脂肪因子与餐后高血糖的研究进展

近年研究发现,脂肪组织是具有内分泌功能的器官。它分泌瘦素、脂联素、肿瘤坏死因子-α、抵抗素、内脂素等脂肪因子。这些细胞因子可能通过参与炎性反应与物质能量的代谢过程,影响胰岛素的生物学效应,影响餐后血糖水平。本文就近年来一些较多关注的脂肪因子与餐后高血糖关系作一综述,为临床控制餐后高血糖,从而降低心血管事件、预防代谢综合征提供依据。     

脂肪因子与妊娠期糖尿病相关性研究进展

妊娠期糖尿病是由多种病因引起的内分泌代谢疾病,可引起糖、蛋白质、脂质代谢紊乱,可导致严重的母婴并发症。脂肪因子能通过介导一系列的信号转导通路,广泛参与机体复杂的代谢平衡网络的调节。近年来的研究表明,脂肪因子广泛参与肥胖、2型糖尿病、高血压病等一系列代谢相关性疾病的病理生理过程,其中趋化素、脂联素、抵抗素、内脂素作为脂肪因子,参与2型糖尿病的发生,与胰岛素抵抗相关。通过对脂肪因子的特性探讨,提示孕期监测脂肪因子的变化对预测及干预妊娠期糖尿病具有重要意义。     

内脂素与内皮功能紊乱

内脂素是一种来源于内脏脂肪的新脂肪因子,它可能在心脑血管疾病、糖尿病、代谢综合征和肾脏疾病等动脉粥样硬化性疾病中发挥重要作用。内皮细胞损伤是动脉粥样硬化病灶形成的始动环节。近年来大量研究证实内脂素对血管内皮功能的影响非常复杂,且可能与炎症、氧化应激或血脂紊乱等机制有关。     

急性脑梗死患者餐后高血糖的临床意义（附49例报告）

目的探讨餐后高血糖对急性期脑梗死患者病情严重程度及预后的影响。方法检测202例急性期脑梗死患者的餐后血糖,将所有患者分为餐后高血糖组和餐后血糖正常组,分别对两组患者的神经功能康复状况进行跟踪观察。采用多元统计方法分析餐后高血糖对终点事件的影响。结果餐后高血糖组患者4、12、24周的NIHSS评分均高于餐后正常血糖组,差异均有统计学意义（P〈0．01）。餐后高血糖组患者死亡和再发缺血性血管病变的风险均高于正常血糖组（x2=11．75,24．35,P〈0．01）。结论餐后血糖升高对脑梗死的预后有重要影响,是预后不良及病情复发的重要因素。     

小儿糖尿病如何治疗

小儿糖尿病是由于胰岛素分泌不足所引起的内分泌代谢疾病,以碳水化合物、蛋白质及脂肪代谢紊乱为主,引起空腹及餐后高血糖及尿糖。儿童一旦发生糖尿病将严重影响其身心健康发展,那么,什么是小儿糖尿病?小儿糖尿病有哪些临床表现?小儿糖尿病应如何治疗?本文帮助您了解小儿糖尿病的相关知识,以早期发现小儿糖尿病症状,及时诊断和治疗,避免其对儿童未来健康成长造成较大影响。     

空腹和餐后高血糖在治疗上有何不同

2型糖尿病的发病过程,往往是先有餐后高血糖,而后发展成糖尿病的。这一过程大约需5年时间。多数学者认为,餐后高血糖比空腹高血糖更重要,因为它是引发慢性并发症的重要原因。空腹血糖是指食物消化吸收后,经过机体代谢10小时以上的血糖水平。空     

2型糖尿病患者的体重指数和血糖、血脂水平与脂联素水平的相关性

<正>近年来研究表明,脂肪组织合成和分泌脂肪因子的调节紊乱是2型糖尿病(DM2)的危险因素。脂肪组织是合成肥胖基因的场所,能分泌多种脂肪因子,如脂联素(APN)等。APN具有增加胰岛素敏感性,抗高血糖,抗免疫等多种效用,与糖尿病有密切关系[1]。而人体的APN水平又受诸多因素影响,本文就体重指数、血糖、血脂水平与APN水平的相关性做初步分析。     

浅谈餐后高血糖对心血管疾病的影响

目的：分析餐后高血糖对心血管疾病产生的影响,探讨相关防治措施。方法：随机抽取笔者所在医院内科2006年3月-2010年9月接诊的心血管疾病患者86例,进行餐前和餐后血糖检测,观察餐后血糖对心血管疾病发生率的影响。结果：餐后高血糖患者心血管疾病发生率明显高于空腹患者（P〈0.01）。结论：餐后高血糖对心血管疾病的产生有着密切影响,要给予足够重视。     

脂肪因子对睾丸雄激素生成的调节作用

脂肪组织合成和分泌多种脂肪因子(adipokines),通过神经内分泌或直接作用于睾丸来调节生殖系统功能,在睾丸组织已发现多种脂肪因子的受体。瘦素(leptin)在下丘脑-垂体-性腺轴各个层面影响睾丸发育成熟、雄激素合成以及生精功能;脂联素(adiponectin)受体在睾丸组织表达,脂联素影响间质细胞的激素合成,还通过抗炎作用保护间质细胞;同样,抵抗素(resistin)和趋化素(chemerin)也参与调节睾酮合成。肥胖可导致脂肪因子分泌的改变,从而引起胰岛素敏感性下降、慢性炎症、血管病变等代谢相关的改变,也是导致雄激素下降、男性不育的原因之一。     

代谢综合征的肾脏损害相关作用研究

目的 探讨代谢综合征中各组成因子与及慢性肾病的相关性.方法 选择我院2008年1月～2010年1月期间收治的代谢综合症患者,对其各项因子与慢性肾病进行相关性分析.结果 各组代谢综合征的影响因子相互伴发均对慢性肾病具有一定的影响(p<0.05),而在各类代谢综合征的影响因素中,高血糖合并高血压患慢性肾病的风险性最大,OR值为3.17.同样,代谢综合征中因子越多的患者,其慢性肾病患病率越高,彼此呈等量递增关系.结论 代谢综合征中的各组成因素均对慢性肾病具有一定的影响,其中高血压合并高血糖的影响最大.     

Nutrition and health--carbohydrates, the risks to health from the postprandial glycaemic response and the possibilities for its manipulation

Carbohydrates are the most important source of food-derived energy. The metabolic effects of different types of carbohydrate can vary considerably, partially due to differences in glucose and insulin response. Several studies indicate that postprandial hyperglycaemia is associated with an increased risk of cardiovascular disease in patients with diabetes mellitus. For these patients, and possibly also for individuals with impaired glucose tolerance as well as for the healthy population at large, it may be of benefit to prevent postprandial hyperglycaemia. In order to manipulate the postprandial glycaemic response, an understanding of the underlying mechanisms of this response is crucial. The postprandial blood glucose level is influenced by a number of factors, such as the amount and type of ingested carbohydrates, gastric emptying rate and digestion and secretion of gastrointestinal and other hormones. Different approaches can be chosen to prevent postprandial hyperglycaemia, including changes in the diet and the use of drugs that delay gastric emptying or digestion of carbohydrates. The administration of gastrointestinal hormones or manipulation of the secretion of these hormones, are also possibilities. Investigating the regulation of the postprandial blood-glucose concentration and its possible manipulation could result in new approaches to preventing postprandial hyperglycaemia.     

Clinical significance of blood glucose levels in the pathogenesis of (atherosclerotic) macroangiopathy

Numerous authors suggested postprandial blood glucose elevation as a significant contributor in development of macroangiopathy. Epidemiological studies and animal experiments delivered supportive data about causal relationship between postprandial hyperglycaemia and macroangiopathy in type 2 diabetes. Interestingly there is no chronological correlation between presence of hyperglycaemia and development of macroangiopathy neither in type 2, nor in type 1 diabetics. Strict metabolic control does not result in slowing progression of macroangiopathy (glucose paradox). Premature macroangiopathy documented in the prediabetes phase of type 2 diabetes is strongly related to presence of insulin resistance, hyperinsulinaemia, high blood pressure, and dyslipidaemia; development of atherosclerosis in advanced stage of type 1 diabetes is also rather associated with presence of high blood pressure and dyslipidaemia but not that of hyperglycaemia. With regard to role of postprandial hyperglycaemia it should be emphasized, that not the postprandial blood glucose elevation per se, but rather the postprandial complex metabolic cluster (hyperinsulinaemia, hypertrygliceriadaemia, etc) is supposed to be related with development of macroangiopathy in patients with metabolic syndrome and type 2 diabetes.     

Coffee polyphenols modulate whole-body substrate oxidation and suppress postprandial hyperglycaemia, hyperinsulinaemia and hyperlipidaemia

Postprandial energy metabolism, including postprandial hyperglycaemia, hyperinsulinaemia and hyperlipidaemia, is related to the risk for developing obesity and CVD. In the present study, we examined the effects of polyphenols purified from coffee (coffee polyphenols (CPP)) on postprandial carbohydrate and lipid metabolism, and whole-body substrate oxidation in C57BL/6J mice. In mice that co-ingested CPP with a lipid-carbohydrate (sucrose or starch)-mixed emulsion, the respiratory quotient determined by indirect calorimetry was significantly lower than that in control mice, whereas there was no difference in VO2 (energy expenditure), indicating that CPP modulates postprandial energy partitioning. CPP also suppressed postprandial increases in plasma glucose, insulin, glucose-dependent insulinotropic polypeptide and TAG levels. Inhibition experiments on digestive enzymes revealed that CPP inhibits maltase and sucrase, and, to a lesser extent, pancreatic lipase in a concentration-dependent manner. Among the nine kinds of polyphenols (caffeoyl quinic acids (CQA), di-CQA, feruloyl quinic acids (FQA)) contained in CPP, di-CQA showed more potent inhibitory activity than CQA or FQA on these digestive enzymes, suggesting a predominant role of di-CQA in the regulation of postprandial energy metabolism. These results suggest that CPP modulates whole-body substrate oxidation by suppressing postprandial hyperglycaemia and hyperinsulinaemia, and these effects are mediated by inhibiting digestive enzymes.     

干部人群中餐后高血糖的检出率及其影响因素分析

[目的]了解柳州市干部人群中餐后高血糖的检出情况,探讨其主要影响因素,为干部人群心血管疾病的预防控制提供依据.[方法]对柳州市713名干部测量身高、体质量、腰围(WC)、血压,计算体质量指数(BMI),同时检测空服血糖(FBG)、餐后2h血糖(2hPBG)、血总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)等指标,并进行统计学分析.[结果]餐后高血糖的总检出率达34.9%,其中糖耐量低减(IGT)和糖尿病(DM)的检出率分别为21.0%和13.9%.男性IGT、女性DM检出率均随年龄增高而增高(P＜0.05).随着餐后血糖水平的增高,年龄、BMI、WC、收缩压(SBP)、舒张压(DBP)、TG的平均水平均升高,而HDL-C水平则降低(P＜0.01).2hPBG与WC、年龄、TG、DBP呈正相关(P＜0.001).IGT、DM的检出率均随着BMI、WC的增大而增高(P＜0.001).[结论]本组干部人群中餐后高血糖检出率已达到较高水平,其主要影响因素为年龄、腹型肥胖、高血压、高TG.     

Liquorice flavonoid oil suppresses hyperglycaemia accompanied by skeletal muscle myocellular GLUT4 recruitment to the plasma membrane in KK-Ay mice

For over 4000 years, liquorice has been one of the most frequently employed botanicals as a traditional herbal medicine. Although previous reports have found that liquorice flavonoids possess various health beneficial effects, the underlying mechanism responsible for the anti-diabetic effect of liquorice flavonoids remains unclear. The present study demonstrates that liquorice flavonoid oil (LFO) improves type 2 diabetes mellitus through GLUT4 translocation to the plasma membrane by activating both the adenosine monophosphate-activated protein kinase (AMPK) pathway and Akt pathway in muscle of KK-A^y mice. Furthermore, LFO lowered postprandial hyperglycaemia in a human study. These results indicate that LFO may exert a therapeutic effect on metabolic disorders, such as diabetes and hyperglycaemia, by modulating glucose metabolism through AMPK- and insulin-dependent pathways in skeletal muscle.     

La glycémie postprandiale : du normal au pathologique

Postprandial glucose excursions contribute to both chronic sustained hyperglycaemia and acute glucose fluctuations from peaks to nadirs. Lessons from physiology indicate that non diabetic persons spend half of their life in postprandial states. However, in normal subjects, postmeal glucose increments remain limited in duration and magnitude. Progression from normal stages to frank diabetes is a stepwise process. The first step from normal to impaired glucose tolerance (IGT) is characterised by a glycaemic deterioration limited to the postprandial period. The second step from IGT to diabetes corresponds to a loss of glycaemic control at the end of the night (dawn phenomenon) followed by a progressive increase in fasting glucose and by an additional deterioration of postmeal glucose excursions. This progression is explained by three main disorders (the biological triumvirat): a relentless defect in β-cell function, an insulin resistance that progresses over the time course of the disease, and an hepatic glucose overproduction that reaches a peak at the end of the overnight fast. These observations indicate that the monitoring of glycaemic disorders in type 2 diabetes should include the three parameters of the “glucose triad”: the HbAlc, the fasting glucose and the postmeal values. More generally, the assessment of glycaemic profiles over daytime is helpful for choosing and tailoring the treatments according to whether the prandial or the basal hyperglycaemia is predominant.     

Modification of beta-cell response to different postprandial blood glucose concentrations by prandial repaglinide and combined acarbose/repaglinide application

This study was designed to compare the effects of repaglinide plus acarbose combination treatment to repaglinide alone on postprandial glucose, serum insulin, C-peptide and proinsulin concentrations. A total of 40 patients with Type 2 diabetes (T2DM) (fasting blood glucose: 120-180 mg/dl; postprandial blood glucose: 140-240 mg/dl) were included in this single-centre, controlled, randomised, single-dose, cross-over study. On two consecutive days, patients either received 2 mg repaglinide 15 min before breakfast followed by 100 mg acarbose with breakfast or repaglinide alone. Two fasting (7.30 h, 8.00 h) and five postprandial blood samples (from 8.30 h to 12.00 h) were taken for blood glucose, serum insulin, C-peptide and proinsulin determination. Repaglinide plus acarbose treatment significantly reduced the mean increase in postprandial blood glucose levels (24.2+/-18.2 mg/dl) compared to repaglinide alone (51.1+/-29.0 mg/dl; p<0.001). Serum insulin, C-peptide and proinsulin levels [mean area under the curve (AUC7.30-12.00h)] were significantly lower than those observed with repaglinide monotherapy (e.g. insulin: 1089.2+/-604.5 hr x pmol/l and 1596.8+/-1080.6 hr x pmol/l, resp., p<0.001), suggesting that acarbose modifies the rapid insulin release induced by repaglinide. Prandial treatment with a combination of acarbose and repaglinide results in an additive glucose lowering effect and modified insulin secretion compared to repaglinide alone. Postprandial hyperglycaemia is not abolished by rapid stimulation of insulin release induced by repaglinide. Additional reduction of postprandial blood glucose by acarbose modifies the stimulation of insulin release.     

The Impact of Microbial Composition on Postprandial Glycaemia and Lipidaemia: A Systematic Review of Current Evidence

Postprandial hyperglycaemia is associated with increased risk of cardiovascular disease. Recent studies highlight the role of the gut microbiome in influencing postprandial glycaemic (PPG) and lipidaemic (PPL) responses. The authors of this review sought to address the question: “To what extent does individual gut microbiome diversity and composition contribute to PPG and PPL responses?”. CINAHL Plus, PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched from January 2010 to June 2020. Following screening, 22 studies were eligible to be included in the current review. All trials reported analysis of gut microbiome diversity and composition and PPG and/or PPL. Results were reported according to the ‘Preferred Reporting Items for Systematic Reviews and Meta-Analysis’ (PRISMA) statement. Individual microbiota structure was found to play a key role in determining postprandial metabolic responses in adults and is attributed to a complex interplay of diet, microbiota composition, and metagenomic activity, which may be predicted by metagenomic analysis. Alterations of gut microbiota, namely relative abundance of bacterial phylum Actinobacteria and Proteobacteria, along with Enterobacteriaceae, were associated with individual variation in postprandial glycaemic response in adults. The findings of the current review present new evidence to support a personalised approach to nutritional recommendations and guidance for optimal health, management, and treatment of common metabolic disorders. In conclusion, personalised nutrition approaches based on individual microbial composition may improve postprandial regulation of glucose and lipids, providing a potential strategy to ameliorate cardiometabolic health outcomes.     

Glycaemic index and metabolic disease risk

There is growing evidence that the type of carbohydrate consumed is important in relation to metabolic disease risk, and there is currently particular interest in the role of low-glycaemic-index (GI) foods. Observational studies have associated low-GI diets with decreased risk of type 2 diabetes and CHD, and improvements in various metabolic risk factors have been seen in some intervention studies. However, findings have been mixed and inconsistent. There are a number of plausible mechanisms for the effects of these foods on disease risk, which arise from the differing metabolic responses to low- and high-GI foods, with low-GI foods resulting in reductions in hyperglycaemia, hyperinsulinaemia and late postprandial circulating NEFA levels. Low-GI foods may also increase satiety and delay the return of hunger compared with high-GI foods, which could translate into reduced energy intake at later time points. However, the impact of a low-GI diet on body weight is controversial, with many studies confounded by dietary manipulations that differ in aspects other than GI. There is currently much interest in GI from scientists, health professionals and the public, but more research is needed before clear conclusions can be drawn about relationships with metabolic disease risk.