A study on the hyperinsulinism of late pregnancy.

Much research has demonstrated that in late pregnancy glucose administration causes a marked increase of peripheral insulin levels. To ascertain whether this particular increase is due to increased insulin secretion and/or to reduced hepatic insulin removal, we measured blood glucose, plasma C-peptide and plasma insulin during OGTT in 7 nonpregnant women and in 20 nondiabetic women at third trimester of gestation and 60-90 days after delivery. The C-peptide/insulin molar ratio was calculated for all subjects. Data obtained showed that both plasma insulin and C-peptide response to oral glucose is considerably higher in women at third trimester of pregnancy as compared with that observed in the same subjects after delivery and in nonpregnant women. The basal (overnight fasting) C-peptide/insulin molar ratio did not differ significantly between pregnant and nonpregnant women. After the oral glucose load the molar ratio was sharply reduced in all groups of subjects, but the overall decrease in the pregnant women in the three hours following oral glucose was considerably greater than in postpartum and in nonpregnant women. The increased plasma C-peptide response clearly indicates that in pregnancy oral glucose-induced hyperinsulinism is caused by increased insulin release from pancreatic B-cells. Moreover, the marked overall decrease of the C-peptide/insulin molar ratio suggests, even if it does not definitely prove, that hyperinsulinism after glucose in late pregnancy may be a consequence not only of increased insulin secretion, but also of decreased hepatic extraction of insulin.     

Insulin resistance has no impact on ghrelin suppression in pregnancy

Ghrelin is reduced in various states of insulin resistance. The aim of this study was to examine the relationship between ghrelin and glucose metabolism during pregnancy - a natural insulin-resistant state - in women with normal glucose tolerance (NGT), impaired glucose tolerance (IGT) or gestational diabetes mellitus (GDM) and potential changes 3 months after delivery. A total of 54 women, 37 pregnant and with various degrees of insulin resistance and 24 postpartum (PP, seven of them also studied during pregnancy) were studied. Ghrelin plasma concentrations at fasting and 60' following glucose loading (75 g-2 h-oral glucose tolerance test), area under the curve of plasma glucose (G-AUC(OGTT)) and insulin sensitivity [homeostatic model assessment (HOMA) and oral glucose sensitivity index (OGIS) indices, respectively] were determined. Both baseline and 60' ghrelin concentrations were to a comparable degree ( approximately by 65%) suppressed in NGT, IGT and GDM as compared to the PP group (the latter being indistinguishable from NGT regarding glucose tolerance and insulin sensitivity). In all women studied both during and after pregnancy, ghrelin levels rose from pregnancy to PP (mean increase 313.8%; P < 0.03). There was no correlation between baseline ghrelin and insulin sensitivity as estimated from both baseline (HOMA) and dynamic (OGTT:OGIS) glucose and insulin data. Ghrelin is substantially decreased during pregnancy, but glucose-induced ghrelin suppression is preserved at a lower level. There is apparently no relation to the degree of insulin resistance.     

Evaluation of B-cell secretion and peripheral insulin resistance during pregnancy and after delivery in gestational diabetes mellitus with obesity

Summary Nine pregnant women with gestational diabetes mellitus (GDM) were studied. Six normal pregnant women and six normal nonpregnant women were evaluated as control groups. All the women underwent oral glucose tolerance test and glucose clamp during the third trimester of pregnancy and two months after delivery. During OGTT, glucose, C-peptide and insulin plasma levels were determined. C-peptide and insulin values in the late phase of OGTT were higher during pregancy than after delivery in both groups. In gestational diabetic women, the M-value in the second steady-state during glucose clamp was lower than in controls, both during pregnancy and after delivery. Nevertheless, in both groups the M-value during pregnancy was lower than after delivery. Moreover, in gestational diabetic women there was an inverse correlation between M-value in the second steady-state and ponderal excess index after delivery. In conclusion, the impaired peripheral glucose utilization and the pancreatic pattern of gestational diabetic women compared to normals suggested altered B-cell secretion response, increased peripheral resistance and overweight to be the main changes in GDM.     

Lack of suppression of plasma glucagon levels in late pregnancy persists postpartum only in women with previous gestational diabetes mellitus

Abstract The aim of the present study was to examine fasting (0) and postglucose glucagon levels in normal and gestational diabetes mellitus (GDM) pregnancy, as available data are somewhat conflicting. To this end we studied 18 women with GDM at 26–32 weeks of pregnancy and compared these with 26 normal pregnant women matched for age and BMI. We also examined glucagon suppressibility postpartum (2–4 months) in the same ex-GDM women, in whom normal glucose tolerance was confirmed (WHO criteria) and compared these with 17 controls matched for age and BMI. Glucose, insulin and glucagon levels were measured during a 100 or 75 g oral glucose tolerance test (OGTT) respectively. In pregnant women, baseline and 3 h after glucose ingestion, plasma glucagon levels were significantly higher (p<0.05) in women with GDM compared to normal women. Interestingly, in normal pregnancy a significant increase (p<0.01) of postglucose plasma glucagon levels at 1 and 2 h compared to baseline levels was observed, while there was no change in GDM pregnancy. In postpartum euglycaemic women, there was no difference in basal glucagon levels between the two groups. A differential glucagon response during OGTT was observed: in control women there was a significant glucagon suppression (p<0.01) at 2 h, while there was a significant glucagon increase (p<0.01) 1 h after glucose ingestion, in ex-GDM women. We conclude that (a) absence of the suppressibility of glucagon in ex-GDM women with normal OGTT may indicate insulin resistance and might be involved in the natural history towards glucose intolerance; and (b) nonsuppression of glucagon in normal late pregnancy as well as in pregnancy complicated by GDM may be due to physiological insulin resistance of the cells during this period.     

INSULIN RESISTANCE IN CIRRHOSIS: EVIDENCE FOR A POST-RECEPTOR DEFECT

Receptor and post-receptor abnormalities of insulin action and their possible role in the insulin resistance of cirrhosis were examined in eight biopsy-proven cirrhotic subjects and eight age-weight matched healthy volunteers. To this end, oral glucose tolerance tests (OGTT), insulin dose response curves and insulin binding to circulating monocytes were determined for each subject. The dose-response curves for the cirrhotic subjects were significantly shifted to the right compared to the control subjects, indicating the presence of insulin insensitivity (ED50 223 +/- 30 versus 64 +/- 8 mU/l respectively; P less than 0.001). The magnitude of the right shift of the insulin-dose response curves correlated significantly (P less than 0.001) with the OGTT 2 h insulin levels (r = 0.74) and the insulin areas under the OGTT curves (r = 0.86). In contrast, insulin responsiveness was marginally elevated in the cirrhotic group (maximal glucose disposal 680 +/- 47 versus 574 +/- 21 ml/m2/min; P less than 0.05). Insulin binding to circulating monocytes was normal in the cirrhotic subjects. It is concluded that the insulin resistance of cirrhosis is due to a post-receptor defect in insulin action which reduces insulin sensitivity but not insulin responsiveness.     

Plasma ghrelin levels of gastrectomized and vagotomized patients are not affected by glucose administration

BACKGROUND: Ghrelin is a brain-gut peptide with GH-releasing and appetite-inducing activities, secreted mainly by the stomach. Circulating ghrelin concentrations fall rapidly after nutrient ingestion as well as after oral and intravenous glucose challenge. A number of gut hormones including ghrelin require an intact vagal system, which has been hypothesized to have a major role in initiating the postprandial fall in ghrelin levels. AIM: We aimed to investigate the effect of oral glucose challenge on ghrelin secretion in gastrectomized (GASTRX) and vagotomized patients. DESIGN: Interventional study. PATIENTS: Six GASTRX-vagotomized patients and 11 healthy sex- and body mass index (BMI)-matched subjects. METHODS: An oral glucose tolerance test (OGTT) was performed in all subjects. At baseline, circulating plasma total ghrelin, serum glucose, insulin and GH levels were measured. Serum glucose, insulin, GH and plasma ghrelin levels were determined every 30 min for 2 h. RESULTS: Plasma ghrelin levels at baseline were reduced by 55% in GASTRX-vagotomized patients compared to the control group (P < 0.01). In control subjects, plasma ghrelin levels decreased significantly during the OGTT whereas in GASTRX-vagotomized patients no reduction was registered (26.4 +/- 2.8% vs. 5.5 +/- 3.4%). The OGTT revealed a significantly greater increase in circulating glucose levels and serum insulin levels while GH response was not different in GASTRX-vagotomized patients compared to control subjects. CONCLUSIONS: Our data show that circulating ghrelin levels in GASTRX and vagotomized patients were not suppressed after oral glucose administration, unlike control subjects, suggesting that this effect could be due, at least in part, to the lack of contribution of the vagal nervous system to the regulation of ghrelin.     

Serum insulin and plasma glucagon in human pregnancy — On the pathogenesis of gestational diabetes. A review

Summary The possibility that the deterioration of glucose tolerance during pregnancy might be due to a change in the functional condition of the endocrine pancreas has been examined in normal pregnant women and in non-obese gestational diabetics. Three test-situations were applied to elucidate the problem: 1) an overnight fast; 2) a glucose tolerance test (OGTT); and 3) a protein-rich meal. After the overnight fast, hyperinsulinemia and hyperglucagonemia were found in late pregnancy in both groups. However, on a molar basis, basal insulin increased more than basal glucagon and the molar insulin: glucagon ratio was therefore increased. After oral administration of glucose, the insulin response was enhanced in the late stages of pregnancy both in normal women and in those with gestational diabetes while the depression of glucagon below fasting levels was exaggerated and sustained in both groups. In response to a protein-rich meal in normal late pregnancy, the glucagon response was significantly lower than post partum in the same subjects, whereas that of insulin was unchanged. Finally, in both groups the diminished glucose tolerance in pregnancy was not associated with an abnormally elevated proportion of total insulin immunoreactivity represented by the biologically almost inactive proinsulin. Based upon these findings and those reported in the literature, it is concluded that there is no evidence in support of the idea that the diabetogenicity of pregnancy can be explained by changes in the function of the endocrine pancreas in these patients.     

Insulin resistance and secretion in polycystic ovarian disease

In order to verify the relationship between insulin resistance and hyperandrogenism in Polycystic ovary disease (PCOD), circulating levels of insulin in response to oral glucose tolerance test (OGTT) were assessed in 23 PCOD patients and 10 matched control subjects without obesity, acanthosis nigricans and impaired glucose tolerance. In PCOD patients serum total testosterone (T), dehydroepiandrosterone sulfate (DHEA-S), LH and LH/FSH ratio were significantly higher than in control subjects; whereas urinary 17-ketosteroids (17-KS) and glycemic response to OGTT were not different. PCOD patients were clearly hyperinsulinemic before and during OGTT compared to the control group: mean +/- SD basal insulin (Io) (23.4 +/- 10.3 vs 11.3 +/- 4.6 microU/ml, p less than 0.001) and the sums of insulin levels (sigma I) during OGTT (341.4 +/- 148.9 vs 162.2 +/- 56 microU/ml, p less than 0.001). In the two groups serum T, but not DHEA-S, LH, urinary 17-KS and the degree of obesity, was strongly associated with Io (r = 0.458, p less than 0.01) and sigma I (r = 0.419, p less than 0.02), as well as with insulin resistance as assessed by basal (r = 0.425, p less than 0.02) and postglucose challenge (r = 0.384, p less than 0.05) insulin to glucose ratio. These results confirm that the hyperinsulinism and insulin resistance in PCOD is not related to obesity and suggest that the hyperandrogenism may be partially responsible of the observed imbalance in glucose-insulin homeostasis.     

Cortisol levels during an oral glucose tolerance test in lean and obese women

Because of the similarities between Cushing's syndrome and insulin resistance syndrome,cortisol metabolism in obesity has been investigated in numerous studies. Our study investigates serum glucose, insulin, and cortisol response to oral glucose stimulation in a group of obese and lean normotensive, normolipidemic, and glucose-tolerant premenopausal women. Twenty-one obese [body mass index (BMI) 37Z +/- 6.3 kg/m2) and 14 lean (BMI: 21.5 +/- 1.0 kg/m2) age-matched healthy premenopausal women were included in the study. Serum glucose, insulin, and cortisol levels were measured at 30-minute intervals during 120 minutes of oral glucose tolerance testing (OGTT). Mean serum glucose and insulin levels were significantly higher in the obese group compared with lean subjects, and cortisol levels were similar during OGTT. There was not a significant difference for cortisol area under the curve (AUC) during OGTT between the two groups. No correlation between cortisol AUC, insulin AUC, and glucose AUC was noted for both groups. During OGTT, a decrease in cortisol levels was observed in both groups. The decrement occurred at 30 minutes of the OGTT in the obese group and at 60 minutes of the OGTT in the lean group. At 90 and 120 minutes of the OGTT, serum cortisol levels were similar to basal levels in both the obese group and the lean group. Previous studies reported altered hypotalamic-pituitary-adrenal axis activity, altered levels of urinary cortisol excretion, and increased metabolic clearance of cortisol in obesity. In our study in obese women, the only detected difference from lean subjects was a quicker suppression and recovery in serum cortisol levels after glucose administration.     

Hepatic insulin responsiveness in patients with endogenous hypertriglyceridaemia

Summary Plasma insulin response to oral glucose, insulin resistance, and insulin suppression of hepatic glucose production were studied in 11 normal subjects and 11 hypertriglyceridaemic patients. Patients with hypertriglyceridaemia had a significantly higher insulin response to oral glucose. Insulin resistance was also significantly greater in hypertriglyceridaemic subjects as determined by measuring the steady-state plasma glucose response during a continuous infusion of epinephrine, propranolol, glucose, and exogenous insulin. Insulin suppression of hepatic glucose production was calculated from the results of two studies in which glucose turnover rate was measured by a continuous infusion of³H-2-glucose. The first study was performed under conditions of basal insulin secretion, and the second carried out at steady state exogenous insulin levels of approximately 100 U/ml. The results indicated that basal hepatic glucose production was the same in both groups, and was suppressed to an equal degree by physiological levels of insulin. These data demonstrate that hepatic glucose production can be suppressed to an equal degree in normal and hypertriglyceridaemic subjects at comparable circulating insulin levels, at the same time that resistance to insulin-stimulated glucose uptake is observed in the hypertriglyceridaemic individuals.     

妊娠期糖代谢异常对妊娠的不良影响

目的了解妊娠期糖代谢异常对孕妇和围生儿的影响。方法对10809名孕妇在孕24～28周做50g葡萄糖负荷试验，阳性者再做75gOGTT，据血糖结果分为糖代谢正常（GNGT）组、妊娠糖尿病（GDM）组和妊娠期糖耐量减低（GIGT）组，比较三组妊娠的结局。结果GDM和GIGT组的患病率分别为0．61％和2．50％。GDM组孕妇产后即时出血、剖宫产、妊娠高血压综合征、羊水过多、巨大儿、早产儿和新生儿低血糖的发生率均显著高于GNGT组；GIGT组剖宫产、羊水过多、巨大儿的发生率显著高于GNGT组，低体重儿发生率低于GNGT组。结论妊娠期糖代谢异常对孕产妇和围生儿有不良影响，因此应重视孕期糖代谢异常的筛查、诊断和治疗。     

Asymmetric dimethylarginine level in hyperglycemic gestation

We aimed to evaluate plasma asymmetric dimethylarginine (ADMA) concentrations and its relation with insulin sensitivity/resistance indices in pregnant women with different degrees of carbohydrate intolerance. This study included a two step approach; 50 g glucose challenge test (GCT) followed by 100 g oral glucose tolerance test (OGTT) was used for diagnosis of carbohydrate intolerance within 24-28th weeks of gestation. Pregnant women with positive GCT but negative OGTT (AGCT group, n=30) and gestational diabetics (GDM group, n=58) were compared to healthy pregnant controls (n=50). Plasma ADMA concentration and its relationship with glucose and insulin levels and insulin sensitivity/resistance indices (HOMA-IR, QUICKI, ISIOGTT) were evaluated. Both AGCT and GDM groups were found to have similarly higher plasma ADMA levels than control subjects (3.60±1.21; 4.00±1.70; 2.65±0.82 μmol/l, respectively, P=0.001). ADMA was significantly but slightly correlated with insulin sensitivity/resistance indices and moderately correlated with 2-h insulin level. The 2-h insulin value of the OGTT was the independent influencing constant for ADMA (R=0.57, P=0.0001). In conclusion, plasma asymmetric dimethylarginine level was higher in cases with abnormal glucose challenge test but normal OGTT as well as in gestational diabetics, compared to pregnant women with normal glucose tolerance. The elevated ADMA level in pregnant women with carbohydrate intolerance may possibly be due to elevated insulin level.     

Lack of relationship between beta3-adrenergic receptor gene polymorphism and gestational diabetes mellitus in a Taiwanese population

The Trp64Arg polymorphism of beta(3)-adrenergic receptor (ADRB3) has been reported to be associated with insulin resistance and gestational diabetes mellitus (GDM). The objective of this study is to investigate whether the ADRB3 Arg variant confers susceptibility to GDM in a Taiwanese population. A total of 299 pregnant women (mean +/- SD, 31.1 +/- 4.2 years) was recruited. Two-hour, 75-g oral glucose tolerance tests (OGTT) were conducted at 24 to 31 weeks gestation (28.3 +/- 1.6 weeks). Forty-one GDM subjects and 258 controls with normal glucose tolerance (NGT) level were genotyped for the ADRB3 Trp64Arg polymorphism. The genotype distribution and allele frequency of ADRB3 did not significantly differ between GDM and NGT subjects (9.8% v 14.5%). Body weight gain during pregnancy was not different between ADRB3 genotypes. However, the GDM subjects with the Arg64 variant had higher fasting (P =.04) and postload 120 minutes (P =.03) insulin levels as compared with the GDM subjects with the Trp64Trp allele. In all subjects, the women with the Arg64 allele (n = 76) had significantly higher level of insulin secretion (the ratio of Deltainsulin(60)/Deltaglucose(60)) during OGTT than those without (n = 223) (P =.03) despite similar plasma levels of glucose and insulin in both genotypes. Our results indicated that the ADRB3 Trp64Arg variant is not related to the development of GDM and has no effect on obesity during pregnancy in a Taiwanese population. However, ADRB3 polymorphism might be a possible determinant of insulin resistance.     

Association between silent ST segment depression in exercise electrocardiography and insulin resistance in obese subjects

OBJECTIVES: This study was designed to clarify the association between ST segment depression in exercise electrocardiography (ECG) and insulin resistance in obese subjects. METHODS: A multistage graded submaximal exercise stress test on the bicycle ergometer was performed under CM5-lead ECG monitoring in 114 obese subjects (39 men and 75 women, mean age 50.9 +/- 12.2 years, mean body mass index 28.6 +/- 3.1 kg/m(2)). RESULTS: In 27 patients showing ST segment depression at the final exercise intensities (abnormal ST), insulin resistance index by homeostasis model assessment (HOMA-IR) was higher and insulin sensitivity index was lower than in the remaining 87 patients with normal ST segment level (normal ST). The abnormal ST group showed significantly higher plasma glucose and serum insulin levels during the oral glucose tolerance test (OGTT) than the normal ST group. The abnormal ST group showed a significantly higher prevalence of hypertension, impaired glucose tolerance and metabolic syndrome than the normal ST group. Multiple logistic regression analysis showed that insulin resistance as evaluated by fasting insulin, sigma insulin during OGTT, HOMA-IR, insulin sensitivity index, the levels of uric acid, fasting glucose, systolic blood pressure and maximal oxygen uptake were independently associated with ST segment depression. CONCLUSIONS: These results suggest that insulin resistance may involve pathological ST depression during exercise, as well as previously reported factors such as hyperglycemia, hyperuricemia, hypertension and lower aerobic capacity.     

Circulating ghrelin levels in basal conditions and during glucose tolerance test in acromegalic patients

BACKGROUND: Ghrelin exerts a wide range of metabolic functions. In contrast to the body of information accumulated on the role of ghrelin on energy balance, the possible relevance of the peptide on GH secretion in physiological and pathological conditions has so far been poorly investigated. AIM: The aim of the present study was to evaluate circulating ghrelin levels in acromegalic patients in basal conditions and in response to oral glucose tolerance test (OGTT). PATIENTS: Serum ghrelin, insulin and leptin levels were measured in 31 healthy normal weight subjects as controls, 25 patients with simple obesity and 17 non-diabetic acromegalic patients. Ghrelin and insulin response to OGTT was evaluated in six controls, four obese and six acromegalic patients. RESULTS: The acromegalic patients showed ghrelin levels lower than those observed in normal weight subjects (201+/-20 vs 329+/-32 pmol/l, P<0.05) and similar to those found in obese subjects (165+/-14 pmol/l, P=not significant). Both obese and acromegalic patients had insulin levels significantly higher than controls, while high levels of leptin were detected only in obese subjects. Serum ghrelin levels showed a significant negative correlation with insulin, leptin and body mass index (P<0.05) in normal and obese subjects. No correlation was observed in acromegalic patients, although those with severe insulin resistance showed the lowest ghrelin values (161+/-20 pmol/l). In controls and obese subjects, ghrelin levels showed a significant decrease (25-40%) during OGTT, while no effect was detectable in acromegalic patients. CONCLUSIONS: This study reports that patients with active acromegaly show low levels of circulating ghrelin that are not further reduced by OGTT, this pattern of secretion probably depending on both GH-induced insulin resistance and the putative GH/IGF-I negative feedback control on ghrelin secretion.     

Glucose tolerance after portacaval shunt in liver cirrhosis

The liver plays a key role in glucose homeostasis and insulin metabolism. Altered glucose and insulin levels in peripheral blood are common findings in chronic liver disease. The aim of the present study was to investigate the effect of surgical portosystemic shunt on plasma glucose and insulin responses to glucose administration in a group of cirrhotic patients. For this purpose 10 cirrhotic subjects (8 males and 2 females) aged 42 to 65 years underwent an oral glucose tolerance test (OGTT, 75 g), and an intravenous glucose tolerance test (IVGTT, 0.33 g/kg) before and after undergoing a side-to side portocaval anastomosis (PCS). 6 noncirrhotic, nondiabetic patients matched for sex, age and body weight who underwent abdominal vascular surgery served as controls. In cirrhotic subjects, the PCS resulted in: increased plasma glucose and insulin levels during OGTT; decreased C-peptide level during OGTT; unmodified plasma glucose and insulin concentrations during IVGTT. In control subjects the abdominal surgery did not affect plasma glucose and insulin responses to oral or intravenous glucose loads. These results suggest that in cirrhotic subjects surgical portocaval shunt results in: deterioration of oral but not intravenous glucose tolerance, due to an escape of ingested glucose from the liver; increased peripheral insulin response to oral glucose administration as a consequence of reduction in hepatic removal of the hormone; and decreased pancreatic response to oral glucose due possibly to a greater feed back inhibition of beta-cell. These events seem to be a consequence of the shunt per se and not of a deterioration of hepatocellular function.     

Leptin response to oral glucose tolerance test in obese and nonobese premenopausal women

The objective of this study was to investigate the serum leptin response to oral glucose stimulation in a group of obese and nonobese normotensive, normolipidemic, and glucose-tolerant premenopausal women. Twenty-one obese (BMI: 37.7 +/- 6.3 kg/m2) and 14 nonbese (BMI: 21.5 +/- 1.0 kg/m2) age-matched, healthy premenopausal women were included in the study. Serum glucose, insulin, and leptin levels were measured at 30 min intervals during the 120 min of an oral glucose tolerance test (OGTT). Mean serum glucose, insulin, and leptin levels were significantly higher in the obese group compared to nonobese subjects during OGTT. Except for a 120 min decrement noted in obese women, no changes occurred in serum leptin levels during oral glucose stimulation in both groups. As a conclusion, absence of a significant elevation in serum leptin levels during OGTT in our obese subjects compared to nonobese subjects may be related to their normal metabolic variables despite being abdominally obese and insulin resistant.     

Plasma nitrate/nitrite response to an oral glucose load and the effect of endurance training

To assess the role of circulating nitric oxide (NO) production in glucose homeostasis, plasma nitrate/nitrite (NO(x)) was assessed during oral glucose tolerance tests (OGTTs) on 64 sedentary subjects and in a subset 40 subjects before and after 6 months of endurance exercise training. NO(x) decreased with the oral glucose load (P 相似文献   

Prediction of gestational diabetes mellitus at 24 to 28 weeks of gestation by using first-trimester insulin sensitivity indices in Asian Indian subjects

The aim of the present study was to predict the development of gestational diabetes mellitus (GDM) after 24 weeks of gestation by using first-trimester insulin indices. A total of 298 nondiabetic pregnant women underwent 3-hour oral glucose tolerance test (OGTT) in the first trimester of pregnancy. The normoglycemic women underwent second OGTT between 24 and 28 weeks. Insulin sensitivity and resistance indices were calculated by using the Matsuda index (composite insulin sensitivity from OGTT), quantitative insulin sensitivity check index, and homeostasis model assessment for insulin resistance and sensitivity by using the results of the first-trimester OGTT. These indices were compared between subjects who were diagnosed as having GDM and subjects with normal glucose tolerance in the second OGTT. The overall prevalence of GDM was 15.49% (24 in the first trimester and 16 between 24 and 28 weeks). First-trimester fasting plasma insulin greater than 7.45 μU/mL was able to predict GDM with sensitivity and specificity of 80% and 57.4%, respectively. The negative predictive value for this parameter was 0.97. Values of first-trimester composite insulin sensitivity from OGTT less than 5.5 had sensitivity and specificity of 71.4% and 62.5% for the prediction of GDM. First-trimester hyperinsulinemia preceded the onset of hyperglycemia between 24 and 28 weeks of gestation and would predict the development of GDM with limited sensitivity and specificity.     

Patterns of insulin resistance in the general population of southeast Spain

The aim of this study was to evaluate patterns of insulin resistance in the general population. The study was cross sectional. Clinical, anthropometric, and lipid measurements were made in 1226 persons aged 18-65 years. An oral glucose tolerance test (OGTT) was performed in 1020 subjects, with insulin levels determined at baseline and after 2 h. The homeostasis model assessment insulin resistance index (HOMA IR) and HOMA beta-cell function were calculated. Compared with subjects with normal glucose tolerance, the groups with abnormal OGTT had different baseline insulinemia, 2 h post OGTT insulinemia, HOMA IR and HOMA beta-cell indices. Serum insulin levels at baseline and 2 h after OGTT showed a characteristic pattern for each category of glucose tolerance, resulting from the different insulin responses. In the subjects with normal glucose tolerance, the pattern of the relationships between both types of serum insulin levels was exactly the same, so that it was possible to determine risk groups according to the ratio of baseline serum insulin/2 h insulin. HOMA IR and HOMA beta-cell were significantly associated with the risk of impaired fasting glucose, previously unknown diabetes mellitus, and known diabetes mellitus. These results support the rationale for introducing preventive measures against insulin resistance in the general population.