Lipid and lipoprotein dysregulation in insulin resistant states

Avramoglu, Rita Kohen; Basciano, Heather; Adeli, Khosrow

doi:10.1016/j.cca.2005.12.026

Cited by 268 publications

(199 citation statements)

References 232 publications

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“…Surprisingly, the LT presence was not associated to increased CIMT in our HIV cohort, suggesting a worse role of VLDL per se. In addition, mechanism of VLDL accumulation in HIV+ patients appears more complex than in diabetes type II patients where insulin-resistance plays a central role 34 . Indeed, there was no association between the LT and HOMA index in the present study (See Table 4), by contrast with the frequent occurrence of LT in insulin resistance state in the general population 33 .…”

Section: Discussionmentioning

confidence: 99%

Association of non-HDL cholesterol with subclinical atherosclerosis in HIV-positive patients

Badiou

Thiébaut

Aurillac-Lavignolle

et al. 2008

Journal of Infection

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Section: Discussionmentioning

confidence: 99%

Association of non-HDL cholesterol with subclinical atherosclerosis in HIV-positive patients

Badiou

Thiébaut

Aurillac-Lavignolle

et al. 2008

Journal of Infection

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“…33 VLDL and chylomicrons are overproduced in insulin-resistant subjects compared with healthy controls, 6,7,[43][44][45][46] and this overproduction seems to result, in part, from decreased sensitivity to the acute inhibitory effect of insulin on Table 2 Mean presurgery (M0) and postsurgery evolution at 6 months (M6) and at 12 months (M12) of weight, BMI, insulin resistance, adiponectin, energy expenditure, and energy intake in the GBP and SG groups of obese subjects Table 4 Mean presurgery (M0) and postsurgery evolution at 6 months (M6) and at 12 months (M12) of apoC-II and apoC-III in HDL and non-HDL fractions in the GBP and SG groups of obese subjects VLDL and chylomicron secretion. 5 Moreover, reduced activity of LPL has been shown in insulin-resistant subjects compared with control subjects in fasting and postprandial states. 47,48 This reduction in lipolytic activity seems also to be related to insulin resistance, insulin being a potent activator of LPL.…”

Section: Discussionmentioning

confidence: 99%

“…This typical dyslipidemia of obese, insulin-resistant individuals is characterized by a quartet of abnormalities: hypertriglyceridemia, reduction in high-density lipoprotein cholesterol (HDL-C), increase of small and dense low-density lipoprotein (LDL) and postprandial hyperlipidemia. 5 The pathophysiology of this dyslipidemia is widely explained by the blood accumulation of triglyceride-rich lipoproteins (TRL) from liver (very-low-density lipoprotein [VLDL]) and intestine (chylomicrons) origin. This accumulation has been attributed to the overproduction of both VLDL 6 and chylomicrons 7 and to a defective TRL removal process because of a number of associated mechanisms: reduction of lipoprotein lipase (LPL) activity, 8 changes in the apolipoprotein composition of TRL 9 impairing particle clearance, and defect in the hepatic uptake of TRL and their remnants.…”

Section: Introductionmentioning

confidence: 99%

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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“…Because we studied a middle-aged population, all subjects were likely to present moderate insulin resistance, which was illustrated by a slightly elevated HOMA score. Insulin resistant states have been extensively shown to be associated with increased hepatic and intestinal TRL secretion resulting in hypertriglyceridemia, concomitant increase in apoB and reduction in plasma levels of HDL cholesterol [2,10]. They are generally associated with high amplitude of postprandial lipemia [1,17].…”

Section: Discussionmentioning

confidence: 99%

APOB-516 T allele homozygous subjects are unresponsive to dietary changes in a three-month primary intervention study targeted to reduce fat intake

Hammoud¹,

Gastaldi²,

Maillot³

et al. 2009

Genes Nutr

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Dietary guidelines aim to control fat intake and reduce cardiovascular risk but an important interindividual variability occurs among subjects. The objective was to investigate whether the response of lipid and glucose homeostasis parameters after a three-month diet aimed at reducing cardiovascular risk could be modulated by the -516C/T polymorphism in the apolipoprotein B gene (APOB). Middle-aged men (n = 69) and women (n = 100) with moderate cardiovascular disease risk were advised to reduce total energy and fat intakes and replace saturated dietary fat by monounsaturated and polyunsaturated fat. Subjects were genotyped for APOB-516C/T polymorphism. At the entry and at the end of the three-month period, fasting and postprandial plasma lipid analyses were performed. At entry, subjects homozygous for the APOB-516 T allele exhibited significantly lower fasting plasma concentrations of apolipoprotein B 48, triglycerides and triglyceride-rich lipoproteins-triglycerides compared to C carrier subjects. After the diet period, while C carrier subjects presented a clear improvement of most biological parameters, paradoxically T/T subjects did not modify them. In addition, the apoB 48 postprandial response after a standardized mixed test meal was not improved in T/T subjects after the threemonth diet, contrary to C allele carriers. Even though their phenotype at entry does not show any significant increase of risk factors when compared to other groups, subjects homozygous for the APOB-516 T allele are unresponsive to a healthy diet that improves cardiovascular risk status in the whole population.

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Lipid and lipoprotein dysregulation in insulin resistant states

Cited by 268 publications

References 232 publications

Association of non-HDL cholesterol with subclinical atherosclerosis in HIV-positive patients

Association of non-HDL cholesterol with subclinical atherosclerosis in HIV-positive patients

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

APOB-516 T allele homozygous subjects are unresponsive to dietary changes in a three-month primary intervention study targeted to reduce fat intake

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