Lipodystrophic diabetes mellitus. Investigations of lipoprotein metabolism and the effects of omega-3 fatty acid administration in two patients.
Lipodystrophic diabetes mellitus. Investigations of lipoprotein metabolism and the effects of omega-3 fatty acid administration in two patients.
复制标题
脂肪营养不良型糖尿病。
DOI：
10.1016/0026-0495(88)90151-5
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Fisher,WR
中科院分区：
文献类型：
--
作者：
Stacpoole,PW;Alig,J;Kilgore,LL;Ayala,CM;Herbert,PN;Zech,LA;Fisher,WR
我们研究了omega-6对新陈代谢的影响（红花油）和欧米茄-3富含（鱼油）脂肪酸的饮食（65%碳水化合物，20%脂肪）在两名患者的综合征糖尿病，脂肪营养不良，黑棘皮病，乳糜微粒血症，腹痛。3 H-甘油被用来评估富含甘油三酯的脂蛋白-甘油三酯（TRLP-TG）代谢，并研究了葡萄糖和胰岛素动力学的变化。在omega-6饮食中，两名受试者都表现出TRLP-TG产生和甘油生物合成的正常速率的四至五倍，以及TRLP-TG和TRLP颗粒的部分分解代谢率（FCR）的显著下降。两例受试者的非酯化脂肪酸（NEFA）浓度均升高。在一名患者中，omega-3饮食显著降低血清甘油三酯和新合成的甘油三酯甘油的产生，与NEFA下降有关。在这两名受试者中，血浆甘油再利用用于甘油三酯合成，在omega-6饮食中正常，在omega-3方案中被废除。两种饲料的血浆肝素后脂解活性均正常。在omega-3饮食中，黄瘤和肝肿大减少，并且在血清甘油三酯没有减少的患者中，胰腺炎发作几乎停止。平均24小时血清葡萄糖水平更高，基础和峰值C-肽对碳水化合物餐的反应在omgea-3饮食中减弱。1例患者出现酮尿。我们得出结论，这些患者高甘油三酯血症的原因是由于脂质合成增加，并假设这是继发于高血浆NEFA浓度。此外，这些受试者的omega-3饮食抑制了胰岛素分泌并恶化了葡萄糖耐量。
We investigated the metabolic effects of omega-6 (safflower oil) and omega-3 (fish oil) fatty acid-enriched diets (65% carbohydrate, 20% fat) in two patients with a syndrome of diabetes mellitus, lipodystrophy, acanthosis nigricans, chylomicronemia, and abdominal pain.3H-glycerol was used to evaluate triglyceride-rich lipoprotein-triglyceride (TRLP-TG) metabolism, and changes in glucose and insulin dynamics were also studied. On the omega-6 diet, both subjects demonstrated four- to five-times normal rates of TRLP-TG production and glycerol biosynthesis, and striking decrements in the fractional catabolic rate (FCR) for TRLP-TG and TRLP-particles. Both subjects had elevations in nonesterified fatty acid (NEFA) concentrations. In one patient, the omega-3 diet markedly decreased serum triglycerides and newly synthesized triglyceride glycerol production, in association with a fall in NEFA. In both subjects, plasma glycerol reutilization for triglyceride synthesis, normal on the omega-6 diet, was abolished on the omega-3 regimen. Plasma postheparin lipolytic activity was normal on both diets. On the omega-3 diet, xanthomas and hepatomegaly decreased and, in the patient who had no reduction in serum triglycerides, pancreatitis attacks virtually ceased. Mean 24-hour serum glucose levels were higher, and both basal and peak C-peptide responses to a carbohydrate meal were blunted on the omgea-3 diet. One patient became ketonuric. We conclude the cause of hypertriglyceridemia in these patients was due to increased lipid synthesis and hypothesize that this is secondary to high plasma concentrations of NEFA. In addition, an omega-3 diet in these subjects inhibited insulin secretion and worsened glucose tolerance.