Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Vergès, Bruno; Adiels, Martin; Borén, Jan; Barrett, P. Hugh R.; Watts, Gerald F.; Chan, Dick C.; Duvillard, Laurence; Söderlund, Sanni; Matikainen, Niina; Kahri, Juhani; Robin, Isabelle; Taskinen, Marja‐Riitta

doi:10.1210/jc.2014-2365

Cited by 25 publications

(30 citation statements)

References 28 publications

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“…Moreover, it has been shown in subjects with abdominal obesity that the fractional catabolic rate (FCR) of apoA-I is independently associated with both catabolism and production of VLDL 1 -TG. 50 We also found a significant positive association between the increase in plasma adiponectin and the increase in HDL-C (DM12-M0). A significant negative correlation has already been reported between HDL-apoA-I catabolism and plasma adiponectin, independent of insulin resistance and plasma lipids, suggesting as in our study a direct effect of adiponectin on HDL metabolism.…”

Section: Discussionsupporting

confidence: 52%

Impact of bariatric surgery on apolipoprotein C-III levels and lipoprotein distribution in obese human subjects

Maraninchi¹,

Padilla²,

Béliard

et al. 2017

Journal of Clinical Lipidology

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BACKGROUND: Elevated apolipoprotein C-III (apoC-III) has been postulated to contribute to the atherogenic dyslipidemia seen in obesity and insulin-resistant states, mainly by impairing plasma triglyceride-rich lipoprotein (TRL) metabolism. Bariatric surgery is associated with improvements of several obesity-associated metabolic abnormalities, including a reduction in plasma triglycerides (TGs) and an increase in plasma high-density lipoprotein cholesterol (HDL-C).OBJECTIVES: We investigated the specific effect of bariatric surgery on apoC-III concentrations in plasma, non-HDL, and HDL fractions in relation to lipid profile parameters evolution.METHODS: A total of 132 obese subjects undergoing bariatric surgery, gastric bypass (n 5 61) or sleeve gastrectomy (n 5 71), were studied 1 month before surgery and 6 and 12 months after surgery.RESULTS: Plasma apoC-III, non-HDL-apoC-III, and HDL-apoC-III concentrations were markedly reduced after surgery and strongly associated with reduction in plasma TG. This decrease was E-mail address: rvalero@mail.ap-hm.fr accompanied by a redistribution of apoC-III from TRL to HDL fractions. In multivariate analysis, plasma apoC-III was the strongest predictor of TG reduction after surgery, and the increase of HDL-C was positively associated with plasma adiponectin and negatively with body mass index.CONCLUSION: Marked reduction of apoC-III and changes in its distribution between TRL and HDL consistent with a better lipid profile are achieved in obese patients after bariatric surgery. These apoC-III beneficial modifications may have implications in dyslipidemia improvement and contribute to cardiovascular risk reduction after surgery.

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Section: Discussionsupporting

confidence: 52%

Impact of bariatric surgery on apolipoprotein C-III levels and lipoprotein distribution in obese human subjects

Maraninchi¹,

Padilla²,

Béliard

et al. 2017

Journal of Clinical Lipidology

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Section: Discussionmentioning

confidence: 99%

“…Both apoA-I and HDL-C are known to be low in obesity and the low levels are attributed to HDL's interaction with VLDL mediated by hepatic triglyceride lipase [44]. These metabolic events are in part attributed to insulin resistance [44] and account for our finding that MHO participants have less insulin resistance and higher apoA-I, possibly accounting for a less atherogenic effect, particularly when combined with lower apoB and the apoB : apoA-I ratio [45]. The high C -statistic and retention in the model support prediction of MHO and lower risk attributable to the apoB : apoA-I ratio [45, 46] and support use of the ratio as a measure of cardiovascular risk attributable to obesity.…”

Section: Discussionmentioning

confidence: 99%

Apolipoproteins A-I, B, and C-III and Obesity in Young Adult Cherokee

et al. 2017

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Since young adult Cherokee are at increased risk for both diabetes and cardiovascular disease, we assessed association of apolipoproteins (A-I, B, and C-III in non-HDL and HDL) with obesity and related risk factors. Obese participants (BMI ≥ 30) aged 20–40 years (n = 476) were studied. Metabolically healthy obese (MHO) individuals were defined as not having any of four components of the ATP-III metabolic syndrome after exclusion of waist circumference, and obese participants not being MHO were defined as metabolically abnormal obese (MAO). Associations were evaluated by correlation and regression modeling. Obesity measures, blood pressure, insulin resistance, lipids, and apolipoproteins were significantly different between groups except for total cholesterol, LDL-C, and HDL-apoC-III. Apolipoproteins were not correlated with obesity measures with the exception of apoA-I with waist and the waist : height ratio. In a logistic regression model apoA-I and the apoB : apoA-I ratio were significantly selected for identifying those being MHO, and the result (C-statistic = 0.902) indicated that apoA-I and the apoB : apoA-I ratio can be used to identify a subgroup of obese individuals with a significantly less atherogenic lipid and apolipoprotein profile, particularly in obese Cherokee men in whom MHO is more likely.

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“…Hypertriglyceridaemia is a major contributing factor to the accelerated HDL catabolism observed in type 2 diabetes. It has recently been demonstrated that both increased VLDL 1 production and reduced VLDL 1 catabolism are independent factors associated with increased HDL catabolism in insulin-resistant states [ 96 ]. It is suggested that the increased pool of triacylglycerol-rich lipoproteins (mainly VLDL 1 ), observed in type 2 diabetes, promotes CETP-mediated triacylglycerol enrichment of HDL particles and, as a consequence, enhances HDL catabolism, since HDL-rich particles are very good substrates for hepatic lipase.…”

Section: Lipid Abnormalities In Type 2 Diabetesmentioning

confidence: 99%

Pathophysiology of diabetic dyslipidaemia: where are we?

2015

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Cardiovascular disease is a major cause of morbidity and mortality in patients with type 2 diabetes mellitus, with a two- to fourfold increase in cardiovascular disease risk compared with non-diabetic individuals. Abnormalities in lipid metabolism that are observed in the context of type 2 diabetes are among the major factors contributing to an increased cardiovascular risk. Diabetic dyslipidaemia includes not only quantitative lipoprotein abnormalities, but also qualitative and kinetic abnormalities that, together, result in a shift towards a more atherogenic lipid profile. The primary quantitative lipoprotein abnormalities are increased triacylglycerol (triglyceride) levels and decreased HDL-cholesterol levels. Qualitative lipoprotein abnormalities include an increase in large, very low-density lipoprotein subfraction 1 (VLDL1) and small, dense LDLs, as well as increased triacylglycerol content of LDL and HDL, glycation of apolipoproteins and increased susceptibility of LDL to oxidation. The main kinetic abnormalities are increased VLDL1 production, decreased VLDL catabolism and increased HDL catabolism. In addition, even though LDL-cholesterol levels are typically normal in patients with type 2 diabetes, LDL particles show reduced turnover, which is potentially atherogenic. Although the pathophysiology of diabetic dyslipidaemia is not fully understood, the insulin resistance and relative insulin deficiency observed in patients with type 2 diabetes are likely to contribute to these lipid changes, as insulin plays an important role in regulating lipid metabolism. In addition, some adipocytokines, such as adiponectin or retinol-binding protein 4, may also contribute to the development of dyslipidaemia in patients with type 2 diabetes.

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Interrelationships Between the Kinetics of VLDL Subspecies and HDL Catabolism in Abdominal Obesity: A Multicenter Tracer Kinetic Study

Cited by 25 publications

References 28 publications

Impact of bariatric surgery on apolipoprotein C-III levels and lipoprotein distribution in obese human subjects

Impact of bariatric surgery on apolipoprotein C-III levels and lipoprotein distribution in obese human subjects

Apolipoproteins A-I, B, and C-III and Obesity in Young Adult Cherokee

Pathophysiology of diabetic dyslipidaemia: where are we?

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