Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-8-12
pubmed:abstractText
Resistance to the capacity of insulin to suppress lipolysis may be an important link in the association between abdominal obesity and hypertension. Furthermore, a more active renin-angiotensin system in adipose tissue may contribute to insulin-resistant lipolysis in abdominally obese hypertensive subjects. We determined nonesterified fatty acid concentrations and turnover as well as lipid oxidation under basal conditions and during steady-state euglycemia with two levels of insulinemia (72 and 287 pmol/L) in lean normotensive, abdominally obese normotensive, and abdominally obese hypertensive subjects. To assess the role of the renin-angiotensin system in determining non-esterified fatty acid turnover, we repeated studies in the abdominally obese hypertensive subjects after double-blind random assignment to placebo or enalapril for 1 month each. The main findings were the following: (1) Nonesterified fatty acid flux was significantly higher in abdominally obese hypertensive subjects at both levels of insulinemia than in either abdominally obese normotensive or lean normotensive subjects and correlated significantly with both mean blood pressure and total systemic resistance during the higher level of insulinemia. (2) Enalapril significantly improved insulin-resistant lipolysis in the abdominally obese hypertensive subjects. The improvement in insulin suppressibility of nonesterified fatty acid flux at the high hormonal concentrations correlated positively with the magnitude of reduction in blood pressure. (3) Basal lipid oxidation and suppression in response to insulin were similarly impaired in both obese groups. Resistance to the antilipolytic actions of insulin is thus a characteristic feature in abdominally obese hypertensive subjects and may be linked to the elevated blood pressure in these individuals. A more active renin-angiotensin system may partly explain the insulin-resistant lipolysis in this form of hypertension.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
120-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:8675251-Adult, pubmed-meshheading:8675251-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:8675251-Antihypertensive Agents, pubmed-meshheading:8675251-Body Constitution, pubmed-meshheading:8675251-Body Mass Index, pubmed-meshheading:8675251-Calorimetry, Indirect, pubmed-meshheading:8675251-Data Interpretation, Statistical, pubmed-meshheading:8675251-Enalapril, pubmed-meshheading:8675251-Fatty Acids, Nonesterified, pubmed-meshheading:8675251-Female, pubmed-meshheading:8675251-Hemodynamics, pubmed-meshheading:8675251-Humans, pubmed-meshheading:8675251-Hypertension, pubmed-meshheading:8675251-Insulin, pubmed-meshheading:8675251-Insulin Resistance, pubmed-meshheading:8675251-Lipolysis, pubmed-meshheading:8675251-Male, pubmed-meshheading:8675251-Obesity, pubmed-meshheading:8675251-Placebos, pubmed-meshheading:8675251-Renin-Angiotensin System
pubmed:year
1996
pubmed:articleTitle
Insulin-resistant lipolysis in abdominally obese hypertensive individuals. Role of the renin-angiotensin system.
pubmed:affiliation
Department of Medicine, College of Wisconsin, Milwaukee, USA.
pubmed:publicationType
Journal Article, Clinical Trial, Comparative Study, Research Support, U.S. Gov't, P.H.S., Randomized Controlled Trial, Research Support, Non-U.S. Gov't