胰岛素对重度肥胖患者葡萄糖和脂质代谢的调节作用
Insulin regulation of glucose and lipid metabolism in massive obesity.
作者信息
Del Prato S, Enzi G, Vigili de Kreutzenberg S, Lisato G, Riccio A, Maifreni L, Iori E, Zurlo F, Sergi G, Tiengo A
机构信息
Unit of Metabolic Diseases, University of Padova, Italy.
出版信息
Diabetologia. 1990 Apr;33(4):228-36. doi: 10.1007/BF00404801.
Eight obese patients and 12 normal individuals underwent a euglycaemic insulin clamp (20 and 40 mU m2-1.min-1) along with continuous infusion of 3-3H-glucose and 1-14C-palmitate and indirect calorimetry. Basal plasma glucose concentration (4.7 +/- 0.3 vs 4.4 +/- 0.2 mmol/l) was similar in the two groups, whereas hepatic glucose production was slightly higher in obese individuals (1.11 +/- 0.06 vs 0.84 +/- 0.05 mmol/min) in spite of higher plasma insulin levels (17 +/- 2 vs 6 +/- 1 mU/l; p less than 0.01). Insulin inhibition of hepatic glucose production was impaired in obese subjects. Glucose disposal by lean body mass was markedly reduced both at baseline (11.7 +/- 1.1 vs 15.6 +/- 0.6 mumol.kg-1.min-1; p less than 0.05) and during clamp (15.0 +/- 1.1 vs 34.4 +/- 2.8 and 26.7 +/- 3.9 vs 62.2 +/- 2.8 mumol.kg-1.min-1; p less than 0.01) Oxidative (12.2 +/- 1.1 vs 17.8 +/- 1 and 16.1 +/- 1.1 vs 51.1 +/- 1.7 mumol.kg-1.min-1; p less than 0.05-0.002) and non-oxidative glucose metabolism (3.9 +/- 1.1 vs 15.0 +/- 2.8 and 12.8 +/- 3.3 vs 38.2 +/- 2.2 mumol.kg-1.min-1; p less than 0.01-0.001) were impaired. Basal plasma concentrations of non-esterified fatty acids (635 +/- 75 vs 510 +/- 71 mumol/l) and blood glycerol (129 +/- 17 vs 56 +/- 5 mumol/l; p less than 0.01) were increased in obese patients.(ABSTRACT TRUNCATED AT 250 WORDS)
8名肥胖患者和12名正常个体接受了正常血糖胰岛素钳夹试验（20和40 mU m²⁻¹·min⁻¹），同时持续输注3-³H-葡萄糖和1-¹⁴C-棕榈酸，并进行间接测热法。两组的基础血浆葡萄糖浓度相似（4.7±0.3 vs 4.4±0.2 mmol/l），然而，尽管肥胖个体的血浆胰岛素水平较高（17±2 vs 6±1 mU/l；p<0.01），但其肝脏葡萄糖生成略高（1.11±0.06 vs 0.84±0.05 mmol/min）。肥胖受试者中胰岛素对肝脏葡萄糖生成的抑制作用受损。瘦体重的葡萄糖处置在基线时（11.7±1.1 vs 15.6±0.6 μmol·kg⁻¹·min⁻¹；p<0.05）和钳夹期间（15.0±1.1 vs 34.4±2.8以及26.7±3.9 vs 62.2±2.8 μmol·kg⁻¹·min⁻¹；p<0.01）均显著降低。氧化（12.2±1.1 vs 17.8±1以及16.1±1.1 vs 51.1±1.7 μmol·kg⁻¹·min⁻¹；p<0.05 - 0.002）和非氧化葡萄糖代谢（3.9±1.1 vs 15.0±2.8以及12.8±3.3 vs 38.2±2.2 μmol·kg⁻¹·min⁻¹；p<0.01 - 0.001）均受损。肥胖患者的基础血浆非酯化脂肪酸浓度（635±75 vs 510±71 μmol/l）和血甘油浓度（129±17 vs 56±5 μmol/l；p<0.01）升高。（摘要截选至250词）
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