Re: Glucose intolerance and Hyperaldosteronism

[Guest guest]

In a message dated 12/20/07 5:02:31 PM, shahall@... writes:

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

>

YES-SEE MY ARTICLE AND AM WORKING ON NEW ONE THAT WILL GIVE MORE DETAILS.

DUE TO EATING TOO MUCH AND LOW K WHICH IMPAIRS INSULIN RELEASE.

May your pressure be low!

Clarence E. Grim, BS, MS, MD

Senior Consultant to Shared Care Research and Consulting, Inc.

(sharedcareinc.com)

Clinical Professor of Internal Medicine and Epidemiology Med. Col. WI

Clinical Professor of Nursing, Univ. of WI, Milwaukee

Specializing in Difficult to Control High Blood Pressure

and the Physiology and History of Survival During

Hard Times and Heart Disease today.

**************************************

See AOL's top rated recipes

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[Guest guest]

I have metabolic syndrome and there seems to be a

connection. Here's a few, you can search pubmed for

more articles.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=ShowDetailView & TermToSear\

ch=17940441 & ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=ShowDetailView & TermToSear\

ch=17885557 & ordinalpos=3 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=ShowDetailView & TermToSear\

ch=17679033 & ordinalpos=4 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=ShowDetailView & TermToSear\

ch=17646573 & ordinalpos=5 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=ShowDetailView & TermToSear\

ch=17575088 & ordinalpos=6 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVDocSum

--- airlinerg <airlinerg@...> wrote:

> Is there a connection between glucose intolerance

> and

> hyperaldosteronism?

>

>

-Lord, keep your arm around my shoulder and your hand over my mouth.-

[Guest guest]

1: Curr Opin Endocrinol Diabetes Obes. 2007 Jun;14(3):210-2. [Click here

to read]

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3159 & itool=Abst\

ractPlus-def & uid=17940441 & db=pubmed & url=http://meta.wkhealth.com/pt/pt-c\

ore/template-journal/lwwgateway/media/landingpage.htm?doi=10.1097/MED.0b\

013e32814db86a> Links Hyperaldosteronism: a commonly occurring

underlying feature of essential hypertension and the metabolic syndrome?

Chun TY

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22C\

hun%20TY%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Result\

sPanel.Pubmed_RVAbstractPlusDrugs2> , Pratt JH

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22P\

ratt%20JH%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Resul\

tsPanel.Pubmed_RVAbstractPlusDrugs2> .

Department of Medicine, Indiana University School of Medicine and the VA

Medical Center, Indianapolis, Indiana, USA.

Individuals with primary aldosteronism make up a substantial proportion

of those with hypertension. Less well appreciated is what appears to be

inappropriately elevated aldosterone secretion in hypertensive patients

who do not meet the criteria for true primary aldosteronism. This

finding is particularly true of African-Americans. An additional,

recently described, aspect of aldosterone excess is its apparent

contribution to insulin resistance as evidenced by the frequent

association of primary aldosteronism with the metabolic syndrome. Thus

in the management of, not only hypertension, but also certain metabolic

conditions, greater consideration should be given to the participation

of aldosterone.

PMID: 17940441 [PubMed - in process]

>

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

> >

> >

>

>

> -Lord, keep your arm around my shoulder and your hand over my mouth.-

>

[Guest guest]

1: J Hypertens. 2007 Oct;25(10):2125-30. [Click here to read]

<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3159 & itool=Abst\

ractPlus-def & uid=17885557 & db=pubmed & url=http://meta.wkhealth.com/pt/pt-c\

ore/template-journal/lwwgateway/media/landingpage.htm?an=00004872-200710\

000-00024> Links A possible association between primary

aldosteronism and a lower beta-cell function. Mosso LM

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22M\

osso%20LM%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Resul\

tsPanel.Pubmed_RVAbstractPlusDrugs2> , Carvajal CA

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22C\

arvajal%20CA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Re\

sultsPanel.Pubmed_RVAbstractPlusDrugs2> , Maiz A

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22M\

aiz%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Results\

Panel.Pubmed_RVAbstractPlusDrugs2> , Ortiz EH

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22O\

rtiz%20EH%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Resul\

tsPanel.Pubmed_RVAbstractPlusDrugs2> , Castillo CR

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22C\

astillo%20CR%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Re\

sultsPanel.Pubmed_RVAbstractPlusDrugs2> , Artigas RA

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22A\

rtigas%20RA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Res\

ultsPanel.Pubmed_RVAbstractPlusDrugs2> , Fardella CE

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22F\

ardella%20CE%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Re\

sultsPanel.Pubmed_RVAbstractPlusDrugs2> .

Department of Nutrition and Diabetes, Faculty of Medicine, Pontificia

Universidad Católica de Chile, Santiago, Chile.

OBJECTIVE: Primary aldosteronism (PA) is the most common secondary cause

of hypertension and recently has been implicated as a cause of impaired

glucose tolerance. We investigated the glucose insulin sensitivity and

insulin secretion in patients with idiopathic primary aldosteronism.

DESIGN: Thirty PA patients and 60 essential hypertensive (EH) patients

as controls were included, matched (1: 2) by their body mass index (BMI)

(29.9 +/- 4.3 versus 29.8 +/- 5.8 m/kg), age (53.7 +/- 9.4 versus 59.9

+/- 8.6 years old) and gender (male/female: 8/22 versus 17/43). In all

patients, we measured insulin, total cholesterol, triglycerides,

C-peptide and fasting glucose levels. Homeostasis model assessment for

insulin resistance (HOMA-IR) and HOMA of pancreatic beta-cell function

(HOMA-betaF) indexes were calculated. We also evaluated the response to

spironolactone in 19 PA patients. RESULTS: PA patients had higher levels

of glucose (5.2 +/- 0.7 versus 4.9 +/- 0.7 mmol/l; P = 0.017). Insulin

levels (10.7 +/- 6.5 versus 11.5 +/- 5.8 uUI/ml, P = 0.525) and HOMA-IR

(2.51 +/- 1.59 versus 2.45 +/- 1.29 uUI/ml x mmol/l, P = 0.854) were

similar in both groups. HOMA-betaF index (138.9 +/- 89.8 versus 179.8

+/- 100.2%, P = 0.049) and C-peptide (0.83 +/- 0.63 versus 1.56 +/- 0.84

ng/dl, P = 0.0001) were lower in PA patients. Potassium was normal in

both groups. Negative correlations between serum aldosterone/plasma

renin activity (SA/PRA) ratio and HOMA-betaF, and between C-peptide and

SA levels were found in all patients. After the spironolactone

treatment, we found an increase of C-peptide and insulin levels without

changes in HOMA-IR or HOMA-betaF. CONCLUSION: Our results showed

differences in glucose metabolism between PA patients and those with

hypertension suggesting that these findings could probably be determined

by a lower beta-cell function influenced by aldosterone. These findings

highlight the importance of aldosterone in glucose metabolism.

PMID: 17885557 [PubMed - in process]

>

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

> >

> >

>

>

> -Lord, keep your arm around my shoulder and your hand over my mouth.-

>

[Guest guest]

1: Am J Hypertens. 2007 Aug;20(8):855-61.

Adiponectin and insulin sensitivity in primary aldosteronism.

BACKGROUND: A high prevalence of metabolic syndrome has been reported in

primary aldosteronism. Low levels of adiponectin, an adipokine with

insulin-sensitizing properties, are considered a hallmark of the

metabolic syndrome. We evaluated the relationship between adiponectin

and insulin sensitivity in primary aldosteronism, with and without

metabolic syndrome, compared with essential hypertension. METHODS: Forty

patients with primary aldosteronism and 40 matched patients with

low-renin essential hypertension (LREH) were studied. Patients with type

2 diabetes were excluded. Each group was divided into two subsets: one

including patients with metabolic syndrome and one including patients

without metabolic syndrome (ie, hypertension alone or associated with

another component of the syndrome). RESULTS: Insulin resistance, defined

by increased homeostasis model assessment (HOMA index), was higher in

patients with primary aldosteronism than in those with LREH only in the

absence of metabolic syndrome (P<.01), whereas in the subsets bearing

the syndrome it was similar. Adiponectin levels were lower in primary

aldosteronism than in patients with LREH (P<.01). Like HOMA index, the

difference was maintained (P<.01) only in the subsets without metabolic

syndrome. Adiponectin levels were inversely correlated with HOMA index

and positively correlated with potassium levels both in primary

aldosteronism (P<.001) or in LREH (P<.05) groups. CONCLUSIONS: Lower

adiponectin as well as lower insulin sensitivity in primary

aldosteronism compared with LREH seem to result from both direct

(aldosterone excess) and indirect (hypokalemia) mechanisms. Therapeutic

interventions aimed at correcting both potassium and adiponectin levels

by specific antihypertensive agents might improve insulin sensitivity,

providing better cardiovascular protection in primary aldosteronism.

PMID: 17679033 [PubMed - indexed for MEDLINE]

>

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

> >

> >

>

>

> -Lord, keep your arm around my shoulder and your hand over my mouth.-

>

[Guest guest]

1: Hypertension. 2007 Oct;50(4):750-5. Epub 2007 Jul 23. Aldosterone

suppresses insulin signaling via the downregulation of insulin receptor

substrate-1 in vascular smooth muscle cells.

Department of Cardiorenal and Cerebrovascular Medicine, Faculty of

Medicine, Kagawa University, Kita-gun, Japan. hitomi@...

Clinical reports indicate that patients with primary aldosteronism

commonly have impaired glucose tolerance; however, the relationship

between aldosterone and insulin signaling pathway has not been

clarified. In this study, we examined the effects of aldosterone

treatment on insulin receptor substrate-1 expression and insulin

signaling pathway including Akt phosphorylation and glucose uptake in

rat vascular smooth muscle cells. Insulin receptor substrate-1 protein

expression and Akt phosphorylation were determined by Western blot

analysis with anti-insulin receptor substrate-1 and phosphorylated-Akt

antibodies, respectively. Glucose metabolism was evaluated using

(3)H-labeled 2-deoxy-d-glucose uptake. Aldosterone (1-100 nmol/L)

dose-dependently decreased insulin receptor substrate-1 protein

expression with a peak at 18 hours (n=4). Aldosterone-induced

degradation of insulin receptor substrate-1 was markedly attenuated by

treatment with the selective mineralocorticoid receptor antagonist

eplerenone (10 micromol/L; n=4). Furthermore, degradation was blocked by

the Src inhibitor PP1 (20 micromol/L; n=4). Treatment with antioxidants,

N-acetylcysteine (10 mmol/L), or ebselen (40 micromol/L) also attenuated

aldosterone-induced insulin receptor substrate-1 degradation (n=4). In

addition, proteasome inhibitor MG132 (1 micromol/L) prevented insulin

receptor substrate-1 degradation (n=4). Aldosterone treatment abolished

insulin-induced Akt phosphorylation (100 nmol/L; 5 minutes; n=4).

Furthermore, aldosterone pretreatment decreased insulin-stimulated (100

nmol/L; 60 minutes; n=4) glucose uptake by 50%, which was reversed by

eplerenone (10 micromol/L; n=4). These data indicate that aldosterone

decreases insulin receptor substrate-1 expression via Src and reactive

oxygen species stimulation by proteasome-dependent degradation in

vascular smooth muscle cells; thus, aldosterone may be involved in the

pathogenesis of vascular insulin resistance via oxidative stress.

PMID: 17646573 [PubMed - indexed for MEDLINE]

>

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

> >

> >

>

>

> -Lord, keep your arm around my shoulder and your hand over my mouth.-

>

[Guest guest]

1: Diabetes Care. 2007 Sep;30(9):2349-54. Epub 2007 Jun 15.

Insulin resistance and hyperinsulinemia are related to plasma

aldosterone levels in hypertensive patients.

Hypertension and Diabetes Unit, Division of Internal Medicine,

Department of Experimental and Clinical Pathology and Medicine,

University of Udine, Udine, Italy.

OBJECTIVE: An association between aldosterone and insulin resistance has

been demonstrated in obesity and primary aldosteronism and in blacks

with the metabolic syndrome. The aim of this study was to evaluate the

relationship of plasma aldosterone with insulin sensitivity in white

subjects. RESEARCH DESIGN AND METHODS: In 356 patients with essential

hypertension and 102 normotensive control subjects of comparable age and

BMI, we measured, after discontinuation of treatment, plasma active

renin, aldosterone, cortisol, glucose, insulin, and C-peptide levels and

calculated markers of insulin sensitivity. Direct assessment of insulin

sensitivity was obtained in a subset of 64 hypertensive patients by a

hyperinsulinemic clamp. RESULTS: Hypertensive patients had significantly

greater fasting plasma insulin and C-peptide concentrations and

homeostasis model assessment (HOMA) indexes than normotensive control

subjects. A positive association with increasing plasma aldosterone

concentrations was demonstrated for plasma glucose, insulin, C-peptides,

and HOMA. Assessment of insulin sensitivity by clamp showed a

significant decrease of the metabolic clearance rate of glucose with

increasing aldosterone levels. Significant correlations were found

between plasma aldosterone, plasma insulin, and C-peptide levels, HOMA,

and glucose metabolic clearance rate. Blood pressure and plasma

potassium, plasma cortisol, and renin levels, but not BMI, were also

directly correlated with plasma aldosterone. Multiple regression

analysis showed that HOMA, together with plasma potassium, cortisol, and

renin levels, was independently correlated with plasma aldosterone.

CONCLUSIONS: This study demonstrates a direct relationship between

aldosterone, insulin resistance, and hyperinsulinemia in white subjects.

In patients with hypertension, this relationship might contribute to

maintenance of high blood pressure and increased cardiovascular risk.

PMID: 17575088 [PubMed - indexed for MEDLINE]

>

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

> >

> >

>

>

[Guest guest]

Thank you a for these great articles. You have opened up my

eyes!

I am not sure if I understand the articles so could you please

explain them in very simple and an easy to understand summary?

Thanks,

airlinerg

>

> > Is there a connection between glucose intolerance

> > and

> > hyperaldosteronism?

> >

> >