Role of vagus nerve in secretion of gastric inhibitory polypeptide in dogs

In order to clarify the role of the vagus nerve in the secretion of gastric inhibitory polypeptide (GIP), experiments were performed on dogs. Response of plasma GIP to intraduodenal instillation of glucose was slightly lower in a group which received atropine, than in a group of normal dogs. The response of plasma GIP to intraduodenal glucose load was not different between vagotomized dogs and normal dogs. Electric stimulation of the vagus nerve did not produce any significant changes in plasma GIP in anesthetized dogs. In conclusion, the present study indicates that the role of the vagus nerve on GIP secretion is tiny, if any, and that the nervous influence does not overcome the effect of intraluminal administration of glucose.     

Elevated plasma glucose-dependent insulinotropic polypeptide associates with hyperinsulinemia in impaired glucose tolerance

OBJECTIVE: The role of gut-derived incretin, glucose-dependent insulinotropic polypeptide (also known as gastric inhibitory peptide [GIP]), in compensatory beta-cell hypersecretion during insulin-resistant states and in transition to beta-cell failure in type 2 diabetes is unknown. RESEARCH DESIGN AND METHODS: We carried out oral glucose tolerance testing followed by blood sampling 10 times for 2 h on 68 age- and BMI-matched participants of the Baltimore Longitudinal Study on Aging (BLSA) with normal glucose tolerance (34 subjects), impaired glucose tolerance (IGT) (18 subjects with both impaired fasting and 2-h plasma glucose levels), and type 2 diabetes (16 subjects with both diabetic fasting and 2-h plasma glucose levels). We assayed plasma glucose, insulin, C-peptide, glucagon, and intact and total GIP levels and quantitated glucose and hormone responses to the oral glucose tolerance test. We also compared GIP and insulin release and sensitivity indexes between groups. RESULTS: After glucose ingestion, subjects with IGT had both hyperinsulinemia and hyperemia, while subjects with type 2 diabetes had both beta- and GIP-cell deficiency. In the former group, there was also a significant positive correlation between the augmented plasma intact and total GIP levels and both fasting and post-oral glucose load plasma insulin levels. CONCLUSIONS: Elevated plasma GIP levels are correlated with hyperinsulinemia in the impaired glucose-tolerant state, whereas type 2 diabetes is associated with a failure to secrete adequate amounts of both GIP and insulin, indicating a common pathway of resistance to and eventually failure of glucose responsiveness in beta- and GIP-cells.     

Increased plasma glucagon-like immunoreactivity in dogs with ileojejunal transposition

To elucidate hormonal and metabolic changes in intestinal adaptation, an experimental study was performed in dogs subjected to ileojejunal transposition. Fasting levels of blood glucose, plasma insulin and gastric inhibitory polypeptide (GIP) did not change significantly throughout 12 weeks. Plasma glucagon measured with an antiserum specific to the C-terminal portion of glucagon slightly increased and plasma total glucagon measured with a non-specific antiserum gradually increased. Glucose tolerance deteriorated at the 4th week in the transposed group. The response of plasma insulin and GIP to glucose in the transposed group did not differ from that of the sham operated group. Plasma glucagon increased significantly during glucose loading at the 12th week. The response of plasma total glucagon to glucose was most prominent, reaching a peak of 3,755 +/- 742 pmol/liter. The value was significantly increased, compared with that of the sham group or normal group (p less than 0.01). Insulin-induced hypoglycemia enhanced a larger increment of plasma total glucagon in the transposed group than in the sham group (p less than 0.05). At the 12th week plasma total amino acids were decreased and several amino acids were reduced. It is concluded that ileojejunal transposition elicited an exaggerated response of plasma total glucagon to glucose and several metabolic derangements and that the transposition offers an excellent model for hyperenteroglucagonemia.     

Effects of atropine and gastric inhibitory polypeptide on hepatic glucose uptake and insulin extraction in conscious dogs.

Previous studies comparing the effects of oral, intraportal, and peripheral venous administration of glucose in conscious dogs demonstrated a significant increase in hepatic extraction of insulin only after oral glucose, but similar hepatic uptake of glucose after oral and intraportal glucose, which was greater than that after peripheral intravenous glucose infusion. This study evaluated the effect of atropine blockade of the parasympathetic nervous system on the increased fractional hepatic extraction of insulin and the role of gastric inhibitory polypeptide (GIP) on augmented hepatic uptake of oral glucose in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery, and catheters in the portal and hepatic veins and carotid artery. Since atropine infusion decreased absorption of glucose, and in order to achieve comparable portal vein levels of glucose and insulin, the dogs receiving atropine were given 1.9 +/- 0.1 g/kg glucose, compared with the control dogs who received 1.1 +/- 0.1 g/kg. The percentage of the glucose load that was absorbed was greater in the dogs not given atropine (80 +/- 4 vs. 44 +/- 7%), but because of the different loads, the absolute amount of glucose absorbed was similar in both groups (20.2 +/- 1.6 vs. 21.7 +/- 4.1 g). Although delayed by atropine, the peak portal vein glucose and insulin concentrations and the amounts presented to the liver were similar in both groups. However, the increased portal vein plasma flow and fractional hepatic extraction of insulin observed after oral glucose was not observed in the dogs infused with atropine. The net hepatic glucose uptake after oral glucose was significantly less at 10, 20, and 45 min in the atropine-treated dogs, and the area under the curve over the 180-min period was 44% less. However, the latter was not statistically significant. Infusion of GIP with peripheral intravenous glucose did not increase hepatic uptake of glucose or the fractional hepatic extraction of insulin compared with peripheral intravenous glucose alone. These results indicate an important role for parasympathetic innervation in the augmented fractional hepatic extraction of insulin, and increased portal vein plasma flow after oral glucose. Although a relationship between the augmented fractional extraction of insulin and the net hepatic glucose uptake may exist, it does not necessarily indicate that the former is required for the latter. Such parasympathetic innervation may be involved in the greater removal of glucose by the liver after oral compared with peripheral glucose administration. The augmented hepatic uptake of glucose and fractional hepatic extraction of insulin after oral glucose doesn not appear to be mediated by gastric inhibitory polypeptide.     

Effect of synthetic human glucose-dependent insulinotropic polypeptide (hGIP) on the release of insulin in man

During an oral glucose tolerance test (oGTT) and an isoglycaemic intravenous glucose infusion, blood glucose and the responses of insulin and glucose-dependent insulinotropic polypeptide (GIP) were measured in six healthy volunteers. On a subsequent occasion a constant infusion of human synthetic GIP (2 pmol kg-1 min-1 for 30 min and 0.5 pmol kg-1 min-1 for another 30 min was given to each subject, again with a simultaneous infusion of glucose to maintain isoglycaemia to the oGTT. During the oGTT, plasma GIP concentrations rose from 92 +/- 18 pmol 1(-1) to 257 +/- 42 pmol 1(-1) 60 min after ingestion of glucose (mean +/- SEM). When glucose was administered intravenously plasma GIP levels did not rise significantly over basal. The infusion of hGIP mimicked the physiological plasma GIP response after oral glucose during the first 60 min of the study. Plasma insulin concentrations were significantly lower between 45 and 60 min than during the oGTT (438 +/- 67 vs. 200 +/- 48 pmol 1(-1); P less than 0.02; 465 +/- 96 vs. 207 +/- 48 pmol 1(-1); P less than 0.01). However, the total and incremental integrated insulin responses during the first 60 min of the study were, though lower, not significantly different from the oGTT experiment when glucose and hGIP were infused simultaneously. Thus, in the presence of mild physiological hyperglycaemia, human GIP is able to enhance the initial insulin response almost equivalently to the stimulus provided by oral glucose. Decreased insulin concentrations during porcine GIP infusions in previous experiments might be due to sequence differences between human and porcine GIP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired incretin response after a mixed meal is associated with insulin resistance in nondiabetic men

OBJECTIVE: To investigate whether features of the insulin resistance syndrome are associated with altered incretin responses to food intake. RESEARCH DESIGN AND METHODS: From a population-based study, 35 men were recruited, representing a wide spectrum of insulin sensitivity and body weight. Each subject underwent a hyperinsulinemic-euglycemic clamp to determine insulin sensitivity. A mixed meal was given, and plasma levels of gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), as well as insulin, glucagon, and glucose were measured. RESULTS: Insulin resistance was associated with impaired GIP and GLP-1 responses to a mixed meal. The total area under the curve (AUC) of the GIP response after the mixed meal was associated with insulin sensitivity (r = 0.54, P < 0.01). There was a significant difference between the highest and the lowest tertile of insulin sensitivity (P < 0.05). GLP-1 levels 15 min after food intake were significantly lower in the most insulin-resistant tertile compared with the most insulin-sensitive tertile. During the first hour, the AUC of GLP-1 correlated significantly with insulin sensitivity (r = 0.47, P < 0.01). Multiple linear regression analysis showed that insulin resistance, but not obesity, was an independent predictor of these decreased incretin responses. CONCLUSIONS: In insulin resistance, the GIP and GLP-1 responses to a mixed meal are impaired and are related to the degree of insulin resistance. Decreased incretin responsiveness may be of importance for the development of impaired glucose tolerance.     

Effect of serial test meals on plasma immunoreactive GIP in non-insulin dependent diabetic patients and non-diabetic controls

Previous reports have shown considerable variation in postprandial gastric inhibitory polypeptide (GIP) response in non-insulin-dependent diabetic (NIDD) patients. One reason for this may be the use of different GIP antisera. Employing antiserum R65, which specifically reacts with the 5000-dalton GIP, we investigated the plasma GIP response to serial test meals in 11 NIDD patients and 11 age- and weight-matched non-diabetic controls. The postprandial GIP response was lower in the NIDD patients than in the non-diabetic controls (p less than 0.05). Although the serum insulin concentrations did not differ between diabetic and non-diabetic subjects, the insulin to glucose ratio was lower in the diabetics than in the non-diabetic subjects (p less than 0.05) indicating some degree of relative insulin deficiency in the diabetic patients. The data suggest that the GIP secretory capacity may be impaired in NIDD patients. Whether the impairment of GIP secretion is associated with impaired insulin secretion requires further investigation.     

Response of extrapancreatic glucagon to glycemic changes under chronic insulin deficiency in dogs

Since the secretion of pancreatic glucagon is largely influenced by the changes in the blood glucose level, the response of extrapancreatic glucagon was investigated in totally pancreatectomized dogs under chronic insulin deficiency. Insulin-induced hypoglycemia did not alter plasma glucagon in the portal vein in a group of 5 pancreatectomized dogs, but the decrease of the blood glucose was small, by 70 mg/100 ml, in spite of a large amount of insulin. The administration of 2-deoxyglucose did not cause any changes in plasma glucagon in the portal vein in a group of 6 pancreatectomized dogs. Glucose-induced hyperglycemia, both transient and continuous, did not cause any changes in plasma glucagon in the portal vein, although blood glucose was significantly elevated. It is concluded that regulation of extrapancreatic glucagon differs from that of pancreatic glucagon.     

不同糖耐量水平人群血浆胰高血糖素样肽-1和葡萄糖依赖的促胰岛素样多肽水平比较

目的 了解不同糖代谢状态的人群空腹及口服葡萄糖耐量实验(oral glucose tolerance test,OGTT)餐后胰高血糖素样态-1(GLP-1)和葡萄糖依赖的促胰岛素多态(GIP)水平.方法 将受试者根据OGTT结果分为3组:正常糖耐量组(NGT,n=61例),糖耐量受损组(IGT,n=53)和2型糖尿病...     

胰岛素强化治疗老年早期糖尿病肾病的疗效

目的 观察胰岛素注射与口服降糖药物对老年早期糖尿病肾病尿蛋白的影响.方法 116例老年早期糖尿病肾病患者随机分为A组(诺和锐及诺和灵N注射)、B组(诺和锐30注射)、C组(甘精胰岛素注射)和D组(口服格列奎酮),治疗12周.观察4组治疗前、后尿微量白蛋白排泄率(UAER)、糖化血红蛋白(HbA.c)、空腹血糖(FBG)、2 h血糖(2 hPG).结果 4组治疗后UAER、HbA1c、FBG、2 hPG较治疗前均有下降,A、B、C治疗组疗效优于D组(P均＜0.05),A组疗效最好.结论 胰岛素注射治疗对老年早期糖尿病肾病有显著疗效,并使血糖控制达标.     

糖耐量受损和2型糖尿病患者脂联素水平的相关性研究

目的探讨在糖耐量受损及2型糖尿病患者中血脂血糖、胰岛素抵抗和血清脂联素之间的关系。方法 166例分为正常对照组（29例）、糖耐量受损组（41例）和糖尿病组（96例）,分别检测血脂、血糖、血胰岛素水平和血清脂联素,采用HOMA-IR法计算胰岛素抵抗指数。分别对正常组是否进展为糖耐量受损,以及糖耐量受损是否进展为糖尿病进行二分类Logistic回归分析。结果正常对照组、糖耐量受损组和糖尿病组血清脂联素水平分别为（15.8±3.6）、（10.7±2.4）和（6.3±2.4）mg/L,3组间差异有显著统计学意义（P〈0.05）。糖耐量受损组的体质指数、总胆固醇、胰岛素水平和胰岛素抵抗显著高于正常组（P均〈0.05）。Logistic回归分析表明体质指数、高密度脂蛋白胆固醇、空腹胰岛素、胰岛素抵抗指数为正常对照进展为糖耐量受损的危险因素。当糖耐量受损组进展为糖尿病组时,空腹胰岛素是唯一有统计学差异的危险因素。脂联素在两个阶段中都为保护因素。结论在糖耐量受损时胰岛素抵抗水平升高,并已伴随脂联素水平下降。血清脂联素测定,可作为2型糖尿病的辅助诊断、及早干预的指标。     

Effect of the fatty acid oxidation inhibitor methyl palmoxirate (methyl 2-tetradecylglycidate) on recovery from insulin-induced hypoglycemia in diabetic dogs

Methyl palmoxirate, an effective hypoglycemic agent administered p.o., has been shown to decrease hepatic glucose production secondary to inhibition of mitochondrial fatty acid oxidation. Because the ability to increase hepatic glucose production is an important counter-regulatory defense against hypoglycemia, we compared the ability of streptozotocin/alloxan-induced diabetic dogs treated p.o. with vehicle or methyl palmoxirate (2.5 mg/kg/day X 7 days) to recover from insulin-induced hypoglycemia. Hepatic glucose production and glucose utilization were determined by isotope dilution before and after acute reduction of plasma glucose by i.v. insulin injection (0.10 or 0.13 U/kg). Diabetic dogs treated with methyl palmoxirate for 6 days had lower overnight fasting plasma glucose levels than vehicle-treated animals (158 +/- 7 vs. 171 +/- 11, respectively, P less than .05). Plasma glucose at 4 hr after the last dose of drug decreased to 115 +/- 5 mg/dl, whereas glucose in the vehicle-treated dogs was unchanged (172 +/- 8 mg/dl). Recovery from insulin-induced hypoglycemia (nadirs of 58 +/- 5 and 42 +/- 4 mg/dl in the vehicle- and methyl palmoxirate-treated groups, respectively) was not significantly different between the two groups of dogs. Restoration of plasma glucose was primarily due to increased hepatic glucose production in both treatment groups, as glucose utilization did not fall significantly below baseline levels. Plasma glucagon levels increased in both vehicle- and methyl palmoxirate-treated dogs in response to hypoglycemia, indicating that release of an important counter-regulatory hormone was not compromised by drug treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of exercise-induced hypoglycemia in depancreatized dogs maintained on long-acting insulin.

Human diabetics on intermediate and long-acting insulin occasionaly become hypoglycemic during exercise. We have shown previously that during exercise, hypoglycemia did not occur in depancreatized insulin-infused dogs because the increments in glucose production and utilization were proportional and of the same magnitude as in normal dogs. Therefore, to elucidate the mechanism of the glucose-lowering effect of strenuous exercise, we measured glucose production and utilization, metabolic clearance of glucose, and serum immunoreactive insulin in postabsorptive depancreatized dogs 8 h after a subcutaneous injection of protamine zinc and crystalline insulin. During rest, plasma glucose was stable, but ranged between hypoglycemia and hyperglycemia. Hyperglycemia was associated with overproduction of glucose, indicating insulin deficiency despite normal or elevated serum immunoreactive insulin. Glucose clearance, as in normal dogs, increased threefold but glucose production increased only marginally (50%) and, consequently, glucose decreased in plasma. The decrease of plasma glucose was directly proportional to the preexercise concentration and production of glucose. The magnitude of inhibition glucose production was not correlated with the serum immunoreactive insulin indicating either that some released insluin was not active or that a moderate immunoreactive insulin increment induced a near-maximal inhibition. It is concluded that in depancreatized dogs injected with protamine zinc insulin, exercise accelerates mobilization of insulin from its injection site presumably because of increased blood and lymph flow. Glucose utilization did not exceed that in normal dogs, but hepatic glucose production failed to increase sufficiently to meet the needs of muscle in exercise.     

6组不同用药方案治疗社区2型糖尿病的成本-效果分析

目的 评价不同用药方案治疗2型糖尿病的经济成本、不良反应及药物疗效.方法 针对筛选出的230例2型糖尿病患者,按不同的用药方案随机分为6组,对其在治疗前和治疗12周结束后的经济效果、不良反应及药物疗效进行分析.6种不同用药方案为:盐酸二甲双胍片(A组),瑞格列奈片(B组),胰岛素注射液(C组),盐酸二甲双胍片联合瑞格列奈片(D组),胰岛素注射液联合二甲双胍片(E组),二甲双胍片联合阿卡波糖片(F组).结果 在各组用药方案中,D、E组在治疗后的空腹血糖(FPG)、餐后2 h血糖(2 h PBG)、糖化血红蛋白(HbA1c)控制较理想,治疗成本相对低.结论 各组治疗2型糖尿病的用药方案疗效均较好,且D方案更符合药物经济学原则.     

Administration of an acylated GLP-1 and GIP preparation provides added beneficial glucose-lowering and insulinotropic actions over single incretins in mice with Type 2 diabetes and obesity

The present study examined the glucose-lowering and insulinotropic properties of acylated GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) peptides in Type 2 diabetes and obesity. GLP-1, GIP, Liraglutide, N-AcGIP(Lys(37)Myr) (N-acetylGIP with myristic acid conjugated at Lys(37)), a simple combination of both peptides and a Lira-AcGIP preparation [overnight preparation of Liraglutide and N-AcGIP(Lys(37)Myr)] were incubated with DPP-IV (dipeptidyl peptidase-IV) to assess peptide stability, and BRIN-BD11 cells were used to evaluate cAMP production and insulin secretion. Acute glucose-lowering and insulinotropic actions were evaluated in Swiss TO mice. Subchronic studies on glucose homoeostasis, insulin secretion, food intake and bodyweight were evaluated in ob/ob mice. Liraglutide, N-AcGIP(Lys(37)Myr), a simple combination of both peptides and the Lira-AcGIP preparation demonstrated improved DPP-IV resistance (P<0.001), while stimulating cAMP production and insulin secretion (1.4-2-fold; P<0.001). The Lira-AcGIP preparation was more potent at lowering plasma glucose (20-51% reduction; P<0.05-P<0.001) and stimulating insulin secretion (1.5-1.8-fold; P<0.05-P<0.001) compared with Liraglutide and N-AcGIP(Lys(37)Myr) or a simple peptide combination. Daily administration of the Lira-AcGIP preparation to ob/ob mice lowered bodyweight (7-9%; P<0.05), food intake (23%; P<0.05) and plasma glucose (46% reduction; P<0.001), while increasing plasma insulin (1.5-1.6-fold; P<0.001). The Lira-AcGIP preparation enhanced glucose tolerance, insulin response to glucose and insulin content (P<0.05-P<0.001). These findings demonstrate that a combined preparation of the acylated GLP-1 and GIP peptides Liraglutide and N-AcGIP(Lys(37)Myr) markedly improved glucose-lowering and insulinotropic properties in diabetic obesity compared with either incretin mimetic given individually.     

Sodium-lithium countertransport and platelet cytosolic free calcium concentration in relation to peripheral insulin sensitivity in postmenopausal women.

1. Peripheral glucose disposal (assessed by the euglycaemic-hyperinsulinaemic clamp technique), Na(+)-Li+ countertransport in erythrocytes and the cytosolic free Ca2+ concentration in platelets were determined in 41 women with impaired glucose tolerance and in 38 women with normal glucose tolerance. The groups were matched for body mass index (range 18-44 kg/m2) and diastolic blood pressure (range 58-109 mmHg). 2. Na(+)-Li+ countertransport was correlated significantly with body mass index, basal plasma insulin concentration and basal plasma glucose concentration, and was inversely correlated with peripheral glucose disposal rate. Stepwise regression analysis showed that Na(+)-Li+ countertransport was positively correlated with basal plasma insulin concentration (r2 = 8.7%). 3. Systolic blood pressure was correlated with fasting plasma insulin concentration (model r2 = 25%) and with Na(+)-Li+ countertransport (model r2 = 34%) in the group with impaired glucose tolerance. In the group with normal glucose tolerance there were no correlations between blood pressure and Na(+)-Li+ countertransport. 4. No correlation was found between platelet cytosolic free Ca2+ concentration and any of the variables measured. 5. It is concluded that Na(+)-Li+ countertransport is correlated with the degree of peripheral insulin sensitivity and with the plasma insulin concentration. Platelet cytosolic free Ca2+ concentration was not correlated with any of these variables, and there was no relationship between Na(+)-Li+ countertransport and the platelet cytosolic free Ca2+ concentration.     

Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus.

In type-2 diabetes, the overall incretin effect is reduced. The present investigation was designed to compare insulinotropic actions of exogenous incretin hormones (gastric inhibitory peptide [GIP] and glucagon-like peptide 1 [GLP-1] [7-36 amide]) in nine type-2 diabetic patients (fasting plasma glucose 7.8 mmol/liter; hemoglobin A1c 6.3 +/- 0.6%) and in nine age- and weight-matched normal subjects. Synthetic human GIP (0.8 and 2.4 pmol/kg.min over 1 h each), GLP-1 [7-36 amide] (0.4 and 1.2 pmol/kg.min over 1 h each), and placebo were administered under hyperglycemic clamp conditions (8.75 mmol/liter) in separate experiments. Plasma GIP and GLP-1 [7-36 amide] concentrations (radioimmunoassay) were comparable to those after oral glucose with the low, and clearly supraphysiological with the high infusion rates. Both GIP and GLP-1 [7-36 amide] dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). With GIP, the maximum effect in type-2 diabetic patients was significantly lower (by 54%; P < 0.05) than in normal subjects. With GLP-1 [7-36 amide] type-2 diabetic patients reached 71% of the increments in C-peptide of normal subjects (difference not significant). Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. In conclusion, in mild type-2 diabetes, GLP-1 [7-36 amide], in contrast to GIP, retains much of its insulinotropic activity. It also lowers glucagon concentrations.     

低张胶体液对失血并腹腔海水浸泡伤实验犬的救治作用

目的：观察低张胶体液对失血并腹腔海水浸泡伤的救治效果。方法：建立腹腔海水浸泡伤动物模型。35只犬随机均分为对照组(A组)、质量分数为5％的葡萄糖治疗组(B组)、0．45％氯化钠治疗组(C组)、0．9％氯化钠治疗组(D组)及低张胶体液治疗组(E组)，观察每组动物腹腔海水浸泡后平均动脉压(MAP)、心排血量(CO)、尿量、血浆渗透压及脑、肺组织的病理学变化。结果：低张胶体液可显著改善MAP及CO，增加尿量，降低血浆渗透压，预防脑、肺水肿的发生。结论：低张胶体液对失血并腹腔海水浸泡伤具有较好的救治效果。     

胰岛素泵不同基础量分段法对2型糖尿病的疗效

目的:比较3种不同胰岛素泵基础量分段法对2型糖尿病患者血糖控制的疗效优劣.方法:240例使用胰岛素泵治疗的2型糖尿病患者,分为3组,3段组、5段组和24段组各80例.观察3组治疗前后血糖值、血糖达标时间、胰岛素用量及低血糖发生率.结果:治疗前后3组血糖值均下降,差异有统计学意义(P＜0.01),3组治疗后血糖值比较差异无统计学意义.与3段组、5段组相比,24段组血糖达标所需时间少,胰岛素用量低,低血糖发生率低,但设置繁杂.5段组胰岛素用量与3段组相似,但达标时间短,低血糖发生率低(P＜0.05),且设置简单、方便.结论:5段法设置简单、方便、疗效好.