Insulin regulation of free fatty acid kinetics in adult cystic fibrosis patients with impaired glucose tolerance.

Insulin regulation of free fatty acid kinetics in adult cystic fibrosis patients with impaired glucose tolerance.
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胰岛素对糖耐量受损成人囊性纤维化患者游离脂肪酸动力学的调节。

DOI:
10.1016/j.metabol.2004.06.015
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发表时间:
2004
期刊:
Metabolism: clinical and experimental
影响因子:
--
通讯作者:
Jensen,MichaelD
Jensen,MichaelD
中科院分区:
--
文献类型:
--
作者:
Moran,Antoinette;Basu,Rita;Milla,Carlos;Jensen,MichaelD

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囊性纤维化(CF)患者在抑制肝脏葡萄糖生成和蛋白水解方面存在胰岛素抵抗,但胰岛素对脂肪游离脂肪酸(FFA)释放的影响尚未研究。本文测定了11例糖耐量减低(IGT)的稳定型成人CF患者和9例正常对照者的[9,10 - 3 H]棕榈酸代谢动力学。基线血浆棕榈酸盐浓度[CF = 99 ± 13(中位数74,范围65 - 187);对照组= 88 ± 9(88,46至138)μmol/L,P = .9]和棕榈酸通量[CF = 114 ± 11(100,72至171);对照组= 105 ± 12(106,54至182)μmol/min,P = 0.9] CF患者和对照组之间无差异。然而,在将胰岛素输注至生理餐后水平的正葡萄糖钳夹期间,CF患者的棕榈酸盐浓度倾向于较高:CF = 18 ± 3(13,10至47)μ mol/L,对照= 12 ± 1(11,8至18)μmol/L,P = 0.08。高胰岛素血症期间较高的棕榈酸盐浓度似乎是由于脂肪组织棕榈酸盐释放的抑制减少,因为CF受试者的平均棕榈酸盐通量[32 ± 5(26,17至66)μmol/min]比对照组[24 ± 2(23,17至34)μmol/min]高33%,P = 0.20。与正常对照受试者相比,CF患者中胰岛素诱导的血浆棕榈酸酯浓度和流量抑制具有相当大的异质性。总之,在临床稳定的糖耐量低减的CF患者中观察到胰岛素抑制脂解的缺陷,类似于CF中氨基酸和葡萄糖代谢的缺陷。这种脂解的定量差异可能是胰岛素诱导的CF中肝脏葡萄糖产生抑制不足的原因,也可能是对能量需求增加的代谢适应。
Cystic fibrosis (CF) patients are insulin-resistant with regards to suppression of hepatic glucose production and proteolysis, but the effect of insulin on adipose free fatty acid (FFA) release has not been studied. [9,10-3H]palmitate kinetics were measured in 11 stable adult CF patients with impaired glucose tolerance (IGT) and 9 normal control subjects. Baseline plasma palmitate concentrations [CF = 99 ± 13 (median 74, range 65 to 187); control = 88 ± 9 (88, 46 to 138) μmol/L, P = .9] and palmitate flux [CF = 114 ± 11 (100, 72 to 171); control = 105 ± 12 (106, 54 to 182) μmol/min, P = 0.9] were not different between CF patients and controls. During a euglycemic clamp with infusion of insulin to physiologic postprandial levels, however, palmitate concentrations tended to be higher in CF patients: CF = 18 ± 3 (13, 10 to 47), control = 12 ± 1 (11, 8 to 18) μmol/L, P = 0.08. The higher palmitate concentrations during hyperinsulinemia appeared to be due to reduced suppression of adipose tissue palmitate release, because mean palmitate flux was 33% greater in CF subjects [32 ± 5 (26, 17 to 66) μmol/min] than controls: [24 ± 2 (23, 17 to 34) μmol/min], P = .20. There was considerably greater heterogeneity in insulin-induced suppression of plasma palmitate concentration and flux in CF patients compared to normal control subjects. In summary, a defect in insulin suppression of lipolysis was seen in clinically stable CF patients with IGT, similar to what has been described in CF for amino acid and glucose metabolism. This quantitative difference in lipolysis may account for inadequate insulin-induced suppression of hepatic glucose production in CF, and may be a metabolic adaptation to increased energy needs.
DOI: 10.1172/jci113733
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DOI: 10.1007/bf00261698
发表时间: 1980
期刊: Diabetologia
影响因子: 8.2
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DOI: --
发表时间: 1992
期刊: Nutrition (Burbank, Los Angeles County, Calif.)
影响因子: --
作者:
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