重视IFG、IGT的防治

糖耐量低减(impaired glucose tolerance，IGT)和空腹血糖异常(impaired fating glueose,IFG)均为糖尿病自然病程中的中间阶段。目前并未被确认为疾病状态，只认为是正常与疾病之间的一种高危状态，称前糖尿病状态(pre-diabetes)。大规模、前瞻性研究已证实：IGT和(或)IFG人群进展为临床糖尿病的危险显著高于正常糖耐量者(NGT)，年发病率约3％-10％，是临床糖尿病的主要后备人群；IGT和(或)IFG是冠心病、高血压及脑血管意外等疾病的重要危险因素；强化生活方式干预(饮食控制、运动)和一定的药物干预。可有效延缓和减少IGT／IFG人群的糖尿病危险。广东省1998年流行病学调查显示，20-74     

Reproducibility of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) classification: a systematic review.

BACKGROUND: The classifications of impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) represent glucose levels above normal, but below the decision threshold for diabetes. We sought to determine what the reproducibility of these classifications was when repeat tests were performed by conducting a systematic review of the literature. METHODS: All primary studies published in English of any study design were included. Studies were excluded if they did not follow the World Health Organization or American Diabetes Association diagnostic criteria, used whole blood as the specimen type, a glucose meter for analysis, or performed repeat testing greater than 8 weeks apart. RESULTS: Five papers had reproducibility data for IGT or IFG, two of which where from the same population but sampled differently. The kappa coefficients, indicating agreement between repeat tests that exceeded chance, indicated poor to fair agreement for IGT (0.04, 0.22, 0.38, 0.42) and moderate agreement for IFG (0.44 and 0.56). Similarly, the observed reproducibility was slightly lower for IGT (33%, 44%, 47%, 48%) compared to IFG (51%, 64%). In two studies for which data were available for both IGT and IFG, the average reproducibility was lower (49%) for the prediabetes group compared to the diabetes group (73%) or the normal group (93%). CONCLUSIONS: Poor reproducibility of IGT and IFG classification suggests caution should be exercised when interpreting a single test result.     

Impaired glucose tolerance and impaired fasting glucose

Impaired glucose tolerance and impaired fasting glucose form an intermediate stage in the natural history of diabetes mellitus. From 10 to 15 percent of adults in the United States have one of these conditions. Impaired glucose tolerance is defined as two-hour glucose levels of 140 to 199 mg per dL (7.8 to 11.0 mmol) on the 75-g oral glucose tolerance test, and impaired fasting glucose is defined as glucose levels of 100 to 125 mg per dL (5.6 to 6.9 mmol per L) in fasting patients. These glucose levels are above normal but below the level that is diagnostic for diabetes. Patients with impaired glucose tolerance or impaired fasting glucose have a significant risk of developing diabetes and thus are an important target group for primary prevention. Risk factors for diabetes include family history of diabetes, body mass index greater than 25 kg per m2, sedentary lifestyle, hypertension, dyslipidemia, history of gestational diabetes or large-for-gestational-age infant, and polycystic ovary syndrome. Blacks, Latin Americans, Native Americans, and Asian-Pacific Islanders also are at increased risk for diabetes. Patients at higher risk should be screened with a fasting plasma glucose level. When the diagnosis of impaired glucose tolerance or impaired fasting glucose is made, physicians should counsel patients to lose 5 to 7 percent of their body weight and engage in moderate physical activity for at least 150 minutes per week. Drug therapy with metformin or acarbose has been shown to delay or prevent the onset of diabetes. However, medications are not as effective as lifestyle changes, and it is not known if treatment with these drugs is cost effective in the management of impaired glucose tolerance.     

Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans

OBJECTIVE: To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS: We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of beta-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS: Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased approximately 30% (P < 0.05), but clamp-determined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced approximately 35% (P < 0.002) and approximately 30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but approximately 15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced approximately 30%. IFG/NGT differed from NFG/IGT by having approximately 40% lower HOMA-%B (P < 0.012) and approximately 50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS: Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity.     

Associations of cardiorespiratory fitness and obesity with risks of impaired fasting glucose and type 2 diabetes in men

OBJECTIVE—The purpose of this study was to examine the associations of cardiorespiratory fitness (hereafter fitness) and various obesity measures with risks of incident impaired fasting glucose (IFG) and type 2 diabetes.RESEARCH DESIGN AND METHODS—This was a prospective cohort study of 14,006 men (7,795 for the analyses of IFG), who did not have an abnormal electrocardiogram or a history of heart attack, stroke, cancer, or diabetes.RESULTS—Of the men, 3,612 (39,610 person-years) and 477 (101,419 person-years) developed IFG and type 2 diabetes, respectively. Compared with the least fit 20% in multivariate analyses, IFG and type 2 diabetes risks in the most fit 20% were 14 and 52% lower, respectively (both P < 0.001). Men with BMI ≥30.0 kg/m², waist girth >102.0 cm, or percent body fat ≥25 had 2.7-, 1.9-, and 1.3-fold higher risks for type 2 diabetes, respectively, compared with those for nonobese men (all P < 0.01), and the results for IFG were similar. In the combined analyses, obese unfit (least fit 20%) men had a 5.7-fold higher risk for type 2 diabetes compared with normal-weight fit (most fit 80%) men. We observed similar trends for the joint associations of BMI and fitness with IFG and those of waist girth or percent body fat and fitness with both IFG and type 2 diabetes.CONCLUSIONS—Low fitness and obesity increased the risks of IFG and type 2 diabetes by approximately similar magnitudes. When considered simultaneously, fitness attenuated but did not eliminate the increased risks of IFG and type 2 diabetes associated with obesity, and the highest risk was found in obese and unfit men.Type 2 diabetes, one of the most costly chronic diseases, is a major risk factor for cardiovascular disease (CVD) mortality (1). Impaired fasting glucose (IFG), a pre-diabetic state, is a strong predictor of type 2 diabetes and CVD (2). Type 2 diabetes rates have increased substantially in recent years, and this trend is expected to continue (3). The American Diabetes Association (ADA) reported that approximately one in five health care dollars in the U.S. is spent caring for someone with diagnosed diabetes (4).Physical inactivity and obesity are well-known independent risk factors for type 2 diabetes (5–7). However, according to objective data on physical activity in the recent National Health and Nutritional Examination Survey, adherence to the recommended amount of physical activity was <5% in U.S. adults (8), and more than one-third of adults were obese in 2005–2006 (9).Previous studies have examined physical inactivity and obesity in relation to the risk of type 2 diabetes (5–7). However, in many studies, physical activity was measured by self-report questionnaire, which may cause an underestimation of the true associations between physical activity and health outcomes (8). Cardiorespiratory fitness (hereafter fitness) obtained from a laboratory maximal exercise test can be a marker for recent physical activity and provide objective information on the relationship between physical activity and health outcomes. Various measures of adiposity and fat distribution, such as percent body fat and waist girth, can more precisely assess the associations between obesity and type 2 diabetes.Although several studies have reported single independent associations between fitness or obesity with type 2 diabetes (10–14), the relative contributions of physical activity or fitness and obesity to the risk of type 2 diabetes are still controversial. Some previous studies concluded that the relative contribution of obesity was more important than physical activity on the risk of type 2 diabetes in women (6,7). However, in our recent study of women using objectively measured fitness instead of self-reported physical activity, obesity and fitness made similar contributions to the risk of type 2 diabetes (15). To date, no study on this issue has been conducted in men.Therefore, we examined the combined associations of fitness and obesity on the risk of type 2 diabetes in a large sample of men with various objective measures of obesity and fat distribution. We also examined the joint associations of these exposures with the risk of IFG, which is a strong predictor of type 2 diabetes and CVD.     

Higher medical care costs accompany impaired fasting glucose

OBJECTIVE: The purpose of this study was to estimate medical costs associated with elevated fasting plasma glucose (FPG) and to determine whether costs differed for patients who met the 2003 (> or = 100 mg/dl) versus the 1997 (> or = 110 mg/dl) American Diabetes Association (ADA) cut point for impaired fasting glucose. RESEARCH DESIGN AND METHODS: We identified 28,335 patients with two or more FPG test results of at least 100 mg/dl between 1 January 1994 and 31 December 2003. Those with evidence of diabetes before the second test were excluded. We categorized patients into two stages of abnormal glucose (100-109 mg/dl and 110-125 mg/dl) and matched each of these subjects to a patient with a normal FPG test (<100 mg/dl) on age, sex, and year of FPG test. All subjects were followed until an FPG test qualified them for a higher stage, dispensing of an anti-hyperglycemic drug, health plan termination, or 31 December 2003. RESULTS: Adjusted annual costs were dollar 4,357 among patients with normal FPG, dollar 4,580 among stage 1 patients, and dollar 4,960 among stage 2 patients (P < 0.001, all comparisons). After removing patients with normal FPG tests whose condition progressed to a higher stage or diabetes, costs in the normal FPG stage were dollar 3,799. Patients in both stages 1 and 2 had more cardiovascular comorbidities than patients with normal FPG. CONCLUSIONS: Our results demonstrate that abnormal glucose metabolism is associated with higher medical care costs. Much of the excess cost was attributable to concurrent cardiovascular disease. The 2003 ADA cut point identifies a group of patients with greater costs and comorbidity than normoglycemic patients but with lower costs and less comorbidity than patients with FPG above the 1997 cut point.     

Cardiometabolic risk in impaired fasting glucose and impaired glucose tolerance: the Atherosclerosis Risk in Communities Study

OBJECTIVE: We compared and contrasted cardiovascular disease (CVD) risk factors, subclinical manifestations of CVD, incident coronary heart disease (CHD), and all-cause mortality by categories of impaired glucose regulation in nondiabetic individuals. RESEARCH DESIGN AND METHODS: The study included 6,888 participants aged 52-75 years who had no history of diabetes or CVD. All-cause mortality and incident CHD were ascertained over a median of 6.3 years of follow-up. RESULTS: Agreement between fasting and postchallenge glucose impairment was poor: 3,048 subjects (44%) had neither impaired fasting glucose (IFG) nor impaired glucose tolerance (IGT), 1,690 (25%) had isolated IFG, 1,000 (14%) had isolated IGT, and 1,149 (17%) had both IFG and IGT. After adjustment for age, sex, race, and center, subjects with isolated IFG were more likely to smoke, consume alcohol, and had higher mean BMI, waist circumference, LDL cholesterol, and fasting insulin and lower HDL cholesterol than those with isolated IGT, while subjects with isolated IGT had higher mean triglycerides, systolic blood pressure, and white cell counts. Measures of subclinical CVD and rates of all-cause mortality and incident CHD were similar in isolated IFG and isolated IGT. CONCLUSIONS: Neither isolated IFG nor isolated IGT was associated with a more adverse CVD risk profile.     

空腹血糖受损患者血脂改变情况分析

目的探讨空腹血糖受损(impaired fasting glucose,IFG)患者血脂成分的改变情况。方法收集23例正常糖耐量(NGT)者和新诊断的44例IFG患者的临床资料,分别测定血脂谱。结果IFG患者血清甘油三酯(TG)水平显著高于NGT组(P<0.05),高密度脂蛋白—胆固醇(HDL-C)值明显低于NGT组(P<0.01)。结论新诊断的IFG患者已经存在血脂代谢异常。     

Impaired glucose tolerance and impaired fasting glucose share similar underlying pathophysiologies

Both impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) are pre-diabetic states. IGT was defined as having normal fasting plasma glucose (< 6.1 mmol/l) and abnormal 2-hr post-challenge plasma glucose. IFG was defined as having abnormal fasting plasma and normal 2-hr post-challenge plasma glucose (< 7.8 mmol/l). To explore whether these two abnormalities share similar underlying pathophysiologies, we evaluated risk factors of IGT and IFT using the models of factor analysis. The present study included 107 subjects with IGT and 52 with IFG. An oral glucose tolerance test and insulin suppression test, which could quantify insulin resistance, were performed on separate days. The risk factors include waist-to-hip ratio (WHR), triglycerides, high-density lipoprotein (HDL)-cholesterol, blood pressure, and fasting plasma glucose, which are associated with metabolic syndrome and insulin resistance. Factor analysis is a commonly used statistical method that could reduce a large number of risk factors into smaller numbers of groups, also called dimension. Accordingly, the complicated data could be interpreted more easily, since the related risk factors are grouped in one dimension. The results showed that the risk factors of IGT and IFG have similar grouping patterns. Triglyceride, insulin resistance, and HDL-cholesterol were grouped in one dimension (the lipid dimension), while WHR, mean blood pressure and fasting plasma glucose were grouped in another dimension (the metabolic dimension). In conclusion, except for WHR, the grouping patterns of the components in both IGT and IFG were nearly identical. These results suggest that IGT and IFG may share similar pathophysiologies.     

The significance of impaired fasting glucose versus impaired glucose tolerance: importance of insulin secretion and resistance

OBJECTIVE: The American Diabetes Association recommended substituting 2hBS (glycemia at the second hour of an oral glucose tolerance test [OGTT]) for fasting blood glucose (FBS) in screening for glucose intolerance. It is debated whether these tests measure the same abnormality and relate to defective insulin secretion or resistance. This study examines the diagnostic effectiveness of FBS versus 2hBS and their relationship with insulin secretion and resistance. RESEARCH DESIGN AND METHODS: Based on history or physical findings suggesting glucose intolerance, we enrolled 398 unselected subjects admitted to a general Internal Medicine ward. After 5 days of a weight-maintaining diet, FBS, 2hBS, and insulin were measured during OGTT. The homeostatic model assessment was used to assess beta-cell function and insulin resistance. RESULTS: Excluding 19 patients with diabetes (5%), we identified 284 subjects with normal glucose tolerance (NGT), 22 with isolated impaired fasting glucose (IFG), 59 with isolated impaired glucose tolerance (IGT), and 14 with associated IFG/IGT. The sensitivity of FBS in predicting 2hBS was 19%, specificity 93%. Positive and negative predictive values were 39% and 83%, respectively. Insulin resistance was absent in NGT and IFG and markedly elevated in IGT and IFG/IGT, whereas defective insulin release was significant only in isolated IFG. CONCLUSIONS: In unselected patients, elevated FBS depends primarily on defective insulin secretion, and impaired 2hBS on insulin resistance. Because these tests measure different alterations, they are useful in combination.     

空腹血糖受损与糖耐量受损者胰岛β细胞功能及胰岛素抵抗的比较

目的：比较空腹血糖受损与糖耐量受损者胰岛β细胞功能及胰岛素抵抗的不同。方法：选择正常糖耐量者40例，空腹血糖受损者32例，糖耐量受损者38例。测体重指数、血压、血脂、空腹及糖负荷后的血糖、血胰岛素。用稳态模式胰岛素抵抗指数HOMA—IR抵抗作为胰岛素抵抗指标，稳态模式HOMA—β作为基础胰岛素分泌指标，糖负荷30min净增胰岛素／净增葡萄糖作为早期胰岛素分泌指数。结果：空腹血糖受损组HOMA-IR较耐量受损组增高，差异有显著性（P〈0．05）。空腹血糖受损组HOMA—β较糖耐量受损组降低，差异有显著性（P〈0.05）。糖耐量受损组净增胰岛素／净增葡萄糖与空腹血糖受损组比较有下降，但差异无统计学意义。结论：空腹血糖受损人群较糖耐量受损人群有着更严重的胰岛素抵抗，空腹血糖受损人群基础状态下胰岛β细胞功能受损，而糖耐量受损人群的早期胰岛素分泌反应减弱。     

Contributions of beta-cell dysfunction and insulin resistance to the pathogenesis of impaired glucose tolerance and impaired fasting glucose

Impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) are intermediate states in glucose metabolism that exist between normal glucose tolerance and overt diabetes. Epidemiological studies demonstrate that the two categories describe distinct populations with only partial overlap, suggesting that different metabolic abnormalities characterize IGT and IFG. Insulin resistance and impaired beta-cell function, the primary defects observed in type 2 diabetes, both can be detected in subjects with IGT and IFG. However, clinical studies suggest that the site of insulin resistance varies between the two disorders. While subjects with IGT have marked muscle insulin resistance with only mild hepatic insulin resistance, subjects with IFG have severe hepatic insulin resistance with normal or near-normal muscle insulin sensitivity. Both IFG and IGT are characterized by a reduction in early-phase insulin secretion, while subjects with IGT also have impaired late-phase insulin secretion. The distinct metabolic features present in subjects with IFG and IGT may require different therapeutic interventions to prevent their progression to type 2 diabetes.