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Titolo:
Hyperlipidaemia is associated with increased insulin-mediated glucose metabolism, reduced fatty acid metabolism and normal blood pressure in transgenic mice overexpressing human apolipoprotein C1
Autore:
Koopmans, SJ; Jong, MC; Que, I; Dahlmans, VEH; Pijl, H; Radder, JK; Frolich, M; Havekes, LM;
Indirizzi:
TNO Anim Nutr, ID, Inst Anim Sci & Hlth, NL-8200 AB Lelystad, Netherlands TNO Anim Nutr Lelystad Netherlands NL-8200 AB 0 AB Lelystad, Netherlands TNO Prevent & Hlth, Gaubius Lab, Leiden, Netherlands TNO Prevent & Hlth Leiden Netherlands Gaubius Lab, Leiden, Netherlands Leiden Univ, Med Ctr, Dept Endocrinol, Leiden, Netherlands Leiden Univ Leiden Netherlands tr, Dept Endocrinol, Leiden, Netherlands Leiden Univ, Med Ctr, Dept Internal Med, Leiden, Netherlands Leiden Univ Leiden Netherlands , Dept Internal Med, Leiden, Netherlands Leiden Univ, Med Ctr, Dept Clin Chem, Leiden, Netherlands Leiden Univ Leiden Netherlands Ctr, Dept Clin Chem, Leiden, Netherlands Leiden Univ, Med Ctr, Dept Internal Med & Cardiol, Leiden, Netherlands Leiden Univ Leiden Netherlands ernal Med & Cardiol, Leiden, Netherlands
Titolo Testata:
DIABETOLOGIA
fascicolo: 4, volume: 44, anno: 2001,
pagine: 437 - 443
SICI:
0012-186X(200104)44:4<437:HIAWII>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
DENSITY-LIPOPROTEIN RECEPTOR; CONSCIOUS NORMAL RATS; PLASMA-LIPOPROTEINS; HEPATIC-UPTAKE; RESISTANCE; HYPERINSULINEMIA; HYPERTENSION; DISEASE; GENE; HYPERTRIGLYCERIDEMIA;
Keywords:
hyperlipidaemia; APOC1; insulin resistance; insulin resistance syndrome; glucose; NEFA; triglycerides; cholesterol; lipoprotein; hypertension;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Koopmans, SJ TNO Anim Nutr, ID, Inst Anim Sci & Hlth, POB 65, NL-8200 AB Lelystad, Netherlands TNO Anim Nutr POB 65 Lelystad Netherlands NL-8200 AB erlands
Citazione:
S.J. Koopmans et al., "Hyperlipidaemia is associated with increased insulin-mediated glucose metabolism, reduced fatty acid metabolism and normal blood pressure in transgenic mice overexpressing human apolipoprotein C1", DIABETOLOG, 44(4), 2001, pp. 437-443

Abstract

Aims/hypothesis. Insulin resistance for glucose metabolism is associated with hyperlipidaemia and high blood pressure. In this study we investigated the effect of primary hyperlipidaemia on basal and insulin-mediated glucoseand on non-esterified fatty acid (NEFA) metabolism and mean arterial pressure in hyperlipidaemic transgenic mice overexpressing apolipoprotein C1 (APOC1). Previous studies have shown that APOC1 transgenic mice develop hyperlipidaemia primarily because of an impaired hepatic uptake of very low density lipoprotein (VLDL). Methods. Basal and hyperinsulinaemic (6 mU . kg(-1) . min(-1)), euglycaemic (7 mmol/l) clamps with 3-H-3-glucose or 9,10-H-3-palmitic acid infusions and in situ freeze clamped tissue collection were carried out. Results. The APOC1 mice showed increased basal plasma cholesterol, triglyceride, NEFA and decreased glucose concentrations compared with wild-type mice (7.0 +/- 1.2 vs 1.6 +/- 0.1, 9.1 +/- 2.3 vs 0.6 +/- 0.1, 1.9 +/- 0.2 vs 0.9 +/- 0.1 and 7.0 +/- 1.0 vs 10.0 +/- 1.1 mmol/l, respectively, p < 0.05). Basal whole body glucose clearance was increased twofold in APOC1 mice compared with wild-type mice (18 +/- 2 vs 10 +/- 1 ml . kg(-1) . min(-1) p < 0.05). Insulin-mediated whole body glucose uptake, glycolysis (generation of (H2O)-H-3) and glucose storage increased in APOC1 mice compared with wildtype mice (339 +/- 28 vs 200 +/- 11; 183 +/- 39 vs 128 +/- 17 and 156 +/- 44 vs 72 +/- 17 mu mol . kg(-1) . min(-1), p < 0.05, respectively), corresponding with a twofold to threefold increase in skeletal muscle glycogenesis and de novo lipogenesis from 3-3H-glucose in skeletal muscle and adipose tissue (p<0.05). Basal whole body NEFA clearance was decreased threefold in APOC1 mice compared with wild-type mice (98 +/- 21 vs 314 +/- 88 ml . kg(-1). min(-1), p < 0.05), Insulin-mediated whole body NEFA uptake, NEFA oxidation (generation of (H2O)-H-3) and NEFA storage were lower in APOC1 mice than in wild-type mice (15 +/- 3 vs 33 +/- 6; 3 +/- 2 vs 11 +/- 4 and 12 +/- 2vs 22 +/- 4 <mu>mol . kg(-1) . min(-1), p < 0.05) in the face of higher plasma NEFA concentrations (1.3 +/- 0.3 vs 0.5 +/- 0.1 mmol/l, p < 0.05), respectively. Mean arterial pressure and heart rate were similar in APOC1 vs wild-type mice (82 +/- 4 vs 85 +/- 3 mm Hg and 459 +/- 14 vs 484 +/- 11 beats min(-1)). Conclusions/interpretation. 1) Hyperlipidaemic APOC1 mice show reduced NEFA and increased glucose metabolism under both basal and insulin-mediated conditions, suggesting an intrinsic defect in NEFA metabolism. Primary hyperlipidaemia alone in APOC1 mice does not lead to insulin resistance for glucose metabolism and high blood pressure.

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Documento generato il 23/01/20 alle ore 18:15:37