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Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1364-1369
Published online before print March 30, 2006, doi: 10.1161/01.ATV.0000219611.50066.bd
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1364.)
© 2006 American Heart Association, Inc.


Atherosclerosis and Lipoproteins

Adiponectin Is an Important Determinant of ApoA-I Catabolism

Bruno Vergès; Jean Michel Petit; Laurence Duvillard; Guillaume Dautin; Emmanuel Florentin; Françoise Galland; Philippe Gambert

From Service Endocrinologie (B.V., J.M.P., F.G.), Diabétologie et Maladies Métaboliques, Centre Hospitalier Universitaire de Dijon, France; INSERM U 498 (B.V., J.M.P., L.D., G.D., E.F., P.G.), Faculté de Médecine, Dijon, France.

Correspondence to Pr Bruno Vergès, Service Endocrinologie, Hôpital du Bocage, BP 77908, 21079 Dijon, France. E-mail bruno.verges{at}chu-dijon.fr

Objective— Plasma concentration of adiponectin is positively correlated with high-density lipoprotein (HDL) cholesterol level. However, the role of adiponectin on HDL metabolism remains unknown. This prompted us to perform an in vivo kinetic study of apoA-I, the main apolipoprotein of HDL, using stable isotopes, in 22 subjects with a wide range of plasma adiponectin, including 11 patients with metabolic syndrome (8 with type 2 diabetes, 3 without type 2 diabetes) and 11 normal individuals.

Methods and Results— In the 22 studied subjects, plasma adiponectin levels ranged from 2.57 to 14.44 µg/mL and apoA-I fractional catabolic rate (FCR) values ranged from 0.142 to 0.340 day–1. A strong negative correlation was found between adiponectin and apoA-I FCR (r=–0.66, P<0.001) in the whole studied population and, to a similar extent, in patients with metabolic syndrome (r=–0.73, P=0.010) and normal subjects (r=–0.68, P=0.020), separately. In multivariable analysis, apoA-I FCR was associated negatively with adiponectin (P=0.005) and positively with HDL triglycerides/cholesterol ratio (P=0.006), but not with age, sex, body mass index (BMI), waist circumference, plasma triglycerides, HDL cholesterol, fasting glycemia, and QUICKI. Both adiponectin and HDL triglycerides/cholesterol ratio explained 62% of the variance of apoA-I FCR and adiponectin on its own explained 43%.

Conclusions— Our kinetic study shows a strong negative correlation between adiponectin and apoA-I FCR, which can explain the positive link between HDL cholesterol and adiponectin. This association is independent of obesity, insulin resistance, and the content of triglycerides within HDL particles. These data suggest that adiponectin may have a direct role on HDL catabolism.

We show a very significant association between adiponectin and apoA-I FCR independent of other factors, such as HDL triglyceride content or clinical and biological indexes of insulin sensitivity. Plasma adiponectin, on its own, explains 43% of apoA-I FCR variance, suggesting that adiponectin may have a direct role on HDL catabolism.


Key Words: adiponectin • apoA-I • HDL cholesterol • insulin-resistance • kinetic




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