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1.
多个流行病学研究显示,亚洲糖尿病高发与经济迅速发展、营养水平快速提高相关,提示环境因素可能在亚洲糖尿病流行中发挥重要作用.营养缺乏造成的生长抑制在营养恢复后可出现代偿性快速生长现象,称为追赶生长.研究发现追赶生长与胰岛素抵抗及2型糖尿病紧密相关[1].  相似文献   

2.
从追赶生长角度剖析胰岛素抵抗相关疾病高发的机制   总被引:1,自引:0,他引:1  
追赶生长为胰岛素抵抗相关疾病的研究提供了新的思路.追赶生长是一个普遍存在的现象,本是生命的一种自我代偿,但与胰岛素抵抗的形成有着密切的关系.追赶生长主要是脂肪的优先和过度生长.目前在其机制、干预等方面还有许多亟待解决的问题.  相似文献   

3.
胰岛素抵抗与胰岛素分泌缺陷是2型糖尿病的主要病理生理学缺陷。绝大多数的欧美2型糖尿病患者均肥胖,而肥胖所致的胰岛素抵抗被认为是导致该人群发生2型糖尿病的最主要因素。但是亚洲2型糖尿病患者中,肥胖者还不到半数。胰岛素抵抗抑或胰岛素分泌功能缺陷是亚洲糖尿病患者早期发病的主要因素尚不明了。本文调查了解中国新诊断的2型糖尿病人群胰岛素抵抗和胰岛素分泌功能的状况并观察格列齐特(达美康缓释片)强化治疗对其的影响。  相似文献   

4.
追赶生长是机体一过性生长抑制后出现的快速生长现象,现已证实追赶生长与胰岛素抵抗存在高度相关性,但其形成的具体机制尚不明确.  相似文献   

5.
在最终将导致2型糖尿病或代谢综合征的各种病理过程中,高胰岛素血症性胰岛素抵抗和内脏型肥胖在早期即可出现.其中一种相当普遍的发病过程即开始于出生前生长受限及幼年时体重自发性追赶增长.进入这种发病过程的儿童在4岁时即使没有肥胖,也有发生高胰岛素血症和体脂增多的倾向.  相似文献   

6.
目的 研究2型糖尿病合并肥胖患者脂联素水平和胰岛素抵抗之间的相关性,探讨脂联素在2型糖尿病合并肥胖患者发生胰岛素抵抗中的作用.方法 选择30例2型糖尿病合并肥胖患者、25例2型糖尿病患者及25例非糖尿病对照人员(其中13例为肥胖者),检测体质指数、腰/臀比值、空腹血糖、糖化血红蛋白、血清空腹胰岛素、血脂、脂联素水平,计算胰岛素抵抗指数和胰岛素敏感指数.分析血清脂联素与胰岛素抵抗的相关性.结果 (1)糖尿病肥胖组的检测体质指数、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素、腰/臀比值均高于对照肥胖组,脂联素、胰岛素敏感指数低于对照肥胖组(P<0.05).(2)糖尿病非肥胖组甘油三酯、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素均高于对照非肥胖组,胰岛素敏感指数、脂联素低于对照非肥胖组(P<0.05).(3)糖尿病肥胖组甘油三酯、胆固醇、体质指数、糖化血红蛋白、空腹血糖、胰岛素抵抗指数、血清空腹胰岛素、腰/臀比值均高于糖尿病非肥胖组,胰岛素敏感指数、脂联素低于糖尿病非肥胖组(P<0.05).结论 脂联素与2型糖尿病肥胖患者的胰岛素抵抗发生有关,脂联素降低易导致胰岛素抵抗,脂联素水平可作为2型糖尿病合并肥胖患者发生胰岛素抵抗的监测标准.  相似文献   

7.
2型糖尿病的发病机理尚未完全阐明,一般认为主要与胰岛素外周靶组织的胰岛素抵抗及胰岛β细胞分泌缺陷有关.但是二者在2型糖尿病发病机理中孰为原发孰为继发,以及各自在糖尿病发病中的地位一直是长期争论不休的问题.近年来发现β细胞膜上也存在胰岛素受体,即β细胞也是胰岛素的靶细胞,β细胞胰岛素信号转导障碍可导致胰岛素分泌缺陷,首次将胰岛素抵抗与β细胞分泌缺陷直接联系起来.为丰富胰岛素抵抗概念的内涵和外延,重新评价胰岛素抵抗在2型糖尿病发病中的作用提供了新的思路.  相似文献   

8.
脂联素与2型糖尿病及其大血管病变   总被引:2,自引:0,他引:2  
脂联素与肥胖、胰岛素抵抗、2型糖尿病及其大血管病变的发生、发展有密切关系,被认为是一种保护性因子.本文从多方面就脂联素与2型糖尿病及其大血病变的关系加以总结.脂联素具有胰岛素抵抗及拮抗动脉粥样硬化的作用,对脂联素在2型糖尿病及其大血管病变方面的基础及临床研究,为改善胰岛素抵抗和防治2型糖尿病大血管病变提供了新的思路.  相似文献   

9.
1胰岛素抵抗与新药的研发 人们目前已共识,2型糖尿病的发病,常用胰岛素分泌双曲线定律来表述,即胰岛素敏感性和胰岛素分泌缺陷是发病的两大要素.有人调查在大量群体中约有25%的个体存在胰岛素抵抗,在2型糖尿病的人群中,胰岛素抵抗的发病率高达75%~85%.也有人用内环境稳定评估模型(HOMA)来评估,正常个体的HOMA-IR的平均值为2.1~2.7;糖耐量受损(IGT)的个体为4.3~5.2;2型糖尿病病人为8.3~9.5.总之表述了胰岛素抵抗广泛的存在于人群中.它强烈预示2型糖尿病发生的可能,而且也是2型糖尿病主要发生机制.为此近些年来,人们在开发大量改善糖代谢的背景下,又把主要目标放在改善胰岛素抵抗的研发上.  相似文献   

10.
目的对于2型糖尿病胰岛素抵抗患者采取中西医结合治疗的具体方法以及治疗效果施行分析与总结。方法将该院在过去两年之内2016年1月—2018年1月所接诊的2型糖尿病胰岛素抵抗患者资料60例施行分析,所选60例2型糖尿病胰岛素抵抗患者采取数字法加以分组,给予对照组2型糖尿病胰岛素抵抗患者口服罗格列酮片进行治疗,研究组2型糖尿病胰岛素抵抗患者在对照组治疗基础之上加用养阴益气汤,两组2型糖尿病胰岛素抵抗患者治疗时间全部为4周,对比两组2型糖尿病胰岛素抵抗患者接受各自治疗措施之后的临床效果以及糖脂代谢改变情况。结果两组2型糖尿病胰岛素抵抗患者接受治疗之后的糖化血红蛋白、三酰甘油、低密度脂蛋白、总胆固醇、高密度脂蛋白以及空腹血糖水平对比差异;两组2型糖尿病胰岛素抵抗患者接受治疗之后的临床效果对比差异有统计学意义(P0.05)。结论临床中针对2型糖尿病胰岛素抵抗患者,为其提供中西医结合治疗效果理想,能够良好调节2型糖尿病胰岛素抵抗患者的糖脂代谢,应该给予大力的推广与应用。  相似文献   

11.
Depending on the definitions used, up to 10% of all live-born neonates are small for gestational age (SGA). Although the vast majority of these children show catch-up growth by 2 yr of age, one in 10 does not. It is increasingly recognized that those who are born SGA are at risk of developing metabolic disease later in life. Reduced fetal growth has been shown to be associated with an increased risk of insulin resistance, obesity, cardiovascular disease, and type 2 diabetes mellitus. The majority of pathology is seen in adults who show spontaneous catch-up growth as children. There is evidence to suggest that some of the metabolic consequences of intrauterine growth retardation in children born SGA can be mitigated by ensuring early appropriate catch-up growth, while avoiding excessive weight gain. Implicitly, this argument questions current infant formula feeding practices. The risk is less clear for individuals who do not show catch-up growth and who are treated with GH for short stature. Recent data, however, suggest that long-term treatment with GH does not increase the risk of type 2 diabetes mellitus and the metabolic syndrome in young adults born SGA.  相似文献   

12.
Fetal growth retardation is associated with decreased postnatal growth, resulting in a lower adult height. In addition, a low birth weight is associated with an increased risk of developing diseases during adulthood, such as insulin resistance, type 2 diabetes mellitus, hypertension, dyslipidemia, and cardiovascular diseases. Children with persistent postnatal growth retardation, i.e., incomplete catch-up growth, can be treated with human GH. The GH/IGF-I axis is involved in the regulation of carbohydrate and lipid metabolism. The question of whether treatment with GH in children born small for gestational age (SGA) has long-term implications with respect to glucose/insulin and lipid metabolism has not been answered yet. In this article, the available data are reviewed.  相似文献   

13.
OBJECTIVE: The aim of this study was to quantify serum adiponectin concentrations in short children born small for gestational age (SGA) compared with those in children born appropriate for gestational age (AGA), and to assess the relationship between the serum levels of adiponectin and insulin-like growth factor binding protein-1 (IGFBP-1) known as a predictor of the development of type 2 diabetes mellitus and cardiovascular disease. SUBJECTS AND METHODS: Sixteen prepubertal short children born SGA and 20 short children born AGA, matched for age, body mass index, height, pubertal status, gestational age, bone age and midparental height, were included in the study. The serum levels of adiponectin, IGFBP-1, insulin and insulin-like growth factor-I (IGF-I) were measured in the fasting state. RESULTS: The levels of serum adiponectin were significantly lower in the SGA than in AGA children (10.5 +/- 4.2 vs. 13.9 +/- 5.1 micro g/ml, P < 0.05). The levels of serum IGFBP-1, insulin and IGF-I were all similar in both groups. Overall, there was a significant positive correlation between adiponectin and IGFBP-1 (r = 0.40, P < 0.05). CONCLUSIONS: Our results suggest that hypoadiponectinaemia in short SGA children without catch-up growth may reflect insulin resistance and imply a higher risk of developing type 2 diabetes mellitus. Additionally, adiponectin may be a more sensitive indicator for latent insulin resistance than IGFBP-1 in short SGA children.  相似文献   

14.
Pancreatic cancer is strongly associated with the development of hyperglycemia, peripheral insulin resistance and diabetes mellitus, especially when presented as new-onset diabetes mellitus. Peripheral insulin resistance and hyperinsulinemia have been suggested to promote growth of pancreatic cancer cells, and therefore a relation between longstanding diabetes mellitus type 2 and pancreatic cancer has been implied. Epidemiological studies, though, give incongruent results to this problem. There are data supporting a tumor-derived influence on glucose metabolism, insulin secretion and eventually the development of diabetes mellitus in early stages of pancreatic cancer. The only possibility for curative intent in pancreatic cancer is to diagnose the disease before symptoms occur. Patients with newly diagnosed diabetes mellitus type 2 or hyperglycemia as a risk group have been recommended for primary screening for pancreatic cancer. To date, there is no specific biomarker to identify patients with an asymptomatic pancreatic cancer. The review discuss the relationship between pancreatic cancer and diabetes mellitus and the possibility of secondary screening of patients with newly diagnosed diabetes mellitus type 2 or hyperglycemia in an artificial neural network. PubMed was searched for articles using the Mesh term ‘pancreatic neoplasms’ combined with ‘insulin resistance’ and ‘glucose metabolism disorders’. Additional articles were retrieved through hyperlinks and by manually searching reference lists in original published articles. In total 36 articles were systematically reviewed.  相似文献   

15.
It has long been known that obesity is a high risk factor for cardiovascular diseases. In more recent years, the analysis of several large epidemiological databases has also revealed that, independently of excess weight, large fluctuations in body weight at some point earlier in life represent an independent risk factor for type 2 diabetes and hypertension-two major contributors to cardiovascular diseases. High cardiovascular morbidity and mortality have indeed been reported in men and women who in young adulthood experienced weight fluctuations (involving the recovery of body weight after weight loss due to disease, famine or voluntary slimming), or when weight fluctuations occurred much earlier in life and involved catch-up growth after fetal or neonatal growth retardation. This paper addresses the pathways from weight fluctuations to chronic metabolic diseases by focusing on the phenomenon of accelerated fat recovery (ie catch-up fat) after weight loss or growth retardation. Arguments are put forward that, during catch-up growth or weight recovery on our modern refined foods, the mechanisms of adaptive thermogenesis that regulate catch-up fat are pushed beyond the limits for which they were meant to operate and turn maladaptive. The consequences are enhanced susceptibilities towards skeletal muscle insulin resistance and overactive sympathetic activity, both of which are major contributors to the pathogenesis of chronic metabolic diseases. Since weight fluctuation earlier in life (independently of excess weight later in life) is an independent risk factor for metabolic diseases, the mechanisms by which body fat is acquired would seem to be at least as important as the consequences of excess fat per se in the pathogenesis of diabetes, hypertension and cardiovascular diseases.  相似文献   

16.
研究表明2型糖尿病可能增加肺癌发生的风险,但其尚缺乏有力的相关机制研究。本文从2型糖尿病和肺癌间的流行病学特点、2型糖尿病患者的肺癌发病率升高、高血糖、胰岛素抵抗、高胰岛素血症、胰岛素样生长因子、血管内皮生长因子、炎症细胞因子、激素调节功能紊乱、免疫系统功能降低、微量元素及降糖药物等方面综述二者可能的相关性,但2型糖尿病加重肺癌的机制仍需要大量研究证明。  相似文献   

17.
The analyses of large epidemiological databases have suggested that infants and children who show catch-up growth, or adiposity rebound at a younger age, are predisposed to the development of obesity, type 2 diabetes and cardiovascular diseases later in life. The pathophysiological mechanisms by which these growth trajectories confer increased risks for these diseases are obscure, but there is compelling evidence that the dynamic process of catch-up growth per se, which often overlaps with adiposity rebound at a younger age, is characterized by hyperinsulinemia and by a disproportionately higher rate in the recovery of body fat than lean tissue (i.e. preferential 'catch-up fat'). This paper first focuses upon the almost ubiquitous nature of this preferential 'catch-up fat' phenotype across the life cycle as a risk factor for obesity and insulin-related complications - not only in infants and children who experienced catch-up growth after earlier fetal or neonatal growth retardation, or after preterm birth, but also in adults who show weight recovery after substantial weight loss owing to famine, disease-cachexia or periodic dieting. It subsequently reviews the evidence indicating that such preferential catch-up fat is primarily driven by energy conservation (thrifty) mechanisms operating via suppressed thermogenesis, with glucose thus spared from oxidation in skeletal muscle being directed towards de novo lipogenesis and storage in white adipose tissue. A molecular-physiological framework is presented which integrates emerging insights into the mechanisms by which this thrifty 'catch-up fat' phenotype crosslinks with early development of insulin and leptin resistance. In the complex interactions between genetic constitution of the individual, programming earlier in life, and a subsequent lifestyle of energy dense foods and low physical activity, this thrifty 'catch-up fat' phenotype--which probably evolved to increase survival capacity in a hunter-gatherer lifestyle of periodic food shortages--is a central event in growth trajectories to obesity and to diseases that cluster into the insulin resistance (metabolic) syndrome.  相似文献   

18.

BACKGROUND:

Insulin resistance has been proposed to be the most likely phenotypic trait that could represent a genetic link between low birth weight and type 2 diabetes, especially in Southeast Asia. Insulin resistance can persist for many years, even decades, before the manifestation of overt diabetes. There have been many studies suggesting a strong genetic basis in the etiology of type 2 diabetes mellitus. There is also ample evidence providing a link with low birth weight and type 2 diabetes in later life. Hence, parental insulin sensitivity could well serve as a representation of the offspring''s future insulin resistance state. Association between maternal insulin sensitivity and the incidence of type 2 diabetes mellitus in low birth weight babies is confounded by many factors and hence, has limited value in the determination of any genetic origin of the disease. Therefore, the present study was done to investigate the relationship between paternal insulin sensitivity and the growth parameters of the foetus to determine a genetic link between poor early growth and the increased risk of type 2 diabetes mellitus in later life.

MATERIALS AND METHODS:

The study was performed on 30 healthy fathers and their babies born from nondiabetic mothers. Each father underwent a low-dose short insulin tolerance test (ITT) as a measure of insulin sensitivity. Placental weight was recorded and a blood sample was collected from the placental side of the umbilical cord at birth for measurement of insulin. Measurement of birth weight, length, and head circumference were recorded and ponderal index was calculated from the formula: weight (kg)/ length (cm)3. Individual parameters of insulin resistance syndrome were measured in the fathers.

RESULTS:

The degree of insulin sensitivity, Km (constant for insulin tolerance test) did not correlate with the fetal growth parameters (Ponderal Index r = 0.031, P = 0.870; weight of baby r = 0.010, P = 0.959; length of baby r = 0.087, P = 0.464; head circumference r = 0.280, P = 0.142) or with the fathers'' anthropometric measures: body mass index (BMI), blood pressure, fasting glucose, insulin, and lipid profiles.

CONCLUSION:

The data suggest that the mechanism linking insulin resistance with low birth weight is not a genetically determined defect.  相似文献   

19.
Hyperglycemic crises in diabetes mellitus type 2.   总被引:3,自引:0,他引:3  
Hyperglycemic crises in type 2 diabetes are not rare and are becoming increasingly recognized as part of the spectrum of the presentation of previously undiagnosed diabetes mellitus and the decompensation of established diabetes mellitus. Contributing factors and associations are being elucidated but remain far from clear, particularly in DKA states. Medications commonly used in the treatment of many comorbid illnesses in patients with diabetes can themselves predispose to HHS. Endocrinopathies can contribute to insulin resistance and directly increase the glycemic load, leading to hyperglycemia. Medications such as the protease inhibitors may in the future lead to a better understanding of the pathophysiology of the metabolic derangements seen in the development of type 2 diabetes mellitus.  相似文献   

20.
Impaired insulin secretion and decreased insulin sensitivity are the main pathophysiologic features responsible for development of hyperglycemia in type 2 diabetes mellitus. Insulin resistance is often associated with increased adipose tissue mass. To examine which variables influence insulin sensitivity, we compared metabolic parameters, serum resistin, leptin, and adiponectin concentrations to the insulin sensitivity, obtained by frequently sampled intravenous glucose tolerance test using the minimal model analysis, in 113 Japanese patients with type 2 diabetes mellitus. Duration of diabetes, fasting plasma glucose, fasting insulin, homeostasis model assessment of insulin resistance index, and serum resistin concentration were significantly higher in the insulin-resistant subgroup compared with the insulin-sensitive subgroup and correlated with insulin sensitivity. Stepwise regression analysis also identified these parameters as independent regulators of insulin sensitivity. The present study reconfirmed that fasting insulin level or homeostasis model assessment of insulin resistance would be a surrogate measure of insulin resistance and demonstrated that insulin resistance increases progressively after the onset of overt diabetes and that the serum resistin level is associated with insulin sensitivity, suggesting that resistin plays an important role in the development of insulin resistance in Japanese patients with type 2 diabetes mellitus.  相似文献   

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