Ignet

Gene Information

Gene symbol: BEST1

Gene name: bestrophin 1

HGNC ID: 12703

Synonyms: BMD, BEST

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	ADIPOQ	1 hits
3	AGT	1 hits
4	AGTR1	1 hits
5	AGTR2	1 hits
6	AKT1	1 hits
7	ALPI	1 hits
8	BGLAP	1 hits
9	BMP2	1 hits
10	BMP4	1 hits
11	BMP7	1 hits
12	COL1A1	1 hits
13	CSH1	1 hits
14	EDN1	1 hits
15	EDNRB	1 hits
16	IDDM2	1 hits
17	IGF1	1 hits
18	INS	1 hits
19	INSR	1 hits
20	KRT124P	1 hits
21	PPARG	1 hits
22	PTH	1 hits
23	REN	1 hits
24	RPS6KB1	1 hits
25	SDU	1 hits
26	SHOX	1 hits
27	TGFA	1 hits
28	TGFB1	1 hits
29	UBASH3B	1 hits

Related Sentences

#	PMID	Sentence
1	9499214	One of insulin-dependent diabetes mellitus (IDDM) complications are bone mineral disorders called diabetic osteopathy.
2	9499214	We observed that BMD in IDDM patients before 40 years old was significantly lower than in healthy subject.
3	11329759	The limitations of angiotensin-converting-enzyme (ACE) inhibitors and the role of angiotensin II-receptor blockers (ARBs) in the treatment of hypertension, heart failure, and diabetic nephropathy are discussed.
4	11329759	ARBs may offer more complete inhibition of angiotensin II than ACE inhibitors.
5	11329759	Some studies of combination ARB and ACE inhibitor therapy for heart failure indicate advantages of the combination over therapy with either class.
6	11773721	Angiotensin II (AT(1)) receptor antagonists, diabetes, and nephropathy: do differences between the renal and systemic circulations explain the outcomes observed with ARBs and ACE inhibitors?
7	12047043	Renoprotective effects of blockade of angiotensin II AT1 receptors in an animal model of type 2 diabetes.
8	12047043	To evaluate the efficacy of angiotensin II receptor blockers (ARBs) for use in the treatment of diabetic nephropathy, we examined the effects of olmesartan medoxomil (olmesartan), an angiotensin II type 1 (AT1) specific ARB, on the progression of nephropathy in Zucker diabetic fatty (ZDF) rats, an animal model of type 2 diabetes.
9	12436944	The renin-angiotensin-aldosterone system (RAS) and arginine vasopressin (AVP) are overactivated in both hypertension and diabetes.
10	12436944	The microvascular and macrovascular benefits of ACE inhibition, ARBs and possible role of AVP antagonists in diabetic patients will be discussed, as will be recommendations for its clinical use.
11	12466317	The review discussed those studies that directly and blindly compared CCB with angiotensin-converting enzyme (ACE) inhibitors and with angiotensin II AT(1) receptor blockers (ARB).
12	12466317	With regard to the outcome of renal complications, both ARB and ACE inhibitors more effectively prevented the progression of renal damage among the patients with overt nephropathy than CCB.
13	12466317	However, ACE inhibitors and ARB more markedly decreased the rate of albumin excretion rate in the range of both microalbuminuria and macroalbuminuria.
14	12784755	[The role of angiotensin II AT1-receptor antagonists in renal and cardiac protection in type-2 diabetes mellitus].
15	12784755	Finally, ACE-inhibitors and ARBs are both first-choice drugs in cardiovascular prevention in type 2 diabetes.
16	12924617	In this population, pharmacological therapy targeting hyperglycemia, hypertension (including ARB/ACE inhibitor), and hyperlipidemia in cases of type 2 diabetes is also necessary.
17	14513876	Leri-Weill syndrome (LWS) is a skeletal dysplasia with mesomelic short stature, bilateral Madelung deformity (BMD) and SHOX (short stature homeobox-containing gene) haploinsufficiency.
18	14727993	Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase.
19	14727993	The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated.
20	14727993	Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms.
21	14871059	These drugs should not be considered as ethical placebo arms in trials, most especially in diabetic nephropathy, nor should they be used without an ACE or ARB in patients with proteinuric renal disease in the absence of documented contraindications or intolerance to ACE, ARB, or non-DHP CCB (which are now considered second-line agents for proteinuric renal disease, and are acceptable placebo or comparison arms in clinical trials).
22	14871059	Given the similarity of actions between the ARB and ACE, it is likely there is considerable overlap of both benefits and side-effects between the two, although ARB may have a lower incidence of cough and hyperkalemia.
23	14871059	Regardless of the choice between an ACE or ARB, however, post hoc analysis of clinical trials [21,47] and observational data clearly indicate that patients with chronic kidney disease, even if considered mild (ie, serum creatinine greater than or equal to 1.4 mg/dL) are at significantly greater risk of cardiovascular morbidity and mortality compared with those with better kidney function.
24	14871059	As stated in a recent review by the authors of the HOPE trial [50], "the frequent practice of withholding ACE [or ARB] in patients with mild renal insufficiency is unwarranted," because not only are these patients precisely those who might benefit most from their use, but safety and tolerability are generally excellent.
25	14871059	These drugs should not be considered as ethical placebo arms in trials, most especially in diabetic nephropathy, nor should they be used without an ACE or ARB in patients with proteinuric renal disease in the absence of documented contraindications or intolerance to ACE, ARB, or non-DHP CCB (which are now considered second-line agents for proteinuric renal disease, and are acceptable placebo or comparison arms in clinical trials).
26	14871059	Given the similarity of actions between the ARB and ACE, it is likely there is considerable overlap of both benefits and side-effects between the two, although ARB may have a lower incidence of cough and hyperkalemia.
27	14871059	Regardless of the choice between an ACE or ARB, however, post hoc analysis of clinical trials [21,47] and observational data clearly indicate that patients with chronic kidney disease, even if considered mild (ie, serum creatinine greater than or equal to 1.4 mg/dL) are at significantly greater risk of cardiovascular morbidity and mortality compared with those with better kidney function.
28	14871059	As stated in a recent review by the authors of the HOPE trial [50], "the frequent practice of withholding ACE [or ARB] in patients with mild renal insufficiency is unwarranted," because not only are these patients precisely those who might benefit most from their use, but safety and tolerability are generally excellent.
29	14871059	These drugs should not be considered as ethical placebo arms in trials, most especially in diabetic nephropathy, nor should they be used without an ACE or ARB in patients with proteinuric renal disease in the absence of documented contraindications or intolerance to ACE, ARB, or non-DHP CCB (which are now considered second-line agents for proteinuric renal disease, and are acceptable placebo or comparison arms in clinical trials).
30	14871059	Given the similarity of actions between the ARB and ACE, it is likely there is considerable overlap of both benefits and side-effects between the two, although ARB may have a lower incidence of cough and hyperkalemia.
31	14871059	Regardless of the choice between an ACE or ARB, however, post hoc analysis of clinical trials [21,47] and observational data clearly indicate that patients with chronic kidney disease, even if considered mild (ie, serum creatinine greater than or equal to 1.4 mg/dL) are at significantly greater risk of cardiovascular morbidity and mortality compared with those with better kidney function.
32	14871059	As stated in a recent review by the authors of the HOPE trial [50], "the frequent practice of withholding ACE [or ARB] in patients with mild renal insufficiency is unwarranted," because not only are these patients precisely those who might benefit most from their use, but safety and tolerability are generally excellent.
33	14871059	These drugs should not be considered as ethical placebo arms in trials, most especially in diabetic nephropathy, nor should they be used without an ACE or ARB in patients with proteinuric renal disease in the absence of documented contraindications or intolerance to ACE, ARB, or non-DHP CCB (which are now considered second-line agents for proteinuric renal disease, and are acceptable placebo or comparison arms in clinical trials).
34	14871059	Given the similarity of actions between the ARB and ACE, it is likely there is considerable overlap of both benefits and side-effects between the two, although ARB may have a lower incidence of cough and hyperkalemia.
35	14871059	Regardless of the choice between an ACE or ARB, however, post hoc analysis of clinical trials [21,47] and observational data clearly indicate that patients with chronic kidney disease, even if considered mild (ie, serum creatinine greater than or equal to 1.4 mg/dL) are at significantly greater risk of cardiovascular morbidity and mortality compared with those with better kidney function.
36	14871059	As stated in a recent review by the authors of the HOPE trial [50], "the frequent practice of withholding ACE [or ARB] in patients with mild renal insufficiency is unwarranted," because not only are these patients precisely those who might benefit most from their use, but safety and tolerability are generally excellent.
37	15000928	Are ARBs or ACE inhibitors preferred for nephropathy in diabetes?
38	15257162	A meta-analysis of seven studies in 58,010 individuals, showed that the 'new' therapies, namely angiotensin-converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor blockers (ARBs) and calcium channel blockers (CCBs) provoke less new diabetes than the conventional 'old' therapies (diuretics and beta-blockers).
39	15257162	ACE inhibitors/ARBs decreased new diabetes by 20% (P < 0.001), whereas CCBs decreased new diabetes by 16% (P < 0.001).
40	15257162	However, when compared with placebo, ACE inhibition by ramipril or by the ARB, candesartan, both decrease the incidence of new diabetes, raising the hypothesis that these agents actually prevent the changes leading to insulin resistance, possibly by lessening the adverse effects of angiotensin II on the endothelium.
41	15614015	Antidiabetic mechanisms of angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists: beyond the renin-angiotensin system.
42	15614015	Several lines of evidence suggest that angiotensin-converting enzyme (ACE) inhibitors and some angiotensin II receptor blockers (ARBs) may improve insulin sensitivity and decrease the risk for type 2 diabetes.
43	15614015	In addition, one ARB in particular, telmisartan, has been found to effectively activate the peroxisome proliferator activated receptor gamma (PPARgamma), a well-known target for insulin-sensitizing, antidiabetic drugs.
44	15614015	Thus, the beneficial metabolic effects of some ACE inhibitors and ARBs may go well beyond their effects on the renin-angiotensin system.
45	15614015	Moreover, the identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARgamma modulating ability suggests new opportunities for developing third-generation ARBs and PPARgamma activators, with enhanced potential for treating hypertension, diabetes and the metabolic syndrome.
46	15614015	Antidiabetic mechanisms of angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists: beyond the renin-angiotensin system.
47	15614015	Several lines of evidence suggest that angiotensin-converting enzyme (ACE) inhibitors and some angiotensin II receptor blockers (ARBs) may improve insulin sensitivity and decrease the risk for type 2 diabetes.
48	15614015	In addition, one ARB in particular, telmisartan, has been found to effectively activate the peroxisome proliferator activated receptor gamma (PPARgamma), a well-known target for insulin-sensitizing, antidiabetic drugs.
49	15614015	Thus, the beneficial metabolic effects of some ACE inhibitors and ARBs may go well beyond their effects on the renin-angiotensin system.
50	15614015	Moreover, the identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARgamma modulating ability suggests new opportunities for developing third-generation ARBs and PPARgamma activators, with enhanced potential for treating hypertension, diabetes and the metabolic syndrome.
51	15614015	Antidiabetic mechanisms of angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists: beyond the renin-angiotensin system.
52	15614015	Several lines of evidence suggest that angiotensin-converting enzyme (ACE) inhibitors and some angiotensin II receptor blockers (ARBs) may improve insulin sensitivity and decrease the risk for type 2 diabetes.
53	15614015	In addition, one ARB in particular, telmisartan, has been found to effectively activate the peroxisome proliferator activated receptor gamma (PPARgamma), a well-known target for insulin-sensitizing, antidiabetic drugs.
54	15614015	Thus, the beneficial metabolic effects of some ACE inhibitors and ARBs may go well beyond their effects on the renin-angiotensin system.
55	15614015	Moreover, the identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARgamma modulating ability suggests new opportunities for developing third-generation ARBs and PPARgamma activators, with enhanced potential for treating hypertension, diabetes and the metabolic syndrome.
56	15671918	The inhibition of the renin-angiotensin system (RAS), using an angiotensin converting enzyme inhibitor (ACEI) or a selective angiotensin receptor AT1 blocker (ARB), may exert favourable metabolic effects capable of preventing T2DM in high risk individuals.
57	15821452	The renin-angiotensin-aldosterone system (RAAS) is involved at all stages of the cardiovascular continuum, because the effector molecules of the RAAS, angiotensin II in particular, have direct pathobiological effects on a variety of tissues, including the endothelium, vascular smooth muscle and the renal mesangium.
58	15821452	Clinical trials of angiotensin II receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors have demonstrated the essential validity of this hypothesis.
59	15821452	What are the clinical effects of combination ARB and ACE inhibitor treatment?
60	15884724	Combining ARB and ACE inhibitors in patient after myocardial infarction increases the rate of adverse events without improving survival.
61	15939809	The adipose-specific protein adiponectin has been recently discovered to improve insulin sensitivity.
62	15939809	Angiotensin type-1 receptor (AT1R) blockers (ARBs) reduce the incidence of type 2 diabetes mellitus by mostly unknown molecular mechanisms.
63	15939809	To identify new antidiabetic mechanisms of ARBs, we studied the regulation of adiponectin by angiotensin II (Ang II) and different ARBs in murine 3T3-L1 adipocytes and obese Zucker rats.
64	15939809	Adiponectin protein expression was markedly stimulated by Ang II (5 nmol/L), which was inhibited by blockade of the AT2R, and further enhanced by the ARB irbesartan.
65	15939809	Irbesartan-mediated adiponectin upregulation started beyond the concentrations needed for AT1R blockade and was also present in the absence of Ang II, implicating an AT1R-independent mechanism of action.
66	15939809	Recently, certain ARBs (irbesartan, telmisartan) were identified as ligands of the peroxisome proliferator-activated receptor (PPAR)gamma.
67	15939809	Blockade of PPARgamma activation by the PPARgamma antagonist GW9662 markedly inhibited irbesartan-induced adiponectin expression.
68	15939809	Finally, administration of irbesartan to obese Zucker rats improved insulin sensitivity and attenuated adiponectin serum depletion.
69	15939809	The present study demonstrates that AT2R activation and certain ARBs induce adiponectin in adipocytes, which was associated with an improvement of parameters of insulin sensitivity in vivo.
70	15939809	ARB-induced adiponectin stimulation is likely to be mediated via PPARgamma activation involving a post-transcriptional mechanism.
71	15939809	The adipose-specific protein adiponectin has been recently discovered to improve insulin sensitivity.
72	15939809	Angiotensin type-1 receptor (AT1R) blockers (ARBs) reduce the incidence of type 2 diabetes mellitus by mostly unknown molecular mechanisms.
73	15939809	To identify new antidiabetic mechanisms of ARBs, we studied the regulation of adiponectin by angiotensin II (Ang II) and different ARBs in murine 3T3-L1 adipocytes and obese Zucker rats.
74	15939809	Adiponectin protein expression was markedly stimulated by Ang II (5 nmol/L), which was inhibited by blockade of the AT2R, and further enhanced by the ARB irbesartan.
75	15939809	Irbesartan-mediated adiponectin upregulation started beyond the concentrations needed for AT1R blockade and was also present in the absence of Ang II, implicating an AT1R-independent mechanism of action.
76	15939809	Recently, certain ARBs (irbesartan, telmisartan) were identified as ligands of the peroxisome proliferator-activated receptor (PPAR)gamma.
77	15939809	Blockade of PPARgamma activation by the PPARgamma antagonist GW9662 markedly inhibited irbesartan-induced adiponectin expression.
78	15939809	Finally, administration of irbesartan to obese Zucker rats improved insulin sensitivity and attenuated adiponectin serum depletion.
79	15939809	The present study demonstrates that AT2R activation and certain ARBs induce adiponectin in adipocytes, which was associated with an improvement of parameters of insulin sensitivity in vivo.
80	15939809	ARB-induced adiponectin stimulation is likely to be mediated via PPARgamma activation involving a post-transcriptional mechanism.
81	15939809	The adipose-specific protein adiponectin has been recently discovered to improve insulin sensitivity.
82	15939809	Angiotensin type-1 receptor (AT1R) blockers (ARBs) reduce the incidence of type 2 diabetes mellitus by mostly unknown molecular mechanisms.
83	15939809	To identify new antidiabetic mechanisms of ARBs, we studied the regulation of adiponectin by angiotensin II (Ang II) and different ARBs in murine 3T3-L1 adipocytes and obese Zucker rats.
84	15939809	Adiponectin protein expression was markedly stimulated by Ang II (5 nmol/L), which was inhibited by blockade of the AT2R, and further enhanced by the ARB irbesartan.
85	15939809	Irbesartan-mediated adiponectin upregulation started beyond the concentrations needed for AT1R blockade and was also present in the absence of Ang II, implicating an AT1R-independent mechanism of action.
86	15939809	Recently, certain ARBs (irbesartan, telmisartan) were identified as ligands of the peroxisome proliferator-activated receptor (PPAR)gamma.
87	15939809	Blockade of PPARgamma activation by the PPARgamma antagonist GW9662 markedly inhibited irbesartan-induced adiponectin expression.
88	15939809	Finally, administration of irbesartan to obese Zucker rats improved insulin sensitivity and attenuated adiponectin serum depletion.
89	15939809	The present study demonstrates that AT2R activation and certain ARBs induce adiponectin in adipocytes, which was associated with an improvement of parameters of insulin sensitivity in vivo.
90	15939809	ARB-induced adiponectin stimulation is likely to be mediated via PPARgamma activation involving a post-transcriptional mechanism.
91	16269993	Others have shown that antihypertensive treatments acting on the renin-angiotensin system (ACE inhibitors, ARBs agents) can reduce the progression of nephropathy in people with hypertension, type 2 diabetes and microalbuminuria.
92	16290123	We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes.
93	16290123	Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each.
94	16290123	However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype.
95	16290123	We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2).
96	16290123	In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes.
97	16290123	We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes.
98	16290123	Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each.
99	16290123	However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype.
100	16290123	We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2).
101	16290123	In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes.
102	16290123	We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes.
103	16290123	Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each.
104	16290123	However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype.
105	16290123	We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2).
106	16290123	In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes.
107	16290123	We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes.
108	16290123	Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each.
109	16290123	However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype.
110	16290123	We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2).
111	16290123	In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes.
112	16298156	The recent discovery that telmisartan and irbesartan, antihypertensive angiotensin II type 1 receptor (AT1-R) blockers (ARBs), were uniquely capable of activating PPARgamma, has provided a novel approach to addressing the multifactorial components of the metabolic syndrome.
113	16298156	This information provides a strategic rationale and pharmacological platform for the development of novel dual ARB/PPARgamma agonists to target the metabolic syndrome and its cardiovascular sequelae, for which therapy is presently insufficient or non-existent.
114	16298156	The recent discovery that telmisartan and irbesartan, antihypertensive angiotensin II type 1 receptor (AT1-R) blockers (ARBs), were uniquely capable of activating PPARgamma, has provided a novel approach to addressing the multifactorial components of the metabolic syndrome.
115	16298156	This information provides a strategic rationale and pharmacological platform for the development of novel dual ARB/PPARgamma agonists to target the metabolic syndrome and its cardiovascular sequelae, for which therapy is presently insufficient or non-existent.
116	17087302	As the first choice drugs, ARB, ACE inhibitor and Ca channel blocker are recommended.
117	17199217	Complete blockade of angiotensin II (Ang II) action with the highly selective Ang II receptor blocker (ARB) valsartan, both as monotherapy and in combination with ACE inhibitors, is well-tolerated and efficacious in patients with renal failure.
118	17199217	Unlike ACE inhibition, ARB treatment leads to no initial reduction in GFR, thus valsartan may be a better agent for the control of BP, with greater renal protection.
119	17376010	Angiotensin II reactivation and aldosterone escape phenomena in renin-angiotensin-aldosterone system blockade: is oral renin inhibition the solution?
120	17376010	This editorial considers the use of the first selective oral renin inhibitor, aliskiren, in reducing angiotensin (Ang) II reactivation or aldosterone (ALDO) escape during renin-angiotensin-aldosterone system (RAAS) inhibition.
121	17376010	RAAS blockade with angiotensin converting enzyme inhibitors (ACEIs) and/or angiotensin receptor AT(1) blockers (ARBs) is very useful for the treatment of arterial hypertension, chronic heart failure (CHF), atherosclerosis and diabetes.
122	17376010	Renin and Ang I accumulate during ACE inhibition, and might overcome the ability of an ACEI to effectively suppress ACE activity.
123	17376010	There is also data suggesting that 30 - 40% of Ang II formation in the healthy human during RAAS activation is formed via renin-dependent, but ACE-independent, pathways.
124	17376010	Moreover, ACE gene polymorphisms contribute to the modulation and adequacy of the neurohormonal response to long-term ACE inhibition, at least in patients with CHF (up to 45% of CHF patients have elevated Ang II levels despite the long-term use of an ACEI) or diabetes.
125	17376010	Furthermore, there is evidence suggesting that aliskiren reduces Ang II reactivation in ACE inhibition and ALDO escape during treatment with an ACEI or an ARB, at least to the degree that this is associated with the RAAS.
126	17487263	Effect of type-1 diabetes mellitus on the regulation of insulin and endothelin-1 receptors in rat hearts.
127	17487263	This project assesses the treatment role with insulin and (or) angiotensin II receptor subtype-1 (AT1-R) blocker (ARB) on insulin receptor and endothelin-1 receptor subtype (ETA-R and ETB-R) regulation in rat hearts suffering from insulin-dependent diabetes mellitus (IDDM).
128	17487263	However, ETB-R expression was significantly reduced in the diabetic group treated with both insulin and an ARB.
129	17487263	The changes in the expression of the insulin, the ETA-Rs, and the ETB-Rs at the various sites of the myocardium and the effect of both insulin treatment and blockade of the AT1-R explain the new benefits related to the halting of myocardial remodeling in IDDM rats.
130	18050531	The recommendations are based on prospective, randomized clinical trials in specific patient populations that evaluated several classes of antihypertensives, including beta-blockers, ARBs, ACE inhibitors, and CCBs, administered as monotherapy or in various combinations.
131	18947897	Earlier it was suggested to use ACE-inhibitors or ARBs.
132	18958580	Evidence from recent studies indicates that in patients with diabetic nephropathy combined therapy with ACE inhibitors (ACEI) and AT1-receptor antagonists (ARB) results in more complete blockade of the renin-angiotensin-aldosterone system (RAS) than monotherapy, and reduces proteinuria.
133	19292617	Femur BMD, CSA, and SM were larger in women with higher BMI, but values scaled in proportion to lean and not to fat or total body mass.
134	19292617	BMD, CSA, and SM vary in proportion to total body lean mass, supporting the view that bones adapt to prevalent muscle loads.
135	19292617	Because lean mass is a progressively smaller fraction of total mass in obesity, femur BMD, CSA, and SM decline relative to body weight in higher BMI categories.
136	19292617	Femur BMD, CSA, and SM were larger in women with higher BMI, but values scaled in proportion to lean and not to fat or total body mass.
137	19292617	BMD, CSA, and SM vary in proportion to total body lean mass, supporting the view that bones adapt to prevalent muscle loads.
138	19292617	Because lean mass is a progressively smaller fraction of total mass in obesity, femur BMD, CSA, and SM decline relative to body weight in higher BMI categories.
139	19292617	Femur BMD, CSA, and SM were larger in women with higher BMI, but values scaled in proportion to lean and not to fat or total body mass.
140	19292617	BMD, CSA, and SM vary in proportion to total body lean mass, supporting the view that bones adapt to prevalent muscle loads.
141	19292617	Because lean mass is a progressively smaller fraction of total mass in obesity, femur BMD, CSA, and SM decline relative to body weight in higher BMI categories.
142	19427492	The renin angiotensin aldosterone system in hypertension: roles of insulin resistance and oxidative stress.
143	19427492	Indeed, there is a mounting body of evidence that the resultant insulin resistance in cardiovascular tissue and kidneys contributes to the development of endothelial dysfunction, HTN, atherosclerosis, CKD, and CVD.77 RAAS-associated signaling by way of the AT1R and MR, triggers tissue activation of the NADPH oxidase enzymatic activation and increased production of ROS.
144	19427492	Oxidative stress in cardiovascular tissue is derived from both NADPH oxidase and mitochondrial generation of ROS, and is central to the development of insulin resistance, endothelial dysfunction, HTN, and atherosclerosis.
145	19427492	Several strategies are available for RAAS blockade, including ACE inhibitors, ARBs, and MR blockers, which have been proven in the clinical trials to result in improved CVD and CKD outcomes.
146	19453256	Sex differences in the association between adiponectin and BMD, bone loss, and fractures: the Rancho Bernardo study.
147	19453256	We evaluated sex differences in the prospective association between adiponectin with BMD, bone loss, and fractures.
148	19453256	Adiponectin, an adipose-derived protein with insulin-sensitizing properties, is also expressed in bone-forming cells.
149	19453256	Sex differences in the association between adiponectin and BMD, bone loss, and fractures: the Rancho Bernardo study.
150	19453256	We evaluated sex differences in the prospective association between adiponectin with BMD, bone loss, and fractures.
151	19453256	Adiponectin, an adipose-derived protein with insulin-sensitizing properties, is also expressed in bone-forming cells.
152	19453255	Bone morphogenetic protein 7 (BMP7) gene polymorphisms are associated with inverse relationships between vascular calcification and BMD: the Diabetes Heart Study.
153	19453255	Four single nucleotide polymorphisms (SNPs) in the BMP2 gene, 2 SNPs in BMP4, and 16 SNPs in BMP7 were tested for association with measures of VC using CT (coronary and carotid arteries, abdominal aorta), and BMD was measured using DXA (lumbar spine, hip, and distal radius) and quantitative CT (QCT; thoracic and lumbar spine) in 920 European Americans from 374 Diabetes Heart Study families: 762 with type 2 diabetes.
154	19453255	Association was observed between several measures of BMD and BMP7 rs17404303 (thoracic spine QCT p = 0.03; lumbar spine QCT p = 0.02; hip DXA p = 0.06, dominant models).
155	19453255	In addition, 6 of 16 BMP7 SNPs showed significant and opposing effects on the bivariate PCA for VC and BMD (two-sided exact test, p = 0.0143).
156	19453255	Bone morphogenetic protein 7 (BMP7) gene polymorphisms are associated with inverse relationships between vascular calcification and BMD: the Diabetes Heart Study.
157	19453255	Four single nucleotide polymorphisms (SNPs) in the BMP2 gene, 2 SNPs in BMP4, and 16 SNPs in BMP7 were tested for association with measures of VC using CT (coronary and carotid arteries, abdominal aorta), and BMD was measured using DXA (lumbar spine, hip, and distal radius) and quantitative CT (QCT; thoracic and lumbar spine) in 920 European Americans from 374 Diabetes Heart Study families: 762 with type 2 diabetes.
158	19453255	Association was observed between several measures of BMD and BMP7 rs17404303 (thoracic spine QCT p = 0.03; lumbar spine QCT p = 0.02; hip DXA p = 0.06, dominant models).
159	19453255	In addition, 6 of 16 BMP7 SNPs showed significant and opposing effects on the bivariate PCA for VC and BMD (two-sided exact test, p = 0.0143).
160	19453255	Bone morphogenetic protein 7 (BMP7) gene polymorphisms are associated with inverse relationships between vascular calcification and BMD: the Diabetes Heart Study.
161	19453255	Four single nucleotide polymorphisms (SNPs) in the BMP2 gene, 2 SNPs in BMP4, and 16 SNPs in BMP7 were tested for association with measures of VC using CT (coronary and carotid arteries, abdominal aorta), and BMD was measured using DXA (lumbar spine, hip, and distal radius) and quantitative CT (QCT; thoracic and lumbar spine) in 920 European Americans from 374 Diabetes Heart Study families: 762 with type 2 diabetes.
162	19453255	Association was observed between several measures of BMD and BMP7 rs17404303 (thoracic spine QCT p = 0.03; lumbar spine QCT p = 0.02; hip DXA p = 0.06, dominant models).
163	19453255	In addition, 6 of 16 BMP7 SNPs showed significant and opposing effects on the bivariate PCA for VC and BMD (two-sided exact test, p = 0.0143).
164	19453255	Bone morphogenetic protein 7 (BMP7) gene polymorphisms are associated with inverse relationships between vascular calcification and BMD: the Diabetes Heart Study.
165	19453255	Four single nucleotide polymorphisms (SNPs) in the BMP2 gene, 2 SNPs in BMP4, and 16 SNPs in BMP7 were tested for association with measures of VC using CT (coronary and carotid arteries, abdominal aorta), and BMD was measured using DXA (lumbar spine, hip, and distal radius) and quantitative CT (QCT; thoracic and lumbar spine) in 920 European Americans from 374 Diabetes Heart Study families: 762 with type 2 diabetes.
166	19453255	Association was observed between several measures of BMD and BMP7 rs17404303 (thoracic spine QCT p = 0.03; lumbar spine QCT p = 0.02; hip DXA p = 0.06, dominant models).
167	19453255	In addition, 6 of 16 BMP7 SNPs showed significant and opposing effects on the bivariate PCA for VC and BMD (two-sided exact test, p = 0.0143).
168	19587550	Angiotensin II receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors improve markers of kidney disease and slow kidney disease progression in diabetic and nondiabetic patients; this kidney protection may be in addition to their antihypertensive activity in those with advanced proteinuric nephropathy.
169	19587550	Key beneficial effects of ARBs and ACE inhibitors throughout the kidney disease continuum are primarily explained by blood pressure lowering effects and partially by their direct blockade of angiotensin II.
170	19641839	Serum osteocalcin/bone-specific alkaline phosphatase ratio is a predictor for the presence of vertebral fractures in men with type 2 diabetes.
171	19641839	We analyzed the relationships between bone markers (osteocalcin [OC], bone-specific alkaline phosphatase [BAP], urinary N-terminal cross-linked telopeptide of type-I collagen) or BMD and HbA(1c), urinary C-peptide, insulin-like growth factor-I (IGF-I), parathyroid hormone, 1,25(OH)(2) vitamin D, and the presence of prevalent vertebral fractures.
172	19665690	AT(1) receptor blockers increase insulin-like growth factor-I production by stimulating sensory neurons in spontaneously hypertensive rats.
173	19665690	Insulin-like growth factor-I (IGF-I) is an important cardioprotective substance.
174	19665690	We previously reported that sensory neuron stimulation increases IGF-I production by releasing calcitonin gene-related peptide (CGRP) in spontaneously hypertensive rats (SHRs).
175	19665690	Because angiotensin II (Ang II) inhibits sensory neuron activation by interacting with Ang II type 1 (AT(1)) receptors, it is possible that AT(1) receptor blockers (ARBs) increase IGF-I production in SHRs.
176	19665690	Plasma, renal, and cardiac levels of CGRP and IGF-I in SHRs were significantly lower than those in normotensive Wistar Kyoto rats (WKYs) (P < 0.01), which increased to levels found in WKYs after the administration of ARBs.
177	19665690	The administration of nifedipine decreased MABP but did not increase CGRP or IGF-I levels in SHRs.
178	19665690	Although ARBs reversed decreases in CGRP release and cAMP levels in the presence of Ang II in DRG isolated from WKYs, they increased CGRP release and cAMP levels in the absence of Ang II in DRG isolated from SHRs.
179	19665690	Cellular levels of Ang II were not detected in DRG isolated from WKYs or SHRs, but messenger RNA (mRNA) levels for angiotensin-converting enzyme in DRG were significantly higher in SHRs than in WKYs (P < 0.01).
180	19665690	Thus, it is likely that decreases in CGRP release and cAMP levels in DRG isolated from SHRs are mainly caused by AT(1) receptor activation by Ang II through an autocrine mechanism.
181	19665690	These observations suggest that ARBs might increase CGRP release from sensory neurons by sensitizing VR-1 activation through increases in cAMP levels, which thereby increased the production of IGF-I in SHRs.
182	19888010	Using data from the National Ambulatory Medical Care Survey, logit models tested for trends in the probability that visits by adult diabetes patients to their primary care providers included recommended treatment measures, such as a prescription for an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin-II receptor blocker (ARB), blood pressure measurement, and diet/nutrition or exercise counseling.
183	19888010	Results indicated that the probability that visits included prescription of an ACE or ARB and blood pressure measurement increased significantly over the 1997-2005 period, while the probability that visits documented provision of exercise counseling rose since 2001.
184	19942847	Three substance classes that block RAS-activation are currently available, angiotensin converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor blockade (ARB) and renin inhibitors.
185	19942847	Overall however, there is no profound proof for a specific cardiovascular protection by blockade of the angiotensin II Type 1 (AT1) receptor that exceeds the impact of ACE-inhibition or synergises with ACE-blockade.
186	19942847	In fact, combination of ARBs and ACE-inhibitor result in an increased rate of adverse effects and, therefore, this combination should not be encouraged.
187	19942847	To summarize, the initial hope for a more specific impact on cardiovascular diseases by inhibition of the AT1-receptor in comparison to ACE-inhibition has not come true.
188	20075934	One-year effectiveness and safety of open-label losartan/hydrochlorothiazide combination therapy in Japanese patients with hypertension uncontrolled with ARBs or ACE inhibitors.
189	20329582	The compounds that block the vital stages of the RAAS cascade, such as ACE-inhibitors (ACEI), AT1-receptor blockers (ARB) and aldosterone receptor antagonists, importantly extended our treatment options.
190	20329582	Administration of ACEIs and ARBs interrupts physiological feedback for renal renin release and leads to reactive elevation of circulating active renin and greater production of angiotensin I and angiotensin II with subsequent return of aldosterone secretion to the pre-treatment levels ('escape' phenomenon).
191	21502972	However, ACE inhibitors, ARBs, and combinations of agents in these two classes are limited in the extent to which they inhibit the activity of the renin-angiotensin-aldosterone system (RAAS).
192	21502972	Whether direct renin inhibitors will overcome some of the limitations of ACE-inhibitor and ARB therapy by blocking the deleterious effects of the RAAS remains to be proven.
193	21502972	However, ACE inhibitors, ARBs, and combinations of agents in these two classes are limited in the extent to which they inhibit the activity of the renin-angiotensin-aldosterone system (RAAS).
194	21502972	Whether direct renin inhibitors will overcome some of the limitations of ACE-inhibitor and ARB therapy by blocking the deleterious effects of the RAAS remains to be proven.
195	23866091	The cardio- and renoprotective effects observed with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) monotherapy, together with the availability of a direct renin inhibitor (DRI), led to the investigation of the potential benefits of dual RAS inhibition.
196	23866091	In small studies, ARB and ACE inhibitor combinations were shown to be beneficial in patients with CV or renal disease, with improvement in surrogate markers.
197	23866091	However, in larger outcome trials, involving combinations of ACE inhibitors, ARBs or DRIs, dual RAS inhibition did not show reduction in mortality in patients with diabetes, heart failure, coronary heart disease or after myocardial infarction, and was in fact, associated with increased harm.
198	23866091	The cardio- and renoprotective effects observed with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) monotherapy, together with the availability of a direct renin inhibitor (DRI), led to the investigation of the potential benefits of dual RAS inhibition.
199	23866091	In small studies, ARB and ACE inhibitor combinations were shown to be beneficial in patients with CV or renal disease, with improvement in surrogate markers.
200	23866091	However, in larger outcome trials, involving combinations of ACE inhibitors, ARBs or DRIs, dual RAS inhibition did not show reduction in mortality in patients with diabetes, heart failure, coronary heart disease or after myocardial infarction, and was in fact, associated with increased harm.
201	23922555	The Novel Angiotensin II Receptor Blocker Azilsartan Medoxomil Ameliorates Insulin Resistance Induced by Chronic Angiotensin II Treatment in Rat Skeletal Muscle.
202	23922555	Angiotensin receptor (type 1) blockers (ARBs) can reduce both hypertension and insulin resistance induced by local and systemic activation of the renin-angiotensin-aldosterone system.
203	23922555	The effectiveness of azilsartan medoxomil (AZIL-M), a novel imidazole-based ARB, to facilitate metabolic improvements in conditions of angiotensin II (Ang II)-associated insulin resistance is currently unknown.
204	23922555	The aim of this study was to determine the impact of chronic AZIL-M treatment on glucose transport activity and key insulin signaling elements in red skeletal muscle of Ang II-treated rats.
205	23922555	Furthermore, Ang II reduced insulin-mediated glucose transport activity in incubated soleus muscle, and AZIL-M co-treatment increased this parameter.
206	23922555	Moreover, AZIL-M treatment of Ang II-infused animals increased the absolute phosphorylation of insulin signaling molecules, including Akt [both Ser⁴⁷³ (81%) and Thr³⁰⁸ (23%)] and AS160 Thr⁶⁴² (42%), in red gastrocnemius muscle frozen in situ.
207	23922555	Absolute AMPKα (Thr¹⁷²) phosphorylation increased (98%) by AZIL-M treatment, and relative Thr³⁸⁹ phosphorylation of p70 S6K1, a negative regulator of insulin signaling, decreased (51%) with AZIL-M treatment.
208	23922555	These results indicate that ARB AZIL-M improves the in vitro insulin action on glucose transport in red soleus muscle and the functionality of the Akt/AS160 axis in red gastrocnemius muscle in situ in Ang II-induced insulin-resistant rats, with the latter modification possibly associated with enhanced AMPKα and suppressed p70 S6K1 activation.