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脂肪萎缩性糖尿病的代谢研究:高血糖机制及脂质代谢胰岛素抵抗证据

Metabolic studies in lipoatrophic diabetes: mechanism of hyperglycemia and evidence of resistance to insulin of lipid metabolism.

作者信息

Beylot M, Sautot G, Laville M, Cohen R

机构信息

INSERM U.197, Faculté de Médecine Alexis Carrel, Lyon, France.

出版信息

Diabete Metab. 1988 Jan-Feb;14(1):20-4.

PMID:3292304
Abstract

We determined in 5 control subjects and in one patient with total congenital lipoatrophy (LA) the effect of insulin infusion on glucose flux and some aspects of lipid metabolism. In the post-absorptive state LA had moderate hyperglycemia (9.2 versus 3.80 +/- 0.07 mmol.l-1) and hyperinsulinemia (19 vs 12 +/- 3 mU.l-1) and a massive increase in glucose production (7.51 mg.kg.-1.min-1) and disappearance (7.40 mg.kg-1.min-1) rates (control subjects: 2.29 +/- 0.14 mg.kg-1 min-1). Raising peripheral insulin levels to 28 +/- 3 mU.l-1 suppressed endogenous glucose production in the control subjects whereas in LA significant (2.01 mg.kg-1.min-1) production persisted even when peripheral insulinemia was raised to 58 mU.l-1. Insulin infusion in control subjects increased progressively glucose utilization to a final value of 15.7 +/- 0.7 mg.kg-1.min-1 (corresponding plasma insulin: 482 +/- 44 mU.l-1). Insulin infusion in LA initially lowered glucose level near to normal values and exogenous glucose was infused for an insulin infusion rate of 10 mU.kg-1.min-1; at this insulin infusion rate glucose utilization rate (6.52 mg.kg-1.min-1) was decreased relative to control subjects in spite of higher insulin levels (750 mU.l-1). NEFA, glycerol and ketone bodies (KB) levels were decreased to undetectable levels by insulin infusion in the normal subjects whereas NEFA and glycerol were decreased only in part and KB were not modified in LA. In addition glycerol and KB appearance rates determined in LA were not suppressed by insulin infusion as expected.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们测定了5名对照受试者以及1名完全性先天性脂肪萎缩症(LA)患者中胰岛素输注对葡萄糖通量及脂质代谢某些方面的影响。在吸收后状态下,LA患者存在中度高血糖(9.2 mmol/l,而对照受试者为3.80±0.07 mmol/l)和高胰岛素血症(19 mU/l,而对照受试者为12±3 mU/l),且葡萄糖生成(7.51 mg·kg⁻¹·min⁻¹)和消失(7.40 mg·kg⁻¹·min⁻¹)速率大幅增加(对照受试者:2.29±0.14 mg·kg⁻¹·min⁻¹)。将外周胰岛素水平提高至28±3 mU/l可抑制对照受试者内源性葡萄糖生成,而在LA患者中,即使外周胰岛素血症升至58 mU/l,仍有显著的(2.01 mg·kg⁻¹·min⁻¹)葡萄糖生成。对照受试者中胰岛素输注使葡萄糖利用率逐渐增加至最终值15.7±0.7 mg·kg⁻¹·min⁻¹(相应血浆胰岛素:482±44 mU/l)。LA患者中胰岛素输注最初使血糖水平降至接近正常范围,并以10 mU·kg⁻¹·min⁻¹的胰岛素输注速率输注外源性葡萄糖;在此胰岛素输注速率下,尽管胰岛素水平较高(750 mU/l),但相对于对照受试者,葡萄糖利用率(6.52 mg·kg⁻¹·min⁻¹)仍降低。正常受试者中胰岛素输注使非酯化脂肪酸(NEFA)、甘油和酮体(KB)水平降至无法检测的水平,而在LA患者中,NEFA和甘油仅部分降低,KB未发生改变。此外,LA患者中测定的甘油和KB出现速率并未如预期那样被胰岛素输注所抑制。(摘要截选至250词)

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