肝硬化患者血清肝纤维化指标与糖代谢异常的关系

目的探讨肝硬化患者血清肝纤维化指标与糖代谢异常的关系。方法将91例肝硬化患者按口服葡萄糖耐量试验(OGTT)分为糖代谢正常组和异常组;用放射免疫法测定血浆胰岛素以及血清透明质酸()HA)、层黏蛋白(LN)、Ⅳ型胶原(4C)、Ⅲ型胶原氨端肽(PCⅢ);同步检测肝功能、凝血酶原活动度(PTA);计算胰岛素敏感性指数(ISI)。结果糖代谢异常组空腹及糖负荷后0.5～2h血糖明显升高(P值均<0.05),空腹及糖负荷后2～3h胰岛素显著增高(P<0.05);肝硬化糖代谢异常组肝纤维化四项指标升高均较糖代谢正常组更为明显,其中HA及PCⅢ水平两组的差异有统计学意义(均P<0.05);两组患者肝功能指标及ISI均有明显差异(P<0.05),肝硬化糖代谢异常组肝功能降低,组织胰岛素敏感性下降。结论肝硬化患者反复肝炎活动,肝功能进行性损害,可促进肝纤维化的进展,并导致糖代谢异常和胰岛素抵抗。     

不同糖代谢状态的维吾尔族人糖负荷后丙二醛水平的变化

目的　探讨不同糖代谢状态的维吾尔族人糖负荷后丙二醛 (MDA)水平的变化。　方法　 10 0 2名维吾尔族市民 ,年龄 30～ 6 0岁。进行 75g葡萄糖耐量试验 (OGTT) ,根据血糖结果按1997年ADA标准将人群分成正常糖代谢 (NGT)组、空腹血糖受损 (IFG)组、糖耐量受损 (IGT)组和糖尿病 (DM )组。各组按年龄、性别分层随机抽取 30人 ,共 12 0人。测定空腹及糖负荷后 2h血浆胰岛素、甘油三酯、胆固醇、高密度脂蛋白及MDA。　结果　 (1)IGT组和DM组糖负荷后 2hMDA较空腹时增高 ,差异有非常显著意义 (t=4 75 5 2、16 0 791,P <0 0 1) ;糖负荷后MDA在DM组较NGT组、IFG组、IGT组均显著增高 (Hc =4 4 5 70 8,P <0 0 1) ;空腹MDA四组间差异无显著意义。 (2 )多元逐步回归分析显示 ,糖负荷后MDA增高的相关因素是糖负荷后甘油三酯的增高 (t=2 3882 ,P <0 0 5 )。　结论　糖代谢异常组尤其是DM组 ,糖负荷后MDA水平显著增高 ,与其密切相关的因素是糖负荷后明显增高的甘油三酯水平。控制餐后甘油三酯可能是糖尿病患者预防大血管并发症的关键措施之一。     

肝硬化门脉高压患者糖代谢异常的临床研究

目的：探讨肝硬化门脉高压患者糖代谢异常的病因和机理。方法：对30例肝硬化门脉高压患者，32例Ⅱ型糖尿病患者和15例正常人进行了空腹和餐后血糖，糖化血红蛋白，空腹胰岛素，C肽，胰高血糖素试验，计算胰岛素释放指数和胰岛素敏感性指数，对各组检查结果进行比较分析。结果：肝硬化组存在着糖耐量异常，餐后血糖，糖化血红蛋白，血清胰岛素，C肽和胰高血糖素多种指标显著高于正常对照组（P＜0．01。胰岛素敏感指数显著低于正常对照组（P＜0．01）。肝硬化Child分级比较，随着病情加重，糖代谢紊乱逐渐突出。肝硬化者胰岛素，C肽和胰岛素释放指数显著高于Ⅱ型糖尿病患者（P＜0．01），但胰岛素敏感指数和胰高血糖素比较两组之间无明显差异（P＞0．05）。结论：肝硬化门脉高压患者存在糖代谢异常，这种代谢异常主要是由于肝功能损害，胰岛素抵抗和胰高血糖素升高所致。     

运动对老年高血压患者血压和糖,脂代谢的影响

目的探讨运动对老年高血压患者血压和糖、脂代谢的影响。方法将４３例老年高血压患者随机分为运动组和对照组，两组均接受尼群地平降压治疗，同时运动组进行为期３个月的体育运动。测量两组入组时和３个月后血压、血脂、空腹血糖、胰岛素及负荷后１ｈ和２ｈ血糖及血胰岛素。结果经过３个月规则运动，运动组空腹及糖负荷后１ｈ、２ｈ胰岛素水平、血胆固醇、甘油三酯及低密度脂蛋白较对照组降低（Ｐ值均＜０．０５），高密度脂蛋白较对照组增高（Ｐ＜０．０５）；试验后两组血压均较入组时降低，而运动组服药量较对照组减少（Ｐ＜０．０５）。结论规则的体育运动能降低老年高血压患者空腹及糖负荷后血胰岛素水平，并有利于血脂代谢紊乱的纠正和血压的控制     

体外循环缺血再灌注后心肌缺血胰岛素抵抗与相关因子变化关系的研究

目的:探讨体外循环(cardiopulmonary bypass,CPB)缺血再灌注后,冠状动脉血清胰高血糖素、生长激素及肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的变化与心肌胰岛素抵抗(insulin resistance,IR)的关系及其作用。方法:选择近年在我院行体外循环手术患者48例分为两组:组1主动脉阻断时间≤30min(n=24);组2主动脉阻断时间30min(n=24)。于CPB转流3min(主动脉阻断前)、主动脉开放后15min、45min、75min、2h、4h及8h时分别采集桡动脉、冠状静脉窦血标本,比较对应时点血浆葡萄糖、胰岛素、胰高血糖素、生长激素、TNF-α及计算胰岛素抵抗指数(IRI)的变化。结果:血浆葡萄糖、胰岛素及胰岛素抵抗指数在缺血再灌注后显著不同程度增高,且于再灌注后15min达峰值,差异有统计学意义(P0.05);心肌对葡萄糖的摄取、利用发生严重障碍,与1组比较,组2上述指标增高程度更重、持续更久,差异有统计学意义(P0.05)。检测血清胰高血糖素、生长激素及TNF-α与血浆葡萄糖、胰岛素及胰岛素抵抗指数增高呈一致性,随主动脉阻断时间延长,其增高程度更重、持续更久,差异有统计学意义(P0.05)。结论:在人体外循环中心肌缺血再灌注后冠状动脉血清胰高血糖素、生长激素及TNF-α分泌增加可能是心肌IR的重要因素之一。     

非胰岛素依赖性糖尿病患者的激素代谢变化（附60例报告）

对６０例肥胖型非胰岛素依赖性糖尿病（ＮＩＤＤＭ）患者和３０例单纯性肥胖者（对照组）进行了空腹及糖负荷后血糖、胰岛素、胰高糖素、生长激素水平比较。根据空腹血糖水平（ＦＢＧ）将ＮＩＤＤＭ患者分为ＤＭＡ组和ＤＭＢ组，结果显示：①ＤＭＡ组胰岛素分泌相对不足，胰高糖素分泌基本正常。②ＤＭＢ组胰岛素分泌明显不足，胰高糖素水平明显升高。③ＤＭＡ和ＤＭＢ组空腹及餐后１、２小时生长激素水平明显高于对照组。提示胰高糖     

肝硬化糖代谢紊乱与肝功能Child—pugh分级关系研究

目的探讨肝硬化患者的血浆胰岛素、胰高血糖素和血糖变化以及与肝功能的关系。方法我们对86例肝硬化患者和29例正常人进行糖耐量试验及胰岛素释放试验,测定胰高血糖素,并对结果进行分析。结果肝硬化患者血糖在各个时间点均高于正常值,餐后1h、2h、3h差异有统计学意义（P〈0．05）。肝硬化失代偿组胰岛素水平均高于正常对照组（P〈0．05）。肝功能分级与糖耐量及胰岛素释放结果比较：3组空腹胰岛素水平均增高,3组比较差异有统计学意义（P〈0．05）。餐后各时点血糖及胰岛素水平均增高,胰岛素高峰延迟,差异有统计学意义（P〈0．05）。3组胰高血糖素比较差异有统计学意义（P〈0．05）。结论肝硬化病人不论是在空腹或在餐后都有高胰岛素水平。胰高血糖素亦较正常对照组增高。随着Child—pugh分级的增高,糖耐量降低逐渐加重,胰岛素及胰高血糖素水平亦更加突出。     

病毒性肝炎和肝硬化患者糖代谢研究

为阐明病毒性肝炎及肝硬化患者胰岛Ｂ细胞功能及糖代谢状况，我们作了静脉糖耐量试验（ｉｖＧＴＴ）和胰岛素，Ｃ肽释放试验（ＩＲＴ，ＣＰＲＴ），并同时测定了基础血糖（ＧＳ），胰岛素（ＩＮＳ），Ｃ肽（ＣＰ），皮质醇（Ｆ），生长激素（ＧＨ），生长抑素（ＳＳ）和胰高血糖素（ＧＮ），结果８５例中１７例糖耐量减退，其中慢性肝炎（ＣＨ）组２例，代偿性肝炎肝硬化（ＨＬＣ－Ｉ）组５例，的代偿性肝炎肝硬化（ＨＬＣ－Ⅱ）组，     

男性中国人体脂分布与激素模式

目的　为研究中国人男性激素模式与体脂分布的关系。方法　用核磁共振（ Ｍ Ｒ Ｉ） 测量８８ 名中国男性的体脂分布，并分为腹内脂肪积聚与非腹内脂肪积聚组。同时测定睾酮（ Ｔ Ｔ） 、游离睾酮（ Ｆ Ｔ） 、硫酸去氢表雄酮（ Ｄ Ｈ Ｅ Ａ Ｓ） 、性激素结合球蛋白（ Ｓ Ｈ Ｂ Ｇ） 、生长激素（ Ｇ Ｈ） 、皮质醇（ Ｆ） 、空腹及糖负荷后胰岛素及 Ｃ 肽。结果　腹内脂肪增多者 Ｔ Ｔ 显著下降，不受 Ｂ Ｍ Ｉ影响。皮质醇及糖负荷后２ 小时胰岛素、 Ｃ 肽显著增加。多元逐步回归分析见到， Ｔ Ｔ 对腹内脂肪的影响达１９ ．２２ ％ 。结论　雄性激素减少是腹内脂肪积聚者的特殊改变。     

胰岛素抵抗及胰岛素分泌功能对肝硬化糖代谢的影响

为探讨肝硬化患者胰岛素抵抗及胰岛素分泌功能和糖代谢的改变。地３０例肝硬化２和２６例正常人进行口服葡萄糖耐量及胰岛素释放试验,以Ｈｏｍａ模型计算胰岛素抵抗指数（ＩＲ）及胰岛β细胞功能指数（ＨＤＣＩ）,并对结果进行分析。结果显示,肝硬化组糖耐是较对照组显著降低,血清胰 素水平增高,并呈现释放延迟,ＫＩＲ有ＨＤＣＩ指数高于对照组。结论：肝硬化患者存在胰同素抵抗、肝源怀糖耐量异常及内源性高胰岛素血症或胰岛     

Effect of Intraoperative Amino Acid Infusion on Blood Glucose under General Anesthesia Combined with Epidural Block

Aim: To investigate the effect of intraoperative amino acid infusion on blood glucose in patients under general anesthesia combined with epidural block. Methods: 36 patients were randomly assigned to receive an intraoperative infusion of 18 compound amino acids (group AA) or lactated Ringer solution (group LR) at 2 ml·kg(-1)·h(-1). Nasopharyngeal temperature, and blood glucose, plasma insulin, C-peptide and glucagon concentrations were measured 30 min before induction (T0), 10 min after induction (T1), 30 min and 2 h after skin incision (T2, T3), and 30 min and 2 h postoperatively (T4, T5). Results: Nasopharyngeal temperature values, which decreased during surgery in both groups, were significantly higher in group AA than in group LR from T3 to T5. Compared with T0, the blood glucose concentration increased significantly from T2 in group AA and T3 in group LR to T5. Plasma insulin and C-peptide concentrations did not change significantly in group LR, while both increased significantly in group AA from T1 to T4. The plasma glucagon concentration did not change significantly in either group. Conclusion: Intraoperative amino acid infusion in patients under general anesthesia combined with epidural block may accelerate the increase of blood glucose concentration and stimulate insulin secretion, and can alleviate hypothermia during the later period of surgery and postoperatively.     

Idiopathic reactive hypoglycemia: a role for glucagon?

We previously reported that patients with idiopathic reactive hypoglycemia (plasma glucose concentration lower than 2.5 mmol/L 2-4 h after the ingestion of 75 g of glucose) display reduced or absent counterregulatory response of the glucagon secretion and increased insulin sensitivity. In order to examine the effect of glucagon on the increased insulin sensitivity in these patients, 12 subjects with idiopathic reactive hypoglycemia underwent a two-step hyperinsulinemic (1 mU/kg.min) euglycemic glucose clamp and were compared with 12 normal control subjects matched for age, weight and sex. During the first step of the glucose clamp (only insulin + glucose infusion) the patients with Idiopathic Reactive Hypoglycemia required higher glucose infusion rates to maintain euglycemia than normal subjects (9.09 +/- 0.29 mg/kg. min vs 7.61 mg/kg.min). When basal glucagon secretion was replaced (+ somatostatin and glucagon, second step of the clamp) the glucose infusion rates required to maintain euglycemia in patients with Idiopathic Reactive Hypoglycemia significantly decreased (to 7.17 +/- 0.40 mg/kg.min) and resulted similar to normal subjects (7.64 +/- 0.41 mg/kg.min). Thus, in patients affected by Idiopathic Reactive Hypoglycemia, glucagon secretion may play an important role in the pathogenesis of the increased insulin sensitivity and hypoglycemia.     

Glucose tolerance and pancreatic hormones in thyroidectomized and thyroid hormone-injected cockerels

The effect of surgical thyroidectomy and of T4/T3 injections on basal and glucose-induced concentrations of plasma insulin and glucagon has been investigated in 20-week-old domestic chickens. Birds injected daily (im) for 2 weeks with T4/T3 (50 micrograms/day) had marginally lower fasting glucose concentrations whereas thyroidectomy had no effect. Glucose tolerance to an intravenous injection of glucose (0.5 g/kg) was impaired in T4/T3 injected animals although the peak hyperglycemia was identical with sham-operated animals. This was associated with significantly reduced basal and glucose-induced insulin concentrations. However, fasting plasma glucagon concentrations were significantly elevated in this group as was the magnitude of the glucose-induced suppression of glucagon release 10 min after injection (48% decline vs 34% in sham-operated animals). Basal concentrations of plasma insulin were markedly elevated in thyroidectomized animals and were associated with only mildly depressed plasma glucagon levels. The absolute concentrations of plasma insulin remained higher in the thyroidectomized birds as compared with those of sham-operated or T4/T3 injected animals after the glucose challenge, although within 30 min after glucose injection they had significantly declined below preinjection levels. This was associated both with significantly reduced plasma glucose concentrations 30 min after injection and the lowest absolute levels of plasma glucagon. The rebound in plasma glucagon in sham-operated animals in response to the rapid decline in glucose concentrations was not as pronounced in either thyroidectomized or T4/T3 injected animals. In conclusion these studies illustrate the secretory dynamics of avian pancreatic endocrine islets in response to both absolute glucose levels and glucose requirements as affected by the thyroid state of the bird.     

Somatostatin enhances insulin-mediated glucose disposal in elderly subjects

Somatostatin (SRIH) infusion has been widely used in metabolic studies of carbohydrate metabolism. While the effects of SRIH itself on various aspects of carbohydrate economy have been assessed in young adults, such studies have not been conducted in the elderly, which represent an increasingly important study group. To examine the effect of SRIH on insulin-mediated glucose disposal in the elderly, we studied 12 (7 men and 5 women) healthy nonobese subjects, aged 65-80 yr. Paired 3-h euglycemic insulin clamp studies were performed in random order employing insulin alone (22 mU/m2.min) or insulin with SRIH (250 micrograms/h) and glucagon (0.4 ng/kg.min) to maintain normal basal plasma glucagon levels. Basal plasma insulin, glucose, glucagon, GH, and glucose production and disappearance were similar on each occasion. Steady state (10-180 min) mean plasma insulin [insulin alone, 298 +/- 12 (+/- SE); insulin; glucagon, and SRIH, 304 +/- 15 pmol/L] and glucagon (insulin alone, 85 +/- 7; insulin, glucagon, and SRIH, 96 +/- 9 ng/L) concentrations were similar. At steady state (150-180 min) glucose production was suppressed to similar levels (insulin alone, 26 +/- 7; insulin, glucagon, and SRIH, 36 +/- 13 mumol/kg.min). However, steady state glucose disposal was significantly higher during the SRIH infusion (insulin alone, 295 +/- 26; insulin, glucagon, and SRIH, 346 +/- 32 mumol/kg.min; P less than 0.02). We conclude that SRIH augments insulin-mediated glucose disposal in healthy older subjects at physiological levels of insulin.     

Glucagon regulates orexin A secretion in humans and rodents

Aims/hypothesis

Orexin A (OXA) modulates food intake, energy expenditure, and lipid and glucose metabolism. OXA regulates the secretion of insulin and glucagon, while glucose regulates OXA release. Here, we evaluate the role of glucagon in regulating OXA release both in vivo and in vitro.

Methods

In a double-blind crossover study, healthy volunteers and type 1 diabetic patients received either intramuscular glucagon or placebo. Patients newly diagnosed with type 2 diabetes underwent hyperinsulinaemic–euglycaemic clamp experiments, and insulin–hypoglycaemia tests were performed on healthy volunteers. The primary endpoint was a change in OXA levels after intramuscular glucagon or placebo administration in healthy participants and patients with type 1 diabetes. Secondary endpoints included changes in OXA in healthy participants during insulin tolerance tests and in patients with type 2 diabetes under hyperinsulinaemic–euglycaemic conditions. Participants and staff conducting examinations and taking measurements were blinded to group assignment. OXA secretion in response to glucagon treatment was assessed in healthy and obese mice, the streptozotocin-induced mouse model of type 1 diabetes, and isolated rat pancreatic islets.

Results

Plasma OXA levels declined in lean volunteers and in type 1 diabetic patients injected with glucagon. OXA levels increased during hyperinsulinaemic hypoglycaemia testing in healthy volunteers and during hyperinsulinaemic euglycaemic conditions in type 2 diabetic patients. Plasma OXA concentrations in healthy lean and obese mice and in a mouse model of type 1 diabetes were lower after glucagon treatment, compared with vehicle control. Glucagon decreased OXA secretion from isolated rat pancreatic islets at both low and high glucose levels. OXA secretion declined in pancreatic islets exposed to diazoxide at high and low glucose levels, and after exposure to an anti-insulin antibody. Glucagon further reduced OXA secretion in islets pretreated with diazoxide or an anti-insulin antibody.

Conclusions/interpretation

Glucagon inhibits OXA secretion in humans and animals, irrespective of changes in glucose or insulin levels. Through modifying OXA secretion, glucagon may influence energy expenditure, body weight, food intake and glucose metabolism.     

The effect of manipulation of basal pulsatile insulin on insulin action in Type 2 diabetes.

AIM: Disordered insulin pulsatility is associated with insulin resistant states including Type 2 diabetes. However, whether abnormal basal insulin pulses play a role in the pathogenesis of insulin resistance or are simply an associated feature remains undetermined. We investigated this relationship further by studying the effect of overnight (10 h) pulsatile insulin infusion on subsequent insulin sensitivity. METHODS: We studied 17 Type 2 diabetic patients who underwent one of two protocols. In protocol A (10 patients) on two separate nights we infused insulin 0.1 mU/kg/min either in a constant infusion or in pulses every 13 min. Octreotide (0.43 microg/kg/h) was given to suppress endogenous insulin secretion and physiological replacement of glucagon (30 ng/kg/h) administered. Insulin sensitivity was measured using a hyperinsulinaemic euglycaemic clamp (2 mU/kg/min) next morning. In protocol B (seven patients), we employed the same experimental procedure but used a basal insulin infusion rate of 0.09 mU/kg/min in 7-min or 13-min pulses. RESULTS: Appropriate pulse patterns were confirmed in each protocol. In protocol A, after overnight infusions, glucose infusion rates required to maintain euglycaemia at steady state hyperinsulinaemia were similar (33.9 +/- 5.2 vs. 31.2 +/- 4.1 micromol/kg/min; P = NS). In protocol B, after overnight infusions the glucose infusion rates required during hyperinsulinaemia were significantly lower during 7-min pulses (39.9 +/- 5.7 vs. 44.7 +/- 5.6 micromol/kg/min; P < 0.05). CONCLUSION: There was no demonstrable priming effect derived from overnight pulsatile insulin compared with constant insulin infusion on subsequent insulin sensitivity in Type 2 diabetic subjects. The failure of 7-min pulses to exhibit an advantageous effect over 13-min pulses raises questions about the natural frequency of basal insulin pulses and their biological effect.     

Regulation of glucose kinetics in trauma patients by insulin and glucagon.

The current study was undertaken to evaluate the contribution of insulin and glucagon to regulation of glucose metabolism in man following severe, traumatic injury by manipulating concentrations of insulin and glucagon with infusions of somatostatin. Glucose kinetics were assessed with [U-14C, 6-(3)H]glucose in severely injured patients and compared with data obtained from patients recovering from minor, elective operative procedures. Glucose production was significantly increased in subjects with traumatic injury compared with control subjects (13.0 +/- 0.63 mumol/kg/min v 8.6 +/- 0.27 mumol/kg/min). There was no impairment in glucose oxidation by the injured patients. Modulation of insulin and glucagon with somatostatin indicated that non-insulin-mediated glucose uptake (NIMGU) was significantly elevated in injured patients (12.2 +/- 0.94 mumol/kg/min v 7.4 +/- 0.61 mumol/kg/min). Hepatic glucose output (HGO) in the absence of glucagon was also significantly elevated in injured patients (12.2 +/- 1.20 mumol/kg/min v 5.8 +/- 1.08 mumol/kg/min). Indirect calorimetry showed a 27% increase in resting energy expenditure (REE). Increased protein oxidation accounted for 56% of the increase in REE. Changes in carbohydrate and lipid oxidation accounted for 28% and 15% of the increase in REE. There was no correlation between the injury severity score of the injured patient and the degree of metabolic abnormality. It is concluded from these studies that (1) injured patients have a high rate of glucose turnover in the absence of glucagon and insulin; (2) the reliance on glucose as a source of energy is not diminished in injured subjects; and (3) increases in protein oxidation account for the majority of the increased REE found in injured patients.     

Effect of insulin on glucagon secretion mediated via glucose metabolism of pancreatic a cells in ducks

Summary A possible action of insulin via glucose metabolism on the pancreatic A cell response to glucose, was studied in ducks. 2-Deoxyglucose, a non-metabolizable analogue of glucose was used. In normal ducks, the hyperglycaemia induced by 2-deoxyglucose (IV: 0.5 g/kg) resulted in hyperglucagonaemia, while the same degree of hyperglycaemia, induced by glucose infusion (IV injection 25 mg/kg, and infusion 5 mg/kg/min) immediately suppressed glucagon secretion. In diabetic ducks, two days after subtotal pancreatectomy, glucose responsiveness of the A cell was abolished, but could be restored by insulin treatment before (IM 0.2 U/kg insulin+8 g/kg glucagon every 6 h) and during (IV 3.6 mU/kg+infusion 0.9 mU/kg/min) the glucose test (IV: 0.5 g /kg). The normal response of the A cell to glucose was not observed in diabetic insulin-treated ducks after the administration of 2-deoxyglucose (IV: 0.5 g/kg). These data suggest an inhibitory effect of the metabolism of glucose on the release of glucagon. In addition, the action of insulin on the A cell may be mediated by its effect on glucose metabolism within the A cell.     

Further support for heterogeneity of insulin response and insulin sensitivity in non-obese subjects with glucose intolerance

The relationship of insulin secretion and insulin sensitivity was studied in 67 age- and body weight-matched non-obese subjects, classified as having a normal glucose tolerance or glucose intolerance (50 g oral glucose load). Insulin response was studied by means of a 2 h glucose infusion. For the determination of insulin sensitivity a 1 h priming dose-constant insulin infusion technique was used. The per cent decrease of plasma glucose level at comparable steady-state insulin levels served as a measure of body sensitivity to exogenous insulin. In patients with glucose intolerance the early (delta IRI area 0-5 min) and late (delta IRI area 30-120 min) insulin responses to iv glucose were significantly reduced in comparison to controls. Controls and subjects with glucose intolerance showed considerable heterogeneity of insulin responses. Patients with glucose intolerance and relative insulin deficiency were not less responsive to insulin than subjects with normal glucose tolerance. There was, however, a wide variation of insulin sensitivity within the two groups. There was a weak significant inverse correlation between insulin response to glucose and insulin sensitivity for the two groups combined and for controls and subjects with glucose intolerance separately. The results demonstrate that the majority of non-obese patients with glucose intolerance and relative insulin deficiency does not exhibit a reduced responsiveness to insulin and therefore hypoinsulinaemia but not insulin resistance is the primary defect for an abnormal glucose tolerance in these group of subjects.