罗格列酮对糖耐量异常干预的临床研究

目的观察罗格列酮对糖耐量异常患者的治疗效果。方法比较119例糖耐量异常患者在饮食加运动控制的基础上口服罗格列酮和安慰剂干预治疗，经治疗1年后，检测空腹血糖（FPG）及葡萄糖耐量试验（OGTT）后2h血糖（2hPG），总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白（HDL）、胰岛素抵抗指数、空腹胰岛素（FINS）和OGTT后2h胰岛素（PINS）水平的变化。结果罗格列酮组和安慰剂组治疗前糖耐量比较差异无统计学意义（P〉0．05）。罗格列酮组与安慰剂组相比FPG、2HPG、TC、TG、LDL、FINS、PINS及糖尿病发病率均明显下降，HDL—C升高。结论罗格列酮能够降低糖耐量异常（IGT）人群糖尿病的发病率，在调节血脂、减轻胰岛素抵抗的同时，可使糖耐量异常明显改善。     

高血压患者动态血压变化与糖代谢异常55例分析

目的 探讨糖代谢异常对高血压患者动态血压变化的影响。方法 对55例既往无糖尿病的高血压患者行24小时动态血压监测和糖耐量试验（OGTT），根据OGTT分为糖耐量正常（NGT）、糖耐量减低（IGT）和新发现2型糖尿病（2-DM）3组。结果 从NGT至IGT至2-DM，非杓型血压发生率逐渐增高（分别为52．17％、64．70％和80．00％，P〈0．01），且2-DM患者夜间高血压的发生率较NGT及IGT显著增加（分别为13．04％、17．64％和33．33％，P〈0．01）；IGT组的24小时舒张压负荷、24小时舒张压和夜间舒张压均显著低于NGT组和2-DM组（P〈0．05），且脉压增大；并且发现，从NGT至IGT至2-DM过程中，胰岛素抵抗指数逐渐增加（分别为1．41、1．66和1．92，P〈0．05），胰岛素敏感指数在IGT阶段较NGT增高（39．90比33．83，P〈0．05），而到2-DM阶段较NGT下降（27．15比33．83，P〈0．05）；Logistic回归分析显示，影响脉压的主要因素为餐后血糖。结论 糖代谢异常的高血压惠者其24h血压的昼夜节律紊乱，其中以IGT患者的舒张压降低和脉压增大为著，而脉压增大与餐后血糖及血浆胰岛素水平相关。     

不同糖耐量人群胰岛素抵抗的比较

【目的】研究不同糖耐量人群胰岛素抵抗程度的差异。【方法】将412名门诊患者按OGTT分为4组：糖尿病组（NDM，n=180），空腹血糖受损组（IFG，n=35），糖耐量异常组（IGT，n=46），糖耐量正常组（NGT，n=151）。测定血压、血脂（TG和HDL）、体质指数（BMI）；应用胰岛素抵抗（HOMA-IR）及胰岛素作用指数（IAI）对不同糖耐量人群进行测定。【结果】DM、IFG及IGT组均较NGT组IAI下降，HOMA-IR增高，DM组表现得尤为显著；而IFG组与IGT组比较，亦有显著的IAI下降及HOMA-IR增高（P〈0．05）。【结论】不同糖耐量人群随着糖调节不同程度的受损HOMA-IR和IAI均有增幅变化，这两种指标可较准确的评估胰岛素敏感性。IFG与IGT人群胰岛素抵抗的机制可能有所不同。     

糖耐量低减人群治疗依从性现状分析

糖耐量低减（impaired glucosetolerance，IGT）是糖调节受损（impaired glucose regulation，IGR）的两种状态之一，是糖尿病发病过程中的中间阶段。s1999年世界卫生组织（WH（））制定的IGT诊断标准：空腹血糖（FPG）〈7．0mmol／L；葡萄糖耐量实验口服75g，葡萄糖2h后血糖（OGTT2hPG）≥7．8mmol／L，且〈11．1mmol／L。     

空腹血糖及糖化血红蛋白用于筛查糖耐量减退的比较性研究

目的比较空腹血糖（FPG）和糖化血红蛋白（HbAlc）在筛查糖耐量减退（IGT）中的应用价值。方法到我院门诊为明确有无血糖异常而就诊者336人，测定空腹血糖、糖化血红蛋白，并行口服葡萄糖耐量试验（OGTT）。结果按照1999年WHO的DM诊断标准，本研究人群空腹血糖〈6．1者124例，≥6．1-〈7．0者56例，≥7．0者156例；糖化血红蛋白〈6．1者84例，≥6．1者252例；OGTT2 hPG〈7．8者92例，≥7．8-〈11．1者99例，≥11．1者145例。结论糖化血红蛋白和空腹血糖均不适用于筛查IGT人群，但糖化血红蛋白比空腹血糖提示病人是否存在血糖异常更敏感。     

不同糖耐量人群胰岛素抵抗和胰岛B细胞分泌功能的临床研究

目的 探讨不同糖耐量人群胰岛素抵抗和胰岛B细胞的分泌功能。方法 根据口服葡萄糖耐量（OGTT）结果，将147例入选者分为糖耐量正常（NGT）组，糖耐量减退（IGT）组和糖尿病（DM）组，测定空腹和服糖后2h真胰岛素（FTI,TI2h）、空腹游离脂肪酸（FFA）、瘦素（kp）、胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）和低密度脂蛋白胆固醇（LDL-C），计算胰岛素抵抗指数（HOMA-IR）和胰岛素分泌指数（HOMA-β），并对有些数据作相关分析。结果 IGT组和DM组的血糖、TI、FFA、Lep、TG、LDL-C含量及HOMA-IR高于NGT组（均P〈0.01），HDLTC含量及HOMA-β均低于NGT组（均P〈0．01）；DM组HOMA-IR和HOMA-B分别高于和低于IGT组（均P〈0．01）。TG与FFA之间以及Lep与FFA之间呈正相关（r分别为0．7061、0．3436，均P〈0．01）；FFA与HOMA-IR正相关（r=0．5452，P〈0.001），与HOMA-β负相关（r=-0．3634，P〈0、01）；FFA、Lep与HOMA-IR独立相关（标准回归系数分别为0．2902、0．3217，均P〈0、05），FFA与HOMA-β独立相关（标准回归系数为-0．4906，P〈0．001）。结论糖代谢异常早期阶段存在明显胰岛素抵抗，胰岛B细胞分泌功能障碍随着病程的进展逐渐加重，脂毒性在这一过程中起重要作用。     

糖耐量受损者胰岛素抵抗和β细胞功能的研究

目的　探讨糖耐量受损 (IGT)患者胰岛素抵抗、β细胞功能和相关的代谢改变。 方法　对 6 4例血糖正常者 (NGT)和 97例IGT患者进行口服葡萄糖耐量试验 (OGTT)、胰岛素释放试验 ,并测定其血脂、血压、体重指数 (BMI)和腰臀比值 (WHR)。结果　与NGT组比较 ,IGT组空腹胰岛素水平、OGTT后胰岛素曲线下面积显著升高 (P <0 0 5 ) ;胰岛素敏感指数、初期胰岛素分泌指数明显降低 (P <0 0 1) ;胰岛素敏感指数依次与腰臀比值、BMI、甘油三脂 (TG)、高密度脂蛋白 胆固醇 (HDL C)、空腹血糖和舒张压相关 ;IGT患者TG、舒张压、收缩压、BMI和腰臀比值明显增高 ,HDL C明显降低。结论　IGT患者存在胰岛素抵抗和 β细胞功能异常并伴有多种代谢紊乱。     

ADA(美国糖尿病学会)糖尿病诊断新标准值得商榷

目的 探讨ADA（美国糖尿病学会1997年）糖尿病诊断新标准是否优于WHO（世界卫生组织1985年）诊断标准。方法 口服75g葡萄糖进行糖耐量试验（OGTT），测空腹血糖和糖负荷后2h血糖值。结果 ADA糖尿病诊断标准比WHO空腹血糖（FPG）诊断标准，可提高敏感性10.1%；按ADA标准诊断的75例糖尿病患者中有15例（20％）按WHO标准诊断为糖耐量低减（IGT），而且漏诊了餐后高血糖、糖尿病患者36例（32．4％）。ADA标准诊断，诊断空腹血糖异常（IFG）人群中按WHO标准有42例（37．8％）诊断为糖尿病，有60例（42．6％）诊断为IGT。结论 ADA诊断标准化WHO标准（FPG）虽可提高FPG诊断敏感性10．1％，但并不优于WHO诊断标准OGTT试验2h血糖（2h PG)值的敏感性。因此，认为WHO标准OGTT试验2h PG值有高敏感性和特异性，作为临床必要的诊断手段在临床工作中应该保留，临床医生要重视2h PG值。     

糖耐量异常患者社区健康教育的现状与展望

糖耐量异常（impaired glucose tolerance,IGT）是指空腹血糖正常,负荷后血糖异常,但未达到糖尿病诊断标准的一种状态。目前普遍认为糖耐量异常反映了由血糖正常到糖尿病（diabetesmellitus,DM）的过渡阶段。有报道胰岛素抵抗可能是大多数IGT和2型糖尿病（T2DM）患者共同的遗传特征。研究显示大部分糖尿病患者均经过糖耐量异常阶段,年转化率为2％-14％,每5-10年约有1／3的IGT患者发展成为糖尿病^[1]。     

中青年原发性高血压代谢状态研究

目的研究中青年原发性高血压患者血糖、血脂、血尿酸等代谢状态。方法对69例（研究组）中青年原发性高血压患者检测空腹血糖（FBG）、餐后2h血糖（2hPG）、空腹胰岛素（FINS）、餐后2h胰岛素（2bINS），进行口服糖耐量试验（OGTT）、胰岛素释放试验，检测血脂、血尿酸（UA），评估患者的代谢状态。并与正常对照组（41例）比较。结果研究组患者FPG、2hPG、FINS与对照组比较差异有统计学意义（P〈0．01、P〈0．05、P〈0．05）；血总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、UA与对照组比较差异有统计学意义（均P〈0．01）。OGTT后2hPG7．8-11．1mmol／L的患者占19％。结论中青年原发性高血压部分患者在FPG正常时可能已经出现OGTT减低、空腹胰岛素水平升高，存在胰岛素抵抗；建议早做OGTT，对同时出现血脂、UA代谢紊乱者，应进行早期干预。     

Impairment of glucose tolerance in normal adults following a lowered carbohydrate intake

Some normal people are falsely classified as having impaired glucose tolerance (IGT) if they are given an oral glucose tolerance test (OGTT) when their last meal contained very few carbohydrates. In this study, the duration of carbohydrate restriction was extended to one and three days and the relationship between the carbohydrate restriction and the glucose tolerance after an OGTT was examined. Two different groups of normal subjects were placed on high-carbohydrate (80% carbohydrates) and low-carbohydrate (10%) diets before an OGTT; one group for one day and the other for 3 days. None of the subjects showed impairment of glucose tolerance when placed on the high-carbohydrate regimens. In contrast, 3 of 12 subjects and 2 of 8 subjects placed on the low-carbohydrate diets for 1 and 3 days, respectively, were classified as having IGT. The impairment of glucose tolerance was invariably accompanied by an increase in the fasting plasma free fatty acid level. The longer the period of carbohydrate restriction, the severer was the glucose tolerance impairment. However, the number of subjects who were classified as having IGT did not depend on the duration of carbohydrate restriction. The impairment of glucose tolerance after carbohydrate restriction may be associated with the Randle effect, which is the activation of the glucose-free fatty acid cycle.     

Serum concentration of small dense low-density lipoprotein-cholesterol during oral glucose tolerance test and oral fat tolerance test

BACKGROUND: Small dense low-density lipoprotein (sdLDL) is well known as an atherogenic lipoprotein. We developed a new assay to measure serum concentration of sdLDL-cholesterol (sdLDLC). Using this assay, we reported a unique circadian rhythm of sdLDLC. We determined whether a glucose intake and/or a fat intake affects on serum sdLDLC concentration and determined the modulators of serum sdLDLC concentration. METHODS: Ten healthy volunteers were recruited to perform both a 75 g oral glucose tolerance test (OGTT) and an oral fat tolerance test (OFTT) to determine the effects of glucose and fat ingestion separately. Blood was measured for sdLDLC concentration and other valuables. RESULTS: Serum concentrations of total cholesterol, LDLC, remnant-like particles-cholesterol (RLPC), and apolipoprotein B significantly decreased during OGTT (p<0.05). SdLDLC also decreased and was a minimum at 2 h after glucose ingestion and increased to the baseline by 3 h. The sdLDLC decrease was seen while serum insulin level was high. The change of sdLDLC during OGTT had greater inverse correlationship with that of serum insulin level (r=-0.74, p<0.01) than that of plasma glucose level (r=-0.69, p=0.04). After fat ingestion, triglyceride and RLPC increased remarkably (p<0.01) but sdLDLC, LDLC, apolipoprotein B, and insulin did not change significantly. CONCLUSIONS: Serum concentration of sdLDLC was not affected by a fat intake but by a glucose intake. The change of sdLDLC was associated by that of serum insulin level, suggesting that insulin can be one of the key modulator of serum sdLDLC level as well as LDL metabolism.     

No influence of high- and low-carbohydrate diet on the oral glucose tolerance test in pregnancy

OBJECTIVE: Our objective was to determine the influence of the carbohydrate content of the diet preceding the oral glucose tolerance test (OGTT) in pregnancy on the test results and to evaluate the necessity of the recommended preparatory high-carbohydrate diet. STUDY DESIGN: Thirty-four women from our outpatient clinic were enrolled in this prospective study. After giving informed consent, each women underwent a 90-min lesson (supervised by a dietary assistant) covering the carbohydrate, protein and fat content of different foods. Women were then randomized and in a crossover design started a diet with either a low or a high carbohydrate content. We were aiming at a carbohydrate intake of 40% in the low-carbohydrate week (LCH) and 50% in the high-carbohydrate week (HCH). Compliance was monitored by a detailed food diary which the women kept and which included the weight of the foods they consumed. RESULTS: The actual dietary intakes as calculated from the food diaries showed that the mean caloric intake was 1801 +/- 314 kcal in the LCH and 2118 +/- 312 kcal in the HCH week (<0.001). During the LCH diet, CH intake was 39 +/- 6.1% and 49 +/- 6.6% in the HCH week (P < 0.001). The carbohydrate intake per kilogram bodyweight was 30 +/- 5.3 kcal vs. 35 +/- 5.2 kcal (P < 0.001). The number of patients diagnosed with gestational diabetes was two in the LCH and three in the HCH week (not significant). The sum of the OGTT values (fasting, 1 h and 2 h) after the LCH was 18.9 +/- 2.1 mmol/l vs. 18.8 +/- 2.1 mmol/l after the HCH (P = 0.51). No differences could be found in both groups regarding the fasting, 1-h, or 2-h glucose values. Including patients with a CH difference of at least 5%, 10%, and 15% carbohydrate between the weeks, we still did not observe any differences in the OGTT sum. We also looked at a possible influence of the CH content of the diet on the day before the test and of the last meal before the OGTT results and observed there was none. CONCLUSION: This is the first study which has observed the influence of the previous day's meal on the test results. We conclude from our results that the carbohydrate percentage of the preparatory diet did not influence the results of an OGTT, even when we increased the difference in carbohydrate intake stepwise up to 15%. This might indicate that a preparatory diet before the OGTT is not necessary for women with normal nutritional behavior.     

Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes.

OBJECTIVE: In normal adults, a small (catalytic) dose of fructose administered with glucose decreases the glycemic response to a glucose load, especially in those with the poorest glucose tolerance. We hypothesized that an acute catalytic dose of fructose would also improve glucose tolerance in individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: Five adults with type 2 diabetes underwent an oral glucose tolerance test (OGTT) on two separate occasions, at least 1 week apart. Each OGTT consisted of 75 g glucose with or without the addition of 7.5 g fructose (OGTT + F or OGTT - F), in random order. Arterialized blood samples were collected from a heated dorsal hand vein twice before ingestion of the carbohydrate and every 15 min for 3 h afterward. RESULTS: The area under the curve (AUC) of the plasma glucose response was reduced by fructose administration in all subjects; the mean AUC during the OGTT + F was 14% less than that during the OGTT - F (P < 0.05). The insulin AUC was decreased 21% with fructose administration (P = 0.2). Plasma glucagon concentrations declined similarly during OGTT - F and OGTT + F. The incremental AUC of the blood lactate response during the OGTT - F was approximately 50% of that observed during the OGTT + F (P < 0.05). Neither nonesterified fatty acid nor triglyceride concentrations differed between the two OGTTs. CONCLUSIONS: Low-dose fructose improves the glycemic response to an oral glucose load in adults with type 2 diabetes, and this effect is not a result of stimulation of insulin secretion.     

Lifestyle intervention in individuals with normal versus impaired glucose tolerance

BACKGROUND: Lifestyle intervention is effective in the prevention of type 2 diabetes in individuals with impaired glucose tolerance (IGT). It is currently unknown whether it has beneficial effects on metabolism to a similar extent, in individuals with normal glucose tolerance (NGT) compared to individuals with IGT. MATERIALS AND METHODS: Data from 181 subjects (133 with NGT and at risk for type 2 diabetes and 48 with IGT) who participated in the Tuebingen Lifestyle Intervention Program with increase in physical activity and decrease in caloric intake were included into this study. Body fat distribution was quantified by whole-body magnetic resonance (MR) tomography and liver fat and intramyocellular fat by (1)H-MR spectroscopy. Insulin sensitivity was estimated from an oral glucose tolerance test (OGTT). RESULTS: After 9 +/- 2 months of follow-up, the diagnosis of IGT was reversed in 24 out of 48 individuals. Only 14 out of 133 participants with NGT developed IGT. Body weight decreased in both groups by 3% (both P < 0.0001). Two-hour glucose concentrations during an OGTT decreased in individuals with IGT (-14%, P < 0.0001) but not with NGT (+2%, P = 0.66). Insulin sensitivity increased both in individuals with IGT (+9%, P = 0.04) and NGT (+17%, P < 0.0001). Visceral fat (-8%, P = 0.006), liver fat (-28%, P < 0.0001) and intramyocellular fat (-15%, P = 0.006) decreased in participants with IGT. In participants with NGT these changes were significant for visceral fat (-16%, P < 0.0001) and liver fat (-35%, P < 0.0001). CONCLUSIONS: Moderate weight loss under a lifestyle intervention with reduction in total, visceral and ectopic fat and increase in insulin sensitivity improves glucose tolerance in individuals with IGT but not with NGT. In individuals with NGT, the beneficial effects of a lifestyle intervention on fat distribution and insulin sensitivity possibly prevent future deterioration in glucose tolerance.     

Postprandial triglycerides in response to high fat: role of dietary carbohydrate

BACKGROUND: The postprandial triglyceride response following a meal high in fat (HFM) has been related to atherogenesis and insulin resistance. We examined the influence of dietary carbohydrate and the accompanying insulin secretory response on the postprandial triglyceride response following a HFM. MATERIALS AND DESIGN: High-fat meals of equal fat content (fat 80 g) containing either 20 g (low) or 100 g (high) of carbohydrate (HFM-LC and HFM-HC, respectively), and therefore not isocaloric (4250 kJ of HFM-LC and 5450 kJ of HFM-HC), were consumed by seven (four male, three female) normolipidaemic subjects (aged 32.9 +/- 3.7 years, BMI 24.7 +/- 1.8 kg m-2). Blood and indirect calorimetry data were collected at 0-4 h. RESULTS: HFM-HC produced a significant rise in plasma glucose (Delta0.54 +/- 0.23 mmol L-1, P = 0.05) at 2 h, while a HFM-LC elicited no mean change from baseline. Following a HFM-LC, the plasma insulin incremental area under the curve (AUC) was significantly lower (31.3 +/- 6.7 vs. 83.2 +/- 11.9 mU l-1 h-1, P < 0.0003) and the postprandial triglyceride response AUC was significantly greater (1.66 +/- 0.36 vs. 1.24 +/- 0.31 mmol L-1 h-1, P < 0.006) compared with a HFM-HC. Plasma free fatty acids were suppressed by 44% (P = 0.04) and 66% (P < 0.0001) at 1 h following HFM-LC and HFM-HC, respectively, compared with baseline. There were no significant differences between the meals in energy expenditure, substrate oxidation rates, or respiratory quotient responses. CONCLUSIONS: By design, the HFMs were not isocaloric but the presence of carbohydrate in a HFM invoked an insulin response that significantly reduced the 4 h postprandial triglyceride response even in healthy, normolipidaemic subjects. This phenomenon may have clinical implications, particularly in relation to insulin sensitivity.     

Effects of jejuno-ileal bypass on serum lipoproteins and glucose tolerance in severely obese patients

Plasma insulin and blood glucose during oral glucose tolerance tests (OGTT) and serial determinations of serum lipoprotein fractions before and after jejuno-ileostomy in twenty severely obese (mean weight 137 kg) patients with a mean age of 29 years revealed statistically significant postoperative decreases in all parameters concomitant with a mean weight loss of 42 kg. Before the operation the patients were hyperinsulinaemic and had elevated blood glucose levels during OGTT though no patient had overt diabetes. Serum triglyceride and total cholesterol levels were normal but HDL cholesterol was significantly lower than in controls. During follow-up at least until body weight had levelled off a mean 19 months post-operative, there were statistically significant reductions in blood glucose and plasma insulin as well as serum total cholesterol and lipoprotein fractions. There was no change in serum triglycerides. The low preoperative HDL levels decreased. In a subgroup of these patients we have earlier shown postoperative increases in arterial tissue cholesterol coincident with the present significant decreases in HDL as well as in LDL cholesterol. Correlations between total cholesterol and lipoprotein cholesterol values in serum and blood glucose and plasma insulin at fast and during OGTT and changes in these parameters demonstrate interrelationships between lipid and carbohydrate metabolism. The bypass procedure most likely reduces the intestinal synthesis of HDL which in turn may increase hepatic cholesterol synthesis. Evidently there is a multifactorial aetiology for the low HDL levels in the severely obese both before and after jejuno-ileostomy.     

Relationship of body fat distribution to blood pressure, carbohydrate tolerance, and plasma lipids in healthy obese women

In 110 obese, healthy women, a relationship was sought between distribution of body fat and blood pressure, glucose tolerance, plasma insulin, and fasting plasma lipid and serum uric acid concentrations. The index of body fat distribution was the ratio of waist circumference to hips circumference (WHR). The WHR range in this group was 0.5 to 0.99, with a median value of 0.78. Positive, significant correlations were found between WHR and both systolic and diastolic blood pressure and between WHR and the total integrated plasma glucose and insulin responses during 4 hr oral glucose tolerance tests. No relationship was found between WHR and age, the degree of obesity as defined by the weight-to-height ratio, or concentrations of fasting plasma free fatty acids, plasma triglyceride, plasma cholesterol, or serum uric acid. Subsequently, 27 women in the highest quartile of the WHR range (0.83 to 0.99) were compared to 28 age- and weight-matched subjects in the lowest quartile of WHR (0.5 to 0.73). Women in the highest quartile had systolic and diastolic blood pressure as well as total plasma glucose and insulin responses during glucose tolerance tests that significantly exceeded mean values of subjects in the lowest quartile. We conclude that in healthy, obese women, a continuum exists that relates increasing fat accumulation in the upper body to progressively higher blood pressure, reduced carbohydrate tolerance, and higher plasma insulin concentrations. These changes occurred independently of age of degree of obesity in this population.     

Effect of new oral antidiabetic agent CS-045 on glucose tolerance and insulin secretion in patients with NIDDM.

OBJECTIVE: To study the effects of CS-045, a newly developed thiazolidine analogue, on glucose tolerance and insulin response to oral glucose load in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Nineteen NIDDM patients (mean +/- SD age 48.9 +/- 9.4 yr) whose previous glycemic control on diet and/or sulfonylurea (SU) therapy was judged stable but unsatisfactory (greater than 7.8 mM) were selected for this study. CS-045 (400 mg/day p.o.) was given alone or together with the previous SU drugs for 12 wk. A 75-g oral glucose tolerance test (OGTT) was performed before and after CS-045 treatment. Results: The following results were found after CS-045 treatment. 1) Fasting plasma glucose (FPG) and HbA1c decreased (n = 19, FPG, 11.0 +/- 2.4 vs. 8.4 +/- 2.7 mM [before vs. after], P less than 0.001; HbA1c, 8.0 +/- 1.1 vs. 7.4 +/- 1.3%, P less than 0.005), and glucose tolerance markedly improved. 2) Fasting insulin (immunoreactive insulin [IRI]) and insulin response during OGTT decreased (n = 19, fasting IRI, 77.4 +/- 49.8 vs. 56.5 +/- 24.6 pM [before vs. after], P less than 0.05; area under the curve of IRI, 540.3 +/- 350.5 vs. 426.4 +/- 216.3 pM.h, P less than 0.05). CONCLUSIONS: CS-045 is effective in improving glucose tolerance without stimulation of insulin secretion in NIDDM, suggesting an effect in improving insulin sensitivity.     

A Higher-Complex Carbohydrate Diet in Gestational Diabetes Mellitus Achieves Glucose Targets and Lowers Postprandial Lipids: A Randomized Crossover Study

OBJECTIVE

The conventional diet approach to gestational diabetes mellitus (GDM) advocates carbohydrate restriction, resulting in higher fat (HF), also a substrate for fetal fat accretion and associated with maternal insulin resistance. Consequently, there is no consensus about the ideal GDM diet. We hypothesized that, compared with a conventional, lower-carbohydrate/HF diet (40% carbohydrate/45% fat/15% protein), consumption of a higher-complex carbohydrate (HCC)/lower-fat (LF) Choosing Healthy Options in Carbohydrate Energy (CHOICE) diet (60/25/15%) would result in 24-h glucose area under the curve (AUC) profiles within therapeutic targets and lower postprandial lipids.

RESEARCH DESIGN AND METHODS

Using a randomized, crossover design, we provided 16 GDM women (BMI 34 ± 1 kg/m²) with two 3-day isocaloric diets at 31 ± 0.5 weeks (washout between diets) and performed continuous glucose monitoring. On day 4 of each diet, we determined postprandial (5 h) glucose, insulin, triglycerides (TGs), and free fatty acids (FFAs) following a controlled breakfast meal.

RESULTS

There were no between-diet differences for fasting or mean nocturnal glucose, but 24-h AUC was slightly higher (∼6%) on the HCC/LF CHOICE diet (P = 0.02). The continuous glucose monitoring system (CGMS) revealed modestly higher 1- and 2-h postprandial glucose on CHOICE (1 h, 115 ± 2 vs. 107 ± 3 mg/dL, P ≤ 0.01; 2 h, 106 ± 3 vs. 97 ± 3 mg/dL, P = 0.001) but well below current targets. After breakfast, 5-h glucose and insulin AUCs were slightly higher (P < 0.05), TG AUC was no different, but the FFA AUC was significantly lower (∼19%; P ≤ 0.01) on the CHOICE diet.

CONCLUSIONS

This highly controlled study randomizing isocaloric diets and using a CGMS is the first to show that liberalizing complex carbohydrates and reducing fat still achieved glycemia below current treatment targets and lower postprandial FFAs. This diet strategy may have important implications for preventing macrosomia.