IMPAIRED GLUCOSE HANDLING IN ACTIVE RHEUMATOID-ARTHRITIS - RELATIONSHIP TO PERIPHERAL INSULIN RESISTANCE
IMPAIRED GLUCOSE HANDLING IN ACTIVE RHEUMATOID-ARTHRITIS - RELATIONSHIP TO PERIPHERAL INSULIN RESISTANCE
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DOI：
10.1016/s0026-0495(98)90005-1
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发表时间：
1988-02-01
影响因子：
9.8
通讯作者：
HALLGREN, R
中科院分区：
文献类型：
--
作者：
SVENSON, KLG;POLLARE, T;HALLGREN, R
对14例活动期类风湿性关节炎(RA)患者(n=14)进行静脉葡萄糖负荷后的葡萄糖代谢研究。与健康对照组相比，患者表现出更强的胰岛素反应和受损的葡萄糖处理能力(P<；.001)。胰岛素敏感性，以正常血糖(M)稳定状态下的葡萄糖利用率衡量，与对照组(5.5±-)相比显著降低(P<；.01)。1.9毫克/公斤体重/分钟[平均值+-]SD]和7.2.+-。分别为12个)。代谢清除率(MCR)的对应值为5.8±-。0.6毫升/公斤体重/分钟和8.2+-。0.4(P<；0.01)。在患者组，k值与外周胰岛素敏感性相关(P<；.01)，而外周胰岛素敏感性与急性时相反应呈负相关(P<；.05)。在糖皮质激素(泼尼松龙每天20 mg)有效抗炎治疗1周期间，K值改善(P<；.001)，胰岛素敏感性趋于改善，胰岛素应答增强(P<；.001)。对5例经磺胺嘧啶抗风湿治疗后病情缓解的患者进行复查。炎症活动以及葡萄糖处理和胰岛素敏感性均达到正常化。这些数据表明，活动期类风湿关节炎患者糖代谢受损与胰岛素抵抗有关。炎症指标和葡萄糖代谢之间的联系可能反映了炎症的一种特殊后果，但必须考虑非特异性疾病表现，如营养不良、缺乏活动和肌减少症的影响。此外，血浆C-肽浓度的测定和C-肽与胰岛素摩尔比的计算表明，活动期RA的高胰岛素血症部分是由于肝脏对胰岛素的提取受损所致。
Glucose metabolism was studied after an intravenous glucose loading in normal-weighted, previously untreated patients (n = 14) with active rheumatoid arthritis (RA). The patients displayed an enhanced insulin response and impaired glucose handling compared with healthy controls (P < .001). The insulin sensitivity, measured as the glucose utilization rate during steady state of euglycemia (M) was significantly decreased (P < .01) among the patients compared to the controls (5.5 .+-. 1.9 mg/kg BW/min [mean .+-. SD] and 7.2 .+-. 12, respectively). The corresponding values for the metabolic clearance rate (MCR) were 5.8 .+-. 0.6 mL/kg BW/min and 8.2 .+-. 0.4, respectively (P < .01). In the patient group the k value correlated with the peripheral insulin sensitivity (P < .01), which, in turn, was inversely related to the acute phase reaction (P < .05). During 1 week of potent anti-inflammatory treatment with corticosteroids (prednisolone 20 mg daily) the k value improved (P < .001), the insulin sensitivity tended to improve and the insulin response increased (P < .001) after an intravenous glucose loading. Five patients who had a remission of their disease on sulphasalazine was antirheumatic therapy were reexamined. A normalization of the inflammatory activity as well as the glucose handling and insulin sensitivity was achieved. The data obtained indicate that impaired glucose handling in active RA is related to insulin resistance. The linkage between inflammatory indices and glucose metabolism might reflect a special consequence of inflammation, but the influence of nonspecific disease manifestations, ie, malnutrition, inactivity, and myopenia, has to be considered. Furthermore, measurement of plasma C-peptide concentrations and the calculation of the C-peptide to insulin molar ratio suggested that the hyperinsulinemia in active RA was partly due to an impaired hepatic extraction of insulin.