycopene implementation was found to be effective in the inhibition of ACE activity, an important indicator of diabetes-related complications.
J Renin Angiotensin Aldosterone Syst 2012 Sep
PMID:The effect of lycopene treatment on ACE activity in rats with experimental diabetes. 2258 36

Renin-angiotensin-aldosterone system (RAAS) inhibitors in combination with other antihypertensive drugs (eg, calcium channel blockers [CCBs] and/or diuretics) are a preferred treatment option for managing uncontrolled hypertension in high-risk patients with chronic kidney disease (CKD), diabetes, or heart failure because RAAS inhibitors provide cardiorenal benefits in addition to lowering blood pressure (BP). However, when prescribing antihypertensive therapies to high-risk patients, physicians must be aware of the risks of treatment-related adverse events of hyperkalemia and peripheral edema associated with RAAS inhibitors and CCBs, respectively. This review discusses the use of single-pill combination antihypertensive therapy to optimize BP control in high-risk patients with CKD, diabetes, and/or heart failure and provides strategies for preventing and managing hyperkalemia and peripheral edema in this group. Single-pill combination therapy can utilize different classes of antihypertensive drugs to reduce BP while mitigating the risks of treatment-related adverse events, reducing pill burden, lowering medical cost, and improving patient compliance.
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PMID:Role of single-pill combination therapy in optimizing blood pressure control in high-risk hypertension patients and management of treatment-related adverse events. 2303 Nov 50

Data from randomized clinical trials and epidemiological evidence identify systemic hypertension as the second most common modifiable risk factor for chronic kidney disease (CKD) progression after diabetes mellitus. CKD may progress silently over the years and early diagnosis and control of hypertension is of major importance in delaying renal function decline. Recent guidelines for the treatment of hypertension suggest the use of a variety of antihypertensive drugs in order to achieve the desired blood pressure levels. Renin-angiotensin system inhibitors have been undoubtedly studied the most and are suggested by guidelines and experts as first choice in patients with hypertension and renal injury, particularly in those with diabetes, as they have repeatedly shown to significantly reduce proteinuria. Other classes of antihypertensive drugs have been studied to a lesser extent and they have their own unique properties and effects. However, it is now common knowledge that adequate blood pressure control is the most important factor for the preservation of renal function, so every drug that effectively lowers hypertension is believed to be renoprotective. The present article will review the latest data on the role and properties of each class of antihypertensive drugs on CKD.
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PMID:The effect of antihypertensive drugs on chronic kidney disease: a comprehensive review. 2305 59

Hyperglycaemia up-regulates intracellular AngII (angiotensin II) production in cardiac myocytes, effects of which are blocked more effectively by renin inhibition than ARBs (angiotensin receptor blockers) or ACEis (angiotensin-converting enzyme inhibitors). In the present study, we determined whether renin inhibition is more effective at preventing diabetic cardiomyopathy than an ARB or ACEi. Diabetes was induced in adult mice for 10 weeks by STZ (streptozotocin). Diabetic mice were treated with insulin, aliskiren (a renin inhibitor), benazeprilat (an ACEi) or valsartan (an ARB) via subcutaneous mini-pumps. Significant impairment in diastolic and systolic cardiac functions was observed in diabetic mice, which was completely prevented by all three RAS (renin-angiotensin system) inhibitors. Hyperglycaemia significantly increased cardiac oxidative stress and circulating inflammatory cytokines, which were blocked by aliskiren and benazeprilat, whereas valsartan was partially effective. Diabetes increased cardiac PRR (prorenin receptor) expression and nuclear translocation of PLZF (promyelocytic zinc finger protein), which was completely prevented by aliskiren and valsartan, and partially by benazeprilat. Renin inhibition provided similar protection of cardiac function to ARBs and ACEis. Activation of PLZF by PRR represented a novel mechanism in diabetic cardiomyopathy. Differential effects of the three agents on oxidative stress, cytokines and PRR expression suggested subtle differences in their mechanisms of action.
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PMID:Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor. 2311 20

The Renin-Angiotensin System (RAS) is recognized as the main biological system involved in cardiovascular and hydroelectrolyte homeostasis. It is well established in literature that RAS blockers retard the progression of renal failure in type 1 [angiotensin converting enzyme (ACE) inhibitors] and in type 2 [angiotensin type 1 receptor (AT1) antagonists] diabetes mellitus and in non-diabetic chronic kidney diseases. More recently, it was shown that newer therapeutic agents, the renin inhibitors, also exert renoprotective actions. Obesity is recognized as a proinflammatory state often associated with kidney diseases. Recent publications have associated the RAS axis imbalance leading to a predominance of Angiotensin II effects with changes in adipokine levels and actions. In this context, the aim of the current review is to present current evidence on the potential role of RAS blockers in modulating the interaction between adipokines and obesity-related renal disorders.
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PMID:The therapeutic role of Renin-Angiotensin System blockers in obesity- related renal disorders. 2327 Apr 35

Colorectal cancer (CRC) cells express renin and chymase through which they can activate angiotensin. Renin expression is induced by hyperglycemic conditions. As angiotensinogen is produced in the liver, CRC cells that can activate angiotensin have an enhanced ability to metastasize to this organ. In human CRC cases, patients with diabetes have higher activities of rennin and angiotensin-II in primary tumors, and on average, have a more progressed disease stage, especially with respect to liver metastasis. These patients exhibit a stronger association with Hemoglobin A1c levels and metastasis compared to patients without diabetes. In a combined diabetes/CRC liver metastasis mouse model, concurrent treatment with anti-angiotensin and hypoglycemic agents shows a synergic effect in terms of reduced liver metastasis and improved survival. The effect of anti-angiotensin treatment and blood sugar control as a baseline management for colon cancer patients with diabetes needs to be examined in clinical trials to establish whether it can prevent liver metastasis.
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PMID:Multiple roles of angiotensin in colorectal cancer. 2329 54

The AKT-mTOR pathway is activated in diabetic nephropathy. Renin-angiotensin system modulators exert beneficial effects on the diabetic kidney. We explored the action of losartan on AKT-mTOR phosphorylation in glomeruli and podocytes. Diabetes mellitus was induced to Sprague-Dawley rats by streptozotocin. Five months later, the rats were commenced on losartan and euthanized 2 months later. Kidneys were processed for immunofluorescence studies. Glomeruli were isolated for Western blot analysis. Diabetes increased activated forms of AKT and mTOR both in glomeruli and podocytes. In diabetic rats, losartan decreased phosphorylated/activated forms of AKT (Thr308) and mTOR (Ser2448) in glomeruli but decreased only activated mTOR in podocytes. However, in both glomeruli and podocytes of healthy animals, an inverse pattern was evident. In conclusion, a new body of evidence indicates the differential activation of AKT-mTOR in glomeruli and podocytes of healthy and diabetic animals in response to losartan.
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PMID:Losartan affects glomerular AKT and mTOR phosphorylation in an experimental model of type 1 diabetic nephropathy. 2345 24


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