妊娠期糖尿病营养治疗进展

妊娠期糖尿病(GDM)营养治疗主要通过评估患者个人情况后制订合适的能量摄入计划,如限制糖类的摄入量,通过血糖指数/血糖负荷理论配合食品交换份法来搭配食物。科学搭配膳食三大营养素可为孕妇提供最佳的营养,促进适当的孕期体质量增加,达到理想的血糖控制水平,为胎儿正常生长发育提供足够的能量。该文就GDM营养治疗的基本治疗和最新进展进行综述。     

A high n-6 polyunsaturated fatty acid diet reduces muscarinic M2/M4 receptor binding in the rat brain

The aim of this study was to examine the influence of different fat diets on muscarinic acetylcholine receptor binding. Nineteen male Sprague–Dawley rats were divided into four groups and fed a diet of either high saturated fat, n-6 polyunsaturated fatty acid (PUFA), n-3 PUFA or low fat (control) for 8 weeks. Using quantitative autoradiography, [³H]pirenzepine binding to muscarinic M1/M4 receptors and [³H]AF-DX384 binding to M2/M4 receptors were measured throughout the brain in all four groups. The main findings were that compared to the low fat control group, M2/M4 receptor binding was significantly reduced in the dorsolateral, dorsomedial and ventromedial parts of the caudate putamen (61–64%, p < 0.05), anterior cingulate cortex (59%, p < 0.01), dentate gyrus and CA1–3 fields of the hippocampus (32–43%, p < 0.01) of rats on a high n-6 PUFA diet; however, no differences in M1/M4 receptor binding densities between the four groups were observed. These results suggest that a diet high in n-6 PUFA, but not of n-3 PUFAs or saturated fat, may selectively alter M2/M4 receptor-mediated signal transduction in the rat brain.     

Changes in the amounts of myelin lipids and molecular species of plasmalogen PE in the brain of an autopsy case with D-bifunctional protein deficiency

Changes in the molecular species of lipids associated with peroxisomal d-bifunctional protein (d-BP) deficiency were investigated in cerebral tissues to elucidate the pathological mechanisms underlying this disorder. Total phospholipids in the gray and white matters of the patient's brain were decreased to approximately 73% and 50% of control levels, respectively, and profound declines in myelin lipids, i.e. galactosyl ceramide and sulfatides, indicated dysmyelination in our patient with d-BP deficiency. Although the total ganglioside amounts in the gray and white matter of this patient's brain were also decreased to 61% and 37% of control levels and GM1 in the white matter was 20% of the control level, the relative amounts of GM2 in both the gray and the white matter of this patient's brain were increased in comparison to those in the control, indicating altered metabolism of gangliosides. In addition, among molecular species of phospholipids, plasmalogen-type and polyunsaturated fatty acid-containing phosphatidylethanolamine were characteristically decreased in the patient's gray matter. These alterations in the molecular species of brain lipids may affect sensitivity to oxidative stress and the membrane fluidity of neural cells, thereby producing the brain pathology of d-BP deficiency.     

ω-3多不饱和脂肪酸对免疫细胞功能的影响

ω-3多不饱和脂肪酸(PUFAs)是重要的营养组成成分.研究发现,ω-3多不饱和脂肪酸对风湿性关节炎、克隆病等自体免疫性疾病有较好的治疗作用.ω-3多不饱和脂肪酸对于机体免疫系统的影响越来越受到重视.近年来,已有大量文献报道.该作者重点总结了ω-3多不饱和脂肪酸对机体各种免疫细胞如T淋巴细胞,中性粒细胞,自然杀伤细胞及单核巨噬细胞的影响,并探讨了PUFAs对各种免疫细胞抑制的可能机制.这些机制包括PUFAs对细胞膜脂质成分的改变、对细胞内信号转导通路及基因表达的影响、对细胞凋亡的诱导以及对类花生酸类物质代谢的影响等,同时对其在炎症性疾病和器官移植中的应用进行了总结和展望.     

多不饱和二十二碳六烯酸对白细胞介素-2α受体的抑制作用

目的：研究多不饱和二十二碳六烯酸(DHA)可通过改变IL-2a受体在细胞膜亚区域的分布和免疫抑制调节。方法：用DHA(22：6)处理Jurkat E6-1T细胞，硬脂酸(18：0)处理作为阴性对照。应用流式细胞仪检测DHA对T细胞表面分子CD25(IL-2Ra)表达的抑制作用。超速离心分离T细胞膜脂肪微区域，应用蛋白印迹法分析检测IL-2Ra所在的T细胞膜亚区域组分，与硬脂酸处理相比较，分析DHA处理对T细胞膜不同亚区域IL-2Ra分布的影响。结果：流式细胞仪检测表明，对照组75umol／L硬脂酸处理，检测到细胞表面CD25阳性表达细胞率为40．14％，75umol／LDHA处理T细胞，细胞表面CD25阳性表达细胞率为19．28％，DHA可抑制T细胞表面分子CD25的表达。蛋白印迹法分析确定IL-2Ra存在于rafts组分中，DHA处理使部分IL-2Ra从膜rafts区域移位到可溶膜区域。结论：膜脂肪微区域为IL-2受体信号转导的功能性亚区域，DHA通过调节IL-2Ra在膜脂肪微区域的分布，使部分IL-2Ra从功能性rafts区域移位到非功能性可溶膜区域，而产生免疫抑制作用。     

ω-3长链多不饱和脂肪酸对培养的少突胶质前体细胞的影响

目的 探讨长链多不饱和脂肪酸(LPFA)对体外培养的成年海马少突胶质前体细胞(OPC)的存活及突起生长影响.方法 采用成组设计,使用从成年大鼠海马分离培养的两种神经祖细胞,分别经花生四烯酸(AA)、二十碳五烯酸(EPA)或二十二碳六烯酸(DHA)处理后,以乳酸脱氢酶(LDH)分析法测定细胞活性;再行免疫细胞荧光染色后做突起的定量测量.结果 EPA、DHA和AA在高浓度(50 μmol/L)时使海马硫酸软骨素蛋白聚糖(NG2)阳性OPC数虽显著增加(P<0.05),而EPA和DHA还可使OPC突起长度显著增长(P<0.05).结论 ω-3LPFA即EPA和DHA对OPC的增生和突起形成有促进作用.     

Altered lipid composition in cortical lipid rafts occurs at early stages of sporadic Alzheimer's disease and facilitates APP/BACE1 interactions

The presence of lipid alterations in lipid rafts from the frontal cortex in late stages of Alzheimer's disease (AD) has been recently demonstrated. Here, we have isolated and analyzed the lipid composition of lipid rafts from different brain areas from control and AD subjects at initial neuropathologic stages. We have observed that frontal cortex lipid rafts are profoundly altered in AD brains from the earliest stages of AD, namely AD I/II. These changes in the lipid matrix of lipid rafts affected both lipid classes and fatty acids and were also detected in the entorhinal cortex, but not in the cerebellum from the same subjects. Paralleling these changes, lipid rafts from AD frontal and entorhinal cortices displayed higher anisotropy for environment-sensitive probes, indicating that lipid changes in AD lipid rafts increased membrane order and viscosity in these domains. The pathophysiological consequences of these alterations in the development and progression of AD were strengthened by the significant, and specific, accumulation of β-secretase within the lipid rafts of AD subjects even at the earliest stages. Our results provide a mechanistic connection between lipid alterations in these microdomains and amyloidogenic processing of amyloid precursor protein.     

A metabolic link between S-adenosylhomocysteine and polyunsaturated fatty acid metabolism in Alzheimer's disease

There is evidence that vascular risk factors contribute to the pathology of Alzheimer's disease. Increased concentrations of circulating homocysteine are associated with vascular risk factors and Alzheimer's disease but the mechanisms involved are unclear. Homocysteine inhibits the hydrolysis of S-adenosylhomocysteine (SAH) which is a product inhibitor of S-adenosylmethionine (SAM) dependent methyltransferase reactions. It has been shown previously that SAH inhibits phosphatidylethanolamine N-methyltransferase (PEMT) in the liver. The activity of PEMT in the liver plays an important role in the methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) and the delivery of essential polyunsaturated fatty acids (PUFAs) to peripheral tissues. In the present study, the plasma concentrations of SAH, SAM and homocysteine and the erythrocyte composition of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and their respective polyunsaturated fatty acid concentrations were determined in 26 patients with Alzheimer's disease and compared to those in 29 healthy control subjects. There was a significant increase in the plasma concentrations of SAH (p < 0.001) and homocysteine (p < 0.001) and a significant increase in the plasma concentrations of SAM (p < 0.001) in the Alzheimer's patients. A significant positive correlation was found between the plasma concentrations of SAH and homocysteine (r = 0.738, p < 0.001). There was a negative correlation between the plasma concentrations of homocysteine and the ratio of SAM/SAH (r = −0.637, p < 0.01). There was a significant decrease in the erythrocyte content of PC (p < 0.001) and an increase in the erythrocyte content of PE (p < 0.001) in the Alzheimer's patients. Plasma SAH concentrations were negatively related to erythrocyte PC concentrations (r = −0.286, p < 0.01) and positively related to erythrocyte PE concentrations (r = 0.429, p < 0.001). The erythrocyte PC from Alzheimer's patients had a significant depletion of docosahexaenoic acid (DHA) (p < 0.001) while there was no significant difference in the DHA content of erythrocyte PE. There was a significant negative correlation between plasma SAH and the DHA composition of erythrocyte PC (r = −0.271, p < 0.001). This data may reflect the inhibition of hepatic PEMT activity by SAH in Alzheimer's disease. The decreased mobilization of DHA from the liver into plasma and peripheral tissues may increases the risk of atherosclerosis and stroke leading to chronic cerebral hypoperfusion. The evidence suggests that a metabolic link between the increased production of SAH and phospholipid metabolism may contribute to cerebrovascular and neurodegenerative changes in Alzheimer's disease.