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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity, hypertension and hyperinsulinism are frequently related and constitute morbid elements of human athero-thrombogenic syndrom. To elucidate physiopathologic mechanisms linking these symptoms, we have developped an experimental model reproducing the morbid triptyque: obesity-hypertension-insulin resistance were induced by hyperlipidic hypercaloric diet. The aim of this study was to investigate cardiovascular modifications elicited by high fat diet. Four male Beagle-Harrier dogs were used in this preliminary study. We investigated before and 7 weeks after the beginning of the hypercaloric hyperlipidic diet morphologic measures, systemic blood pressure (BP) and heart rate (HR), pulmonary blood pressure, cardiac output (CO), systolic ejection volume (SEV), peripheral arterial resistance (PAR) and HR variability on 24 hours' electrocardiogram obtained by Holter method. Echocardiographic modifications of left ventricule was also studied after 20 weeks. Body weight increased (+15.4%) after 7 weeks and remained stable the whole experimental period. This gain was associated with an increase of thoracic and abdominal circonferences (respectively +5.9% and 14.3% at the 7th week). The abdominal increase was significantly more elevated than the thoracic one. This abdominal obesity was associated with an increase in diastolic (+17.9%) and mean (+16.4%) (but not systolic) BP. High fat diet failed to modify arterial pulmonary blood pressures but induced an increase in both CO (3.0 +/- 5.2 vs 4.3 +/- 0.4 ml/min) and SEV (32.4 +/- 5.2 vs 40.8 +/- 2.7 ml/beat). PAR decreased (43.1 +/- 5.9 vs 33.0 +/- 3.2 UW; p = 0.08). Holter method showed a non significant increase of HR (82.0 +/- 7.8 vs 99.5 +/- 5.6 beat/min; p = 0.1) explained by a significant decrease of parasympathetic HR variability (PNN50: 53.5 +/- 4.1 vs 40.9 +/- 4.1%). No echocardiographic modification of left ventricule was found after 20 weeks of high fat diet. This preliminary study shows that, like in humans, high fat diet in dogs induced abdominal obesity with systemic hypertension but failed to provoke left cardiovascular hypertrophy after 20 weeks. This model will allow to characterize the links between cardiovascular and endocrinometabolic alterations occurring during the development of obesity and hypertension.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Experimental hypertension induced by hypercaloric diet]. 894 71

The dyslipidemia classically associated with abdominal obesity is characterised by a metabolic atherogenic triad including an elevation of triglycerides, a low HDL-cholesterol and an excess of small dense LDL fractions. All of these lipid anomalies contribute to an increased cardio-metabolic risk, and are engendered by an excess of visceral adipose tissue. This excess adipose tissue seems to be the direct origin of the dyslipidemia associated with abdominal obesity, causing more free fatty acids to flow into the liver and contributing to insulin resistance.
Arch Mal Coeur Vaiss 2007 Dec
PMID:[Dyslipidemia and abdominal obesity: mechanisms and characteristics (Part I)]. 1822 10

Lifestyle changes form the basis of the therapeutic management of dyslipidemia associated with abdominal obesity and other risk factors associated with an excess of visceral adipose tissue. The use of lipid-lowering agents is justified if the therapeutic objectives are not attained by lifestyle changes alone. New therapeutic approaches are aimed directly at the excess visceral adipose tissue, and the CB1 receptor blockers are particularly promising for improving the overall lipid profile for patients with abdominal obesity.
Arch Mal Coeur Vaiss 2007 Dec
PMID:[Dyslipidemia and abdominal obesity: therapeutic approaches (Part II)]. 1822 11