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Duvillard L.,University of Burgundy | Dautin G.,University of Burgundy | Florentin E.,University of Burgundy | Florentin E.,Institute Federatif Of Recherche 100 | And 4 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2010

Context: Oral contraceptives with estrogen plus progestin are likely to influence apolipoprotein B (apoB)-containing lipoprotein metabolism by changing the expression of different enzymes or receptors that play a major role in this metabolism. However, the precise changes in apoB kinetic parameters induced by oral contraceptives that are now currently used are unknown. Objectives: We studied the impact of Moneva, containing 30 μg ethinylestradiol and 75 μg gestodene, on the apoB production rate and fractional catabolic rate of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL). Design: Using a 16-h [13C]leucine infusion, we performed an apoB kinetic study in nine normolipidemic women before and 3 months after beginning Moneva. Results: On Moneva, serum triglycerides increased moderately (+12%, P = 0.04) in the fed state, whereas serum LDL remained unchanged. LDL particles were richer in triglycerides in women on Moneva (7.5 ± 1.5 vs. 4.3 ± 1.0% of total LDL mass, P < 0.01). The apoB production rate of VLDL, IDL, and LDL increased by 49 (P=0.04), 55 (P=0.05), and51%(P=0.01), respectively. The fractional catabolic rate of apoB in LDL increased by 36% (P=0.04). Consequently, the serum LDL apoB pool size remained unchanged (26.49 ± 6.98 vs. 23.96 ± 5.37 mg/kg). Conclusion: Oral contraception with ethinylestradiol plus gestodene induces an increase in the production rate of apoB-containing lipoproteins all along the VLDL→IDL→LDL cascade. The increased production rate of apoB in LDL is counterbalanced by a higher fractional catabolic rate of apoB in LDL, thus precluding an increase in the concentration of atherogenic LDL particles. Copyright © 2010 by The Endocrine Society. Source


Duvillard L.,University of Burgundy | Duvillard L.,Institute Federatif Of Recherche 100 | Florentin E.,University of Burgundy | Florentin E.,Institute Federatif Of Recherche 100 | And 5 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2011

Objective: It is currently suggested that chronic hyperinsulinemia is a causal factor for the increased production rate of very-low-density lipoproteins (VLDL) associated with metabolic syndrome.However, the involvement of hyperinsulinemia independently of the other abnormalities also observed in metabolic syndrome has never been proven in humans. Design: We used patients with insulinoma showing hyperinsulinemia but no insulin resistance as a model and conducted an apolipoprotein B (apoB) kinetic study in seven patients with insulinoma, seven insulin-resistant (IR) obese patients, and 12 controls. Results: Insulinemia was higher in patients with insulinoma or IR than in controls both in the fasting state [2.4-fold (P = 0.039) and 3.1-fold (P = 0.003), respectively] and in the fed state [3.5-fold (P = 0.006) and 2.6-fold (P = 0.05), respectively]. Patients with insulinoma were not IR (steady state plasma glucose=80±46 mg/dl, a value lower than in IR subjects (231±75, P=0.0013). In the fed state, triglyceridemia and VLDL apoB pool size were higher in IR subjects compared with controls and patients with insulinoma [208 ± 56 vs. 89 ± 30 mg/dl (P < 0.0001) and 96 ± 42 mg/dl (P < 0.0001), respectively, for triglyceridemia and 3.56 ± 0.60 vs. 1.85 ± 0.88 mg/kg (P = 0.004) and 2.32±1.79 (P=0.052)mg/kg for VLDLapoBpool size].The production rate of VLDLapoBin subjects with insulinoma was not significantly different from that in controls (14.56 ± 7.43 vs. 16.40 ± 7.70 mg/kg · d) but was higher in IR subjects compared with these two groups [25.66 ± 12.84 mg/kg · d (P = 0.046 and 0.035, respectively)]. Conclusion: Chronic endogenous hyperinsulinemia is not directly responsible for any increase in the production rate of VLDL apoB in humans. Copyright © 2011 by The Endocrine Society. Source

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