Insulin receptor binding to monocytes and erythrocytes during normal human pregnancy

In normal human pregnancy glucose tolerance deteriorates gradually in spite of a steady increase in plasma insulin levels. To see whether this change in insulin resistance is accompanied by changes in insulin receptor binding, insulin binding to monocytes and erythrocytes was measured serially during pregnancy and again post-partum in fifteen normal women. Insulin binding to monocytes increased from week 12 to week 24 of gestation (P less than 0.001) and it decreased from week 32 to week 36 (P less than 0.05). After delivery a new increase in insulin binding to monocytes was seen (P less than 0.05). Insulin binding to erythrocytes increased from week 30-32 to week 36 (P less than 0.05), decreased from week 36 to delivery (P less than 0.01) and decreased further post-partum (P less than 0.001). Insulin receptor binding was not significantly correlated to plasma insulin, estradiol, estriol, progesterone or cortisol. The insulin receptor binding to monocytes, but not to erythrocytes, paralleled the insulin resistance found in human pregnancy.     

Fatty acid binding protein 2 and insulin resistance

BACKGROUND: An A54T polymorphism of the fatty acid binding protein 2 (FABP2) gene was found to be associated with insulin resistance in nondiabetic Pima Indians. Design This is a cross-sectional study to examine the role of this polymorphism in insulin resistance in 71 healthy and normotensive Caucasian subjects with normal glucose tolerance. Insulin sensitivity (%S, ISI(M), ISI(S)) and beta-cell function (%B, dI/dG, 1stPHS, 2ndPHS) were estimated based on published models. Their genotypes were determined using a polymerase chain reaction-restriction fragment length polymorphism assay. The relationship between genotypes and phenotypes was examined. RESULTS: After genotyping, we identified 34 AA, 32 AT and five TT subjects. The TT subjects were pooled together with the AT subjects during the analysis due to their low number. No difference was noted in gender distribution, clinical features, or fasting lipid profile between the two genotypic groups (AA vs. AT/TT). The AT/TT group had lower %S and ISI(S) than the AA group (P = 0.0118 and P = 0.0170, respectively). The difference in ISI(M) was marginal (P = 0.0544). However, no difference was noted in beta-cell function between the two groups. Multivariate analysis revealed that this polymorphism was an independent but modest determinant for %S (P = 0.0149), ISI(M) (P = 0.0489) and ISI(S) (P = 0.0175). It independently contributed 6.04% (95% CI, 0.02-20.53%), 4.28% (95% CI, 0.08-17.63%) and 4.94% (95% CI, 0.01-18.75%) of the variation of %S, ISI(M) and ISI(S), respectively. CONCLUSIONS: We demonstrated that the A54T polymorphism at the FABP2 locus is a risk factor for insulin resistance in a Caucasian population.     

Urinary kallikrein excretion in normal and hypertensive pregnancy at term

To study the urinary kallikrein excretion before the delivery of term pregnancy we measured its excretion preterm (between 32-36 gestational week) in 13 patients with normotensive pregnancy and 17 patients with pregnancy-induced hypertension and one to five days before the delivery at term in 18 and 22 patients, respectively. In normotensive pregnancy urinary kallikrein excretion remained unchanged during the late third trimester until delivery (12.6 +/- 1.7 ncat in 24 hours in preterm, 10.8 +/- 1.2 before delivery). In pregnancy-induced hypertension and particularly in pre-eclampsia urinary kallikrein excretion was lower than in normotensive pregnancy and the decrease became more marked as the time of delivery approached (respective values: in pregnancy induced hypertension 9.2 +/- 1.2 and 7.0 +/- 0.7; in pre-eclampsia 7.6 +/- 1.3 and 7.3 +/- 0.9). The decrease in urinary kallikrein excretion suggests progressive disturbances in the interactions of renal vasoactive systems (the kallikrein-kinin system, the renin-angiotensin system and prostaglandins) with resultant changes in renal hemodynamics.     

Relation between insulin kinetics and insulin sensitivity in pregnancy

BACKGROUND: Different time-concentration profiles of plasma insulin following insulin modification of a frequently sampled intravenous glucose-tolerance-test (FSIVGTT) were observed in a study investigating maternal metabolism and fetal macrosomia. We aimed to investigate whether these differences were related to the volume of distribution of insulin, insulin clearance, or both. DESIGN: Forty-four women were studied between 33 and 35 weeks' gestation using an insulin-modified FSIVGTT. Specific insulin was assayed with an enzyme-linked immunosorbent assay. Insulin sensitivity was calculated using the minimal model and the homeostasis model assessment (HOMA). The volume of distribution and clearance of insulin were calculated from measurements between 2 and 155 min after insulin modification using a one-compartment model. RESULTS: In accordance with the method for deriving the volume of distribution, there was a significant negative correlation between the increment in insulin concentration and the volume of distribution (rho=-0.92, P<0.0001). The insulin increment was also related negatively to the clearance of insulin (rho=-0.88, P<0.0001). There was a significant correlation between the volume of distribution and both the insulin sensitivity index (rho=0.56, P<0.0001) and HOMA-%S (rho=0.30, P=0.048), and between the clearance of insulin and both the insulin sensitivity index (rho=0.83, P<0.0001)) and HOMA-%S (rho=0.34, P=0.025). CONCLUSION: The different time-concentration profiles of plasma insulin resulted from differences in the volume of distribution and clearance of insulin. There was a correlation between insulin kinetics and the insulin sensitivity index. Further research is required to investigate possible mechanisms by which insulin kinetics may be related to insulin sensitivity.     

Relationship of insulin clearance and secretion to insulin sensitivity in non-diabetic Mexican Americans

The antecedents of type II diabetes, while still controversial, are thought to involve decreased insulin sensitivity and compensatory hypersecretion of insulin. Mexican Americans have a three-fold excess risk of type II diabetes and non-diabetic Mexican Americans are characterized by hyperinsulinaemia and insulin resistance. Few data exist, however, on whether there are defects in insulin secretion and/or clearance in this population. We examined insulin sensitivity, secretion and clearance using combined insulin and C-peptide measurements analysed by the minimal model technique of Bergman and colleagues in 10 non-obese, normoglycaemic Mexican Americans and 11 age, sex and obesity-matched non-Hispanic whites. Mexican Americans had significantly decreased insulin sensitivity (SI 4.06 s. 7.56, P = 0.017), higher first phase insulin secretion (1.03 nM vs. 0.72 nM) and decreased insulin clearance (0.099 vs. 0.161) than non-Hispanic whites. Thus, normal Mexican Americans have higher rather than lower insulin secretion suggesting that lower insulin sensitivity may be an early defect in this ethnic group. In addition, they have reduced insulin clearance. Moreover, insulin sensitivity and insulin clearance were positively correlated. We thus speculate that decreased insulin clearance may represent a further autoregulatory mechanism in addition to increased insulin secretion to compensate for decreased insulin sensitivity.     

Urinary tract infection during pregnancy affects the level of leptin,ghrelin and insulin in maternal and placental blood

Abstract

Aim. We examined ghrelin, leptin and insulin in maternal blood during normal pregnancy and pregnancy complicated by urinary tract infection (UTI), as well as in cord blood at labor. Methods. A total of 36 delivering women with history of UTI during the third trimester of pregnancy were enrolled in the study; 12 healthy pregnant women served as a control. Infection markers (CRP and procalcitonin) were determined in maternal blood during the course of UTI and at labor. Ghrelin, leptin and insulin were determined during labor in venous maternal and in umbilical cord blood. Results. We found negative correlation between infection markers in maternal blood during UTI, and level of tested hormones in cord blood, indicating potential risk of placental impairment due to energetic imbalance. We noted lower level of leptin in mothers with UTI and no change in leptin from umbilical blood comparing subjects with and without UTI. Low level of ghrelin was observed in maternal and cord blood when pregnancy was complicated by UTI. Insulin concentrations were high in mothers with UTI and low in their newborn's cord blood. Increased maternal insulin level could indicate peripheral insulin resistance caused by the infection. Conclusion. UTI during pregnancy affects the concentration of hormones responsible for regulating energetic homeostasis within the placenta.     

Insulin inhalation with absorption enhancer at meal-times results in almost normal postprandial insulin profiles

Background: Conventional insulin therapy with subcutaneous injections of regular insulin at meal‐times result in plasma insulin peaks that are lower and appear later than meal related insulin peaks in healthy individuals. The present study was designed in order to evaluate the resulting insulin concentrations in peripheral blood after inhalation of micro crystalline human insulin together with an absorption enhancer [dioctyl sodium sulphosuccinate (DOSS)] via a powder inhaler. Methods: Ten insulin dependent middle‐aged non‐obese diabetic patients (mean diabetes duration 21 years) were included. Blood samples for glucose and insulin were taken immediately before and 13 times, up to 300 min, after insulin inhalation. The mass median aerodynamic diameter of the particles was 3·2 μm. The inhaled insulin dose was 39 U. Results: Within 5 min after the end of the 2 min inhalation procedure the mean increase of insulin was 7·0 μU ml^–1, and the mean maximum concentration, 12·1 μU ml^–1, was reached between 20 and 30 min. There was then a slow decline until base‐line was reached after around 210 min and there were no adverse events. Conclusions: Inhalation of a mixture of 39 U of insulin and enhancer resulted in a rapid plasma insulin peak with a slow decline, similar to the normal postprandial insulin profile.     

Exercise increases insulin clearance in healthy man and insulin-dependent diabetes mellitus patients

Exercise is known to decrease insulin secretion, but the effect on insulin clearance is unclear. We examined the effect of exercise on insulin clearance with euglycaemic insulin clamp in 28 healthy men either 12 h after a marathon run (n=14) or 44 h after a 2-h treadmill exercise (n=14), and in seven insulin-dependent diabetes mellitus (IDDM) patients 12 h after a marathon run, and after a resting, control day. During the post-exercise insulin infusion, steady-state plasma insulin concentration was reduced by 9% in healthy men after both types of exercise, and by 16% in the diabetic subjects compared with the control study (P<0·05 in all). In healthy men, C-peptide concentrations were more than one-third lower during insulin infusion, both after the marathon run (P<0·001) or treadmill exercise (P<0·02) compared with the control study. Insulin clearance was significantly increased by exercise both in healthy men (9%, P<0·05) and in IDDM subjects (15%, P<0·05). After exercise, endogenous insulin secretion in healthy men is reduced and insulin clearance is enhanced both in healthy men and in IDDM patients. Decreased insulin availability may allow enhanced muscle lipid utilization and spare glucose after long-term exercise.     

The influence of body weight and cell size on lipogenesis and lipolysis of isolated rat fat cells

Abstract. A method for fractionating isolated fat cells is described. After fixation with osmium tetroxide, the cells are passed through a series of polyamide filters of decreasing mesh width and the number of cells on each filter is counted. — Isolated fat cells from ad libitum fed rats weighing 85–580 g were incubated with [U-¹⁴ C]-glucose (0.55 mM), fixed with osmium tetroxide and fractionated according to size. When the cells were obtained from one animal the conversion of glucose to neutral lipids per cell increased with increasing cell size just as well in the absence of insulin as in the presence of insulin (10 mU/ml). The following results were obtained from comparisons between animals of different weight: in the absence of insulin, the lipogenesis for cells of the same size remained constant irrespective of the rat weight, whereas in the presence of insulin the lipogenesis for cells of the same size decreased markedly when the rat weight exceeded about 300 g. It is Concluded that factors other than the cell size per se (e.g. age, degree of obesity) determine the responsiveness to insulin. — The hormone-stimulated lipolysis was studied on unfractionated cell samples from ad libitum fed rats of different weights and the following was found: the glycerol release per 10⁶ cells induced by ACTH and norepinephrine in maximally stimulating concentrations increased with increasing mean cell size or rat weight. In contrast, the glucagon-induced lipolysis of cells from rats weighing 300–400 g was smaller than that of cells from rats weighing 100–120 g.     

糖负荷后血尿酸与胰岛素分泌及胰岛素敏感性/抵抗的相关性分析

目的研究不同糖负荷人群血尿酸(SUA)水平与胰岛素分泌及胰岛素抵抗的关系。方法 389例符合要求的研究对象行口服糖耐量试验(OGTT),测量空腹SUA,OGTT 0、30、60、120min血糖(GLU)和胰岛素(INS)水平,按照OGTT结果将研究对象分为糖耐量正常组(NGT组,n=88)、糖尿病前期组(preDM,n=119)、糖尿病组(DM,n=182),计算研究对象的胰岛素分泌指数(IGI)、120min胰岛素分泌指数(AUC INS_(120)/AUC GLU_(120))、胰岛素抵抗指数(HOMA-IR)、及Matsuda指数;将SUA按四分位水平分组,比较各糖负荷组不同SUA水平胰岛素分泌及胰岛素抵抗差异;计算SUA与胰岛素分泌及HOMA-IR的直线回归方程。结果 DM组SUA水平低于PreDM组[(346.66±90.60)mmol/Lvs.(367.36±92.34)mmol/L],但是略高于NGT组(339.34±89.51)mmol/L,差异有统计学意义(P0.01);DM组IGI指数、AUC INS_(120)/AUC GLU_(120)指数随着SUA升高有降低趋势(P0.01),Matsuda指数随着SUA水平升高有降低趋势(P0.05)。SUA与IGI、AUC INS_(120)/AUC GLU_(120)、HOMAIR、Matsuda指数的二元一次方程分别是Y=4.050+0.144 X,Y=2.343+0.206 X,Y=1.288+0.176 X,Y=129.373-0.202 X。结论 SUA与胰岛素分泌及胰岛素敏感性显著相关,DM组胰岛素分泌随着SUA水平升高而升高,胰岛素敏感性随着SUA水平升高而降低。SUA与胰岛素分泌及胰岛素敏感性的二元一次方程可大概评估胰岛素功能。     

Genetic variance and lipolysis regulation: implications for obesity

Catecholamines are the major lipolytic hormones in human fat cells, and lipolytic catecholamine resistance is described in obesity. Studies on twins and in rare genetic disorders suggest a strong heredity component of catecholamine-induced lipolysis. Polymorphisms in catecholamine receptor signalling pathways have been described, several of which associate with obesity. Many polymorphisms in adrenoceptor genes are functional in transfected cell lines. The importance of polymorphisms in catecholamine signalling pathways for lipolysis regulation is discussed. A Trp64Arg polymorphism in the β₂-receptor, which associates with obesity, is accompanied by changes in lipolytic sensitivity of the receptor in human fat cells. Similarly, a Gln 16Glu and an Arg 16411e variation in the β₂-adrenoceptor cause marked variations in the lipolytic sensitivity of this receptor in human adipocytes. Furthermore, β₂-adrenoceptor gene polymorphisms associate with obesity. A dinucleotide (CA) intron repeat in hormone-sensitive lipase gene is linked to obesity and markedly decreases the ability of catecholamines to activate the lipase and thereby lipolysis in human fat cells. However, an Arg 389Gly polymorphism in the β₂-adrenoceptor, which alters receptor function in transfected cell lines, has no effect on lipolysis in human fat cells and is not associated with obesity. Thus, polymorphism in human genes that are involved in catecholamine signal transduction have effects on fat cell lipolysis and also relate to obesity. The lipolysis effects of these polymorphisms cannot always be predicted from gene transfer experiments on artificial cell lines. It is possible that genetic variance in catecholamine signalling pathways, through alterations in adipocyte lipolysis, may promote obesity.     

Alcohol consumption and insulin resistance in young adults

BACKGROUND: Alcohol may have a cardioprotective effect. One possible mechanism is by reducing insulin resistance, a known cardiovascular risk factor. The aim of this study was to assess the relationship between alcohol consumption, insulin resistance and other parameters determining glucose tolerance in 154 young men and women. SUBJECTS AND METHODS: Subjects completed a questionnaire documenting weekly alcohol consumption. Insulin sensitivity and glucose tolerance were measured using the intravenous glucose tolerance test with minimal model analysis. Height, weight, usual level of exercise, smoking habits and socio-economic status were also recorded. RESULTS: Insulin sensitivity correlated inversely with body mass index (r = - 0.529, P < 0.001) but not with level of physical fitness. Women were significantly less insulin sensitive than men (4.19 and 5.63 104 min-1 pmol-1 L-1, respectively; P < 0.001). Insulin sensitivity correlated positively with alcohol consumption and this trend remained significant allowing for body mass index and gender (beta = 0.17, P < 0.014). First-phase insulin secretion showed a weak but non-significant trend in the opposite direction. Fasting glucose, fasting insulin and glucose tolerance showed no relationships with alcohol consumption. CONCLUSION: These data suggest a close relationship between alcohol consumption and insulin resistance in young adults. Regular alcohol consumption is associated with decreased insulin resistance and this may partly explain the cardioprotective effect of alcohol.     

胰岛素对Reh细胞胰岛素受体和胰岛素样生长因子Ⅰ型受体表达及细胞增殖的影响

本研究探讨胰岛素对Reh细胞胰岛素受体(IR)和胰岛素样生长因子Ⅰ型受体(IGF-ⅠR)表达的影响及对Reh细胞的促增殖作用。用CCK-8法检测Reh细胞的增殖;采用实时PCR法检测Reh细胞IR和IGF-ⅠRmRNA的表达。结果表明,胰岛素对Reh细胞具有浓度和时间依赖性的促增殖作用,当胰岛素浓度为10-9 mol/L时其促增殖作用最强,进一步提高浓度,胰岛素的促增殖作用不再增强。与对照组相比,胰岛素有明显的促增殖作用(P<0.05)。胰岛素10-9mol/L作用24、48及72 h,IR mRNA表达量与对照组相比的比值分别为2.2520±0.7431、1.9956±0.9692和3.9766±1.3189,IGF-ⅠR表达量与对照组相比的比值分别为1.0803±0.2238、1.6026±0.6158和3.1013±0.1008。胰岛素刺激后IR和IGF-ⅠR的mRNA相对表达量与对照组相比均明显增加,差别有统计学显著意义(P=0.022和P=0.00)。结论:胰岛素能促进Reh细胞的增殖,其机制可能与IR和IGF-ⅠR上调有关。IR和IGF-ⅠR的高表达与白血病细胞的生长有着密切关系。     

Gastro-entero-pancreatic hormones in normal pregnancy: response to a protein rich meal

Abstract. The plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) were studied following the ingestion of a protein rich meal in late pregnancy and postpartum in 11 normal women. In pregnancy, the fasting plasma concentrations of glucose (mean ± SEM in pregnancy: 4.1 ± 0.1 mmol1^-1, postpartum: 4.7 ± 0.1 mmol1^-1, p<0.01), gut GLI (25± 3 v. 33± 2 pmol-eqv 1^-1, P<0.01) and PP (7.9 ± 1.0 v. 13.0± 1.2 pmol 1¹, P<0.01) were decreased, gastrin and GIP unaltered, and insulin (90± 9 v. 72 ± 5 pmol 1¹, P<005) and glucagon (17±1 v. 13 ± 1 pmol 1^-1, P<0.01) increased.
The gastrin, GIP and glucagon responses to the meal were unaffected by pregnancy, whereas the responses of gut GLI (integrated responses in pregnancy: 1217 ± 325 pmol-eqv 1^-1 postpartum 2223± 404 pmol-eqv 1^-1, P<005) and PP (9801 &± 1440 v. 14,078 ± 1543 pmol 1^-1, P<001) were impaired and the insulin response enhanced (27,973 ± 6814 v. 11,409 ± 3102 pmol 1^-1, P<001) in pregnancy.
The physiological implications of these findings are at present not known in detail. They may, however, be important for the altered carbohydrate metabolism in pregnancy and also for the changes occurring during gestation in gastrointestinal physiology.     

Variations in leptin and insulin levels within one swimming season in non-obese female cold water swimmers

Aim: We examined whether cold water swimming for seven consecutive months changes basal leptin and insulin concentrations and insulin sensitivity in healthy non-obese women.

Materials and methods: Fourteen recreational female swimmers aged 45?±?8.7 years, regularly swimming outdoors during winter months were exposed to cold water at least twice a week. Fasting blood samples were collected in October, January and April. Serum leptin, insulin and glucose concentrations were tested and insulin sensitivity was calculated using updated model HOMA2.

Results: Repeated cold water baths significantly increased insulin sensitivity and decreased insulin and leptin concentrations (p?=?0.006, p?=?0.032, p?=?0.042, respectively). Leptin concentration positively correlated with body-mass index (BMI) and insulin level (r?=?0.412, r?=?0.868, respectively). Insulin level inversely correlated with insulin sensitivity and positively with glucose (r = ?0.893, r?=?0.166, respectively). No associations between leptin and insulin sensitivity were found.

Conclusion: Regular cold water swimming may stimulate metabolic changes suggesting that leptin and insulin participate in adaptive metabolic mechanisms triggered by repeated cold exposure accompanied by mild exercise in healthy non-obese women.     

Effect of glibenclamide on insulin release at moderate and high blood glucose levels in normal man

Insulin release occurs in two phases; sulphonylurea derivatives may have different potencies in stimulating first- and second-phase insulin release. We studied the effect of glibenclamide on insulin secretion at submaximally and maximally stimulating blood glucose levels with a primed hyperglycaemic glucose clamp. Twelve healthy male subjects, age (mean ± SEM) 22.5 ± 0.5 years, body mass index (BMI) 21.7 ± 0.6 kg m^?2, were studied in a randomized, double-blind study design. Glibenclamide 10 mg or placebo was taken before a 4-h hyperglycaemic clamp (blood glucose 8 mmol L^?1 during the first 2 h and 32 mmol L^?1 during the next 2 h). During hyperglycaemic clamp at 8 mmol L^?1, the areas under the Δinsulin curve (AUC_Δinsulin , mean ± SEM) from 0 to 10 min (first phase) were not different: 1007 ± 235 vs. 1059 ± 261 pmol L^?1 × 10 min (with and without glibenclamide, P = 0.81). However, glibenclamide led to a significantly larger increase in AUC_Δinsulin from 30 to 120 min (second phase): 16 087 ± 4489 vs. 7107 ± 1533 pmol L^?1 × 90 min (with and without glibenclamide respectively, P < 0.03). The same was true for AUC_ΔC-peptide: no difference from 0 to 10 min but a significantly higher AUC_ΔC-peptide from 30 to 120 min on the glibenclamide day (P < 0.01). The M/I ratio (mean glucose infusion rate divided by mean plasma insulin concentration) from 60 to 120 min, a measure of insulin sensitivity, did not change: 0.26 ± 0.05 vs. 0.22 ± 0.03 μmol kg^?1 min^?1 pmol L^?1 (with and without glibenclamide, P = 0.64). During hyperglycaemic clamp at 32 mmol L^?1, the AUC_Δinsulin from 120 to 130 min (first phase) was not different on both study days: 2411 ± 640 vs. 3193 ± 866 pmol L^?1 × 10 min (with and without glibenclamide, P = 0.29). AUC_Δinsulin from 150 to 240 min (second phase) also showed no difference: 59 623 ± 8735 vs. 77389 ± 15161 pmol L^?1 × 90 min (with and without glibenclamide, P = 0.24). AUC_ΔC-peptide from 120 to 130 min and from 150 to 240 min were slightly lower on the glibenclamide study day (both P < 0.04). The M/I ratio from 180 to 240 min did not change: 0.24 ± 0.04 vs. 0.30 ± 0.07 μmol kg^?1 min^?1 pmol L^?1 (with and without glibenclamide, P = 0.25). In conclusion, glibenclamide increases second-phase insulin secretion only at a submaximally stimulating blood glucose level without enhancement of first-phase insulin release and has no additive effect on insulin secretion at maximally stimulating blood glucose levels. Glibenclamide did not change insulin sensitivity in this acute experiment.     

Mechanism of oestrogen and progesterone effects on lipid and carbohydrate metabolism: alteration in the insulin: glucagon molar ratio and hepatic enzyme activity

As in women receiving oestrogens the administration of 17beta-oestradiol to ovariectomized female rats caused a rise in fasting plasma triglycerides and a fall in plasma glucose. Progesterone, on the other hand, had no significant effects. In the oestradiol treated rats, the portal vein basal insulin levels were slightly reduced. Oestradiol, however, had a marked suppressive effect on the alpha cells of the pancreas resulting in a greater reduction in basal glucagon and impaired glucagon response to alanine infusions. The relative insulin to glucagon (I/G) molar concentration ratio in portal vein blood was increased. Oestradiol also produced a dose dependent increase in the activity of the liver lipogenic enzymes, acetyl CoA carboxylase and fatty acid synthetase. On the other hand, the activity of the gluconeogenic rate limiting enzyme phosphoenol-pyruvate carboxykinase (PEPCK) was inhibited. The cross-over pattern of gluconeogenic intermediates confirmed inhibition of gluconeogenesis at this step, an effect which is similar to that induced by relative insulin 'excess'. Progesterone produced an increase in the portal vein insulin concentrations. Both the basal and the alanine-stimulated glucagon levels were also increased. The I/G molar ratio in portal vein blood of progesterone treated rats remained unaltered and the hepatic lipogenic and gluconeogenic enzyme activities were similar to control animals. These data suggest that insulin activity is increased relative to glucagon in the liver of oestradiol-treated rats due to the rise in portal vein I/G ratio. The changes in liver lipogenic and gluconeogenic enzymes and the alterations in fasting plasma triglycerides and glucose in response to oestrogens could be secondary to this effect.     

妊娠糖尿病子代红细胞膜胰岛素受体与胰岛素抵抗关系的研究

目的探讨妊娠糖尿病（GDM）子代红细胞膜胰岛素受体与胰岛素抵抗之间的关系。方法 32例妊娠糖尿病其儿童,22例正常妊娠其儿童,测定空腹血糖（FBG）、空腹胰岛素（FINS）、餐后2 h血糖（2 hBG）、餐后2 h胰岛素（2 hINS）、胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）,并检测高、低亲和力红细胞膜胰岛素受体数目（R1、R2）和亲和力常数（K1、K2）,计算胰岛素抵抗指数（IRI）。结果 GDM组儿童R1、R2低于对照组（P〈0.05）;GDM组儿童体重、BMI、FINS水平高于正常对照组（P〈0.05）。多元线性逐步回归分析结果显示,进入回归方程的因素有BMI（t=3.362,P〈0.05）、R1（t=-2.613,P〈0.05）、R2（t=-2.541,P〈0.05）,提示以上因素是影响GDM组儿童IR的主要危险因素。结论妊娠糖尿病（GDM）子代存在胰岛素抵抗,且与红细胞膜胰岛素受体数目减少、亲和力下降及肥胖有密切关系。     

不同孕周加用胰岛素对妊娠合并糖尿病孕产妇妊娠结局的影响分析

目的分析对于妊娠合并糖尿病孕产妇在不同孕周加用胰岛素治疗对剖宫产及早产发生率的影响。方法回顾性选取2017年6月至2018年6月同济大学附属第一妇婴保健院收治的采用胰岛素控制的妊娠合并糖尿病孕产妇179例,按照加用胰岛素时孕周的不同将孕产妇分为两组:<32周为早期组(n=96),≥32周为晚期组(n=83)。比较两组孕产妇胰岛素使用后,空腹血糖、餐后2 h血糖、血糖控制达标率与妊娠结局(包括剖宫产、早产、顺产发生率)。结果胰岛素使用后早期组孕产妇空腹与餐后2 h血糖水平(5.48±0.34)mmol/L、(7.08±0.75)mmol/L明显低于晚期组(6.72±0.47)mmol/L、(8.83±1.34)mmol/L,差异具有统计学意义(P<0.05)。早期组孕产妇血糖控制达标率(94.90%)明显高于晚期组(71.08%),差异具有统计学意义(P<0.05)。早期组孕产妇剖宫产率为13.54%,顺产率为79.17%,早产率为7.29%;晚期组孕产妇剖宫产率为32.53%,顺产率为36.14%,早产率为31.33%;两组比较差异具有统计学意义(P<0.01)。早期组孕产妇的不良妊娠结局发生率(7.29%)显著低于晚期组(15.66%),差异具有统计学意义(P<0.05)。结论对于妊娠合并糖尿病孕产妇,在早期加用胰岛素,可明显控制产妇产前空腹、餐后2 h血糖水平,提高血糖控制达标率,降低剖宫产率和早产发生率,效果理想。