Ignite Creation Date:
2024-05-05 @ 11:54 AM
Last Modification Date:
2024-10-26 @ 9:16 AM
Study NCT ID:
NCT00173082
Status:
UNKNOWN
Last Update Posted:
2007-11-29
First Post:
2005-09-12
Brief Title:
Metabolic Syndrome and Insulin Resistance in Primary Aldosteronism
Sponsor:
National Taiwan University Hospital
Organization:
National Taiwan University Hospital
Study Overview
Official Title:
Metabolic Syndrome and Insulin Resistance in Primary Aldosteronism
Status:
UNKNOWN
Status Verified Date:
2007-11
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Primary aldosteronism PA is occasionally associated with impaired glucose tolerance Glucose intolerance in general metabolic syndrome is caused by suppression of insulin release from the pancreas and suppression of insulin sensitivity of the target tissues Several studies have suggested that impaired glucose tolerance in primary aldosteronism is due to an inability of the beta cells to release insulin by potassium depletion It was suggested glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassemia and compensatory increase of insulin sensitivity is observed in PA The increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism The conclusion with respect to the possible causal relationship between diabetes mellitus DM and PA however can be obtained after the evaluation of the effect of surgical pharmacological treatment of PA
Detailed Description:
Primary aldosteronism PA is occasionally associated with impaired glucose tolerance Glucose intolerance in general metabolic syndrome is caused by suppression of insulin release from the pancreas and suppression of insulin sensitivity of the target tissues Several studies have suggested that impaired glucose tolerance in primary aldosteronism is due to an inability of the beta cells to release insulin by potassium depletion It was suggested glucose intolerance in PA is caused by the suppression of insulin release related to hypopotassemia and compensatory increase of insulin sensitivity is observed in PA The increased insulin secretory capacity associated with correction of negative potassium balance may account for the increase in plasma leptin after curing primary aldosteronism The conclusion with respect to the possible causal relationship between DM and PA however can be obtained after the evaluation of the effect of surgical pharmacological treatment of PA From July 2005 to July 2008 patients with primary aldosteronism hospitalized for a comprehensive study of the subtypes of primary aldosteronism before operation will receive informed consent about the insulin sensitivity test In the present study we measured insulin sensitivity via the ability to release insulin by the 75 g oral glucose tolerance test OGTT in PA to clarify the mechanisms of glucose intolerance in PA Seventy-five gram OGTT was performed in PA before and after adrenalectomy Within one minute 75 g of glucose dissolved in 200 cc water was ingested Venous blood samples were drawn at 0 60 120 minutes for determination of plasma glucose and plasma insulin levels Serum potassium levels were measures at 0 minutes Furthermore the adipokines HOMA QUICKI leptin adiponectin homocystine C-reactive protein proinflammatory cytokine and adhesion molecules were also measured
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None