The effects of the menopause on insulin sensitivity, secretion and elimination in non-obese, healthy women

Abstract. We have carried out intravenous glucose tolerance tests with measurement of plasma glucose, insulin and C-peptide concentrations on 66 premeno-pausal and 92 postmenopausal non-obese Caucasian women. After adjustment for the effects of a number of possible confounding variables, including age and body mass index, there was little difference between pre and postmenopausal women in glucose and insulin concentrations either fasting or in response to intravenous glucose. Mathematical modelling analysis of the resultant plasma concentration profiles was used to obtain measures of insulin sensitivity, secretion and elimination, and non-insulin dependent glucose disposal. We found reciprocal differences in mean insulin sensitivity (increased by 50%) and non-insulin dependent glucose disposal (decreased by 30%). Plasma C-peptide response and pancreatic insulin secretion were markedly lower in the postmenopausal group (- 35% and -50% respectively). However, the rate constant for insulin elimination was also lower in these women. As a result, intravenous glucose tolerance test plasma insulin concentrations were not significantly different between the two groups. We conclude that, despite the occurrence of little or no variation in plasma glucose and insulin concentrations, the menopause is associated with significant changes in insulin metabolism.     

Lack of effect of hepatic enzyme induction on metabolic control in patients with type 2 (non-insulin-dependent) diabetes

A placebo-controlled, double-blind crossover study was carried out in 11 non-insulin-dependent (type 2) diabetic patients to find out the effects of a hepatic enzyme inducer (phenobarbital, 100 mg/day for 2 months) on the metabolic control, plasma C-peptide, insulin, serum, and lipoprotein lipid levels. Phenobarbital induced a significant increase in hepatic antipyrine metabolizing activity, but no significant changes were found in fasting or postload blood glucose, plasma C-peptide, or insulin levels during the study. There was a significant increase in serum total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol, as well as in serum total and very low-density lipoprotein triglycerides, during phenobarbital treatment as compared with placebo.     

Impaired first-phase insulin response predicts postprandial blood glucose increment in patients with recently diagnosed type 2 diabetes

OBJECTIVE: The aim of the study was to evaluate the relationship between postprandial blood glucose and first-phase insulin response and, furthermore, to assess whether the intravenous glucagon stimulation test can be used as a predictor for increased postprandial glucose in patients with recently diagnosed type 2 diabetes. MATERIAL AND METHODS: Twenty patients with diet-treated type 2 diabetes, diagnosed within the past 5 years, were included. In random order, on three different days, the patients underwent: 1) a standardized meal tolerance test, 2) an intravenous glucose tolerance test, and 3) an intravenous glucagon stimulation test. The postprandial blood glucose response was defined as the incremental area under the blood glucose curve 0-240 min after the meal. RESULTS: The first-phase insulin response at an intravenous glucose stimulation test was significantly correlated to the postprandial blood glucose increment (R(2)=0.21, p<0.05) and the maximal increment in plasma glucose concentration (R(2)=0.40, p<0.01) during the meal tolerance test. However, the incremental C-peptide value at 6 min in response to intravenous glucagon stimulation did not correlate to the postprandial blood glucose increment (R(2)=0.09, p=0.14). CONCLUSION: Impaired first-phase insulin response is a significant predictor of the increase in postprandial blood glucose in patients with type 2 diabetes in near normal metabolic control, whereas beta-cell function, assessed by glucagon stimulation test, is not.     

Lowering of plasma glucose concentrations with bezafibrate in patients with moderately controlled NIDDM

The goal of this study was to investigate whether treatment with bezafibrate improves glucose tolerance in non-insulin-dependent diabetes mellitus (NIDDM). The study included 37 NIDDM patients with HbA1 concentrations greater than 8.5% and normal kidney and liver function who were being treated with diet alone or diet together with a sulfonylurea drug. One patient withdrew because of constipation. At randomization and after 3 mo of treatment, patients were given a standard mixed-test-meal tolerance test (MTT; 500 cal) after an overnight fast, and plasma glucose, insulin, C-peptide, metabolite, nonesterified fatty acid (NEFA), and triglyceride concentrations were measured at 15- to 30-min intervals. Serum lipid, HbA1, and fructosamine concentrations were measured at monthly intervals. Glucose, NEFA, and triglyceride concentrations were significantly lower throughout the second MTT in bezafibrate patients (P less than 0.01-0.001) but not in the placebo group. Fasting serum insulin and C-peptide levels, but not postprandial concentrations, were reduced only in bezafibrate patients (P less than 0.05). After 3 mo, mean fasting serum triglyceride concentrations fell from 2.2 to 1.4 mM (P less than 0.001), total serum cholesterol concentrations from 6.3 to 5.5 mM (P less than 0.001), and low-density lipoprotein cholesterol concentrations from 4.2 to 3.5 mM (P less than 0.001) in bezafibrate patients. There were no changes in serum lipid concentrations in the placebo group. Treatment of patients with moderately controlled NIDDM with bezafibrate improves glucose tolerance and the serum lipid profile. Bezafibrate treatment may be a useful adjunct to hypoglycemic therapy in patients with NIDDM.     

血清游离脂肪酸与胰岛β细胞功能及胰岛素抵抗

目的观察糖代谢异常不同阶段患者空腹及口服75g葡萄糖后血清游离脂肪酸（free fatty acid,FFA）的变化,探讨FFA随糖代谢异常进展的变化趋势及其与胰岛β细胞功能、胰岛素抵抗的关系。方法 2003年5月-2005年4月对123例受试者通过口服葡萄糖耐量试验（OGTT）分为正常糖耐量组（NGT）20例,糖调节受损组（IGR）30例,初诊2型糖尿病组（NDM）41例,已诊2型糖尿病组（TDM）32例。测定其空腹及口服75g葡萄糖后的FFA、血糖、胰岛素及血脂的水平。结果①空腹FFA、OGTTFFA曲线下面积在IGR组、NDM组、TDM组均较NGT组明显增高,有统计学意义（P〈0.05）;各组OGTT2hFFA数值无差异,但随着2型糖尿病病情发展有逐渐增高的趋势。②空腹FFA、OGTT2hFFA与血糖、血脂均有相关性,且与胰岛β细胞功能有一定的负相关,OGTT2hFFA与胰岛素抵抗指数有一定的正相关。结论 FFA对胰岛β细胞功能及胰岛素抵抗均有影响。     

诺和锐30强化治疗对初诊2型糖尿病患者血糖及胰岛功能的影响

目的探讨诺和锐30强化治疗对初诊2型糖尿病患者血糖及胰岛功能的影响。方法对40例初诊2型糖尿病患者进行2周的诺和锐30治疗,分析治疗前后空腹血糖（FPG）及餐后2h血糖（2hPG）、糖化血红蛋白（HbAlc）、静脉葡萄糖耐量试验第一时项胰岛素及C肽分泌和胰岛素及C肽曲线下面积、胰岛素抵抗指数、胰岛素分泌指数、胰岛素敏感指数、空腹胰岛素（FINS）与FPG比值。结果诺和锐30治疗后,FPG、2hPG、HbAlc、胰岛素抵抗指数均较治疗前明显下降（P〈0．01）;窄腹及第一时项胰岛素和C肽的分泌、胰岛素及C肽曲线下面积、FINS与FPG比值、胰岛素分泌指数、胰岛素敏感指数均较治疗前明显升高（P〈0．01）。结论诺和锐30强化治疗能显著改善初诊2型糖尿病患者的血糖及胰岛功能。     

Fasting plasma C-peptide levels in health and impaired glucose tolerance: relations to blood glucose and relative body weight

Pancreatic B-cell function was studied as part of a health control examination by measuring fasting plasma C-peptide concentration in 433 44-55 year-old males with normal glucose tolerance. Fasting C-peptide levels were correlated with relative body weight (r = 0.48) and fasting blood glucose concentrations (r = 0.43), yielding a multiple correlation coefficient of 0.56, and the multiple regression equation: FCP (nmol/l) = -0.89 + 0.61 X RBW + 0.16 X FBG (mmol/l). (FCP = fasting plasma C-peptide, RBW = relative body weight, FBG = fasting blood glucose). In 26 subjects with impaired glucose tolerance, fasting plasma C-peptide levels were even more strongly correlated with relative body weight (r = 0.63) and fasting blood glucose concentrations (r = 0.47). Subjects older than 52 years had a significantly higher fasting C-peptide level than younger subjects (p less than 0.01). In the 26 subjects with impaired glucose tolerance, fasting plasma C-peptide levels were not significantly different from those in the 433 men with normal glucose tolerance. However, when compared to a group with normal glucose tolerance matched for relative body weight, the subjects with impaired glucose tolerance had an elevated fasting blood glucose level (p less than 0.01) without difference in C-peptide level, suggesting a reduced insulin sensitivity. It is concluded that, in order to evaluate B-cell secretory function by determining fasting plasma C-peptide concentration, the relative body weight and simultaneous blood glucose concentration should be taken into consideration.     

Practical aspects in performing the glucagon test in the measurement of C-peptide secretion in diabetic patients

The secretion of plasma C-peptide after intravenous glucagon stimulation was studied in 15 insulin-treated diabetic patients with onset of diabetes after the age of 30. The mean stimulation of C-peptide secretion caused by glucagon given in the fasting state and by a standardized breakfast were similar. Low blood glucose values (less than 3.5 mmol/l) were found to suppress the stimulating action of glucagon on the pancreas almost completely. When the glucagon test was performed 1.5 hours after a standardized breakfast, the mean concentration of plasma C-peptide was 62% higher than in the test in the fasting state, showing that the stimulating actions of glucagon and breakfast on the secretion of insulin are additive. The results indicate that when determining the level of plasma C-peptide after stimulation with glucagon, in order to distinguish between insulin-dependent and non-insulin-dependent diabetic patients, it is critical to take into account the consequence of low blood glucose values and to standardize the test conditions in regard to pre-test meals.     

Plasma insulin disturbances in primary hyperparathyroidism

Plasma insulin dynamics were evaluated in 10 patients with primary hyperparathyroidism before and after parathyroidectomy and correction of hypercalcemia. Before surgery fasting plasma insulin concentrations and insulin responses to administered glucose, tolbutamide, and glucagon were significantly greater than postoperative values. Hyperinsulinemia was not associated with altered glucose curves during glucose or glucagon tolerance tests, but a relatively greater insulin response to tolbutamide resulted in an increased hypoglycemic effect following its administration. The glucose-lowering action of intravenous insulin was slightly impaired before treatment. Intramuscular injections of parathormone to six normal men for 8 days induced mild hypercalcemia and hypophosphatemia and reproduced augmented plasma insulin responses to oral glucose and intravenous tolbutamide. 4-hr intravenous infusions of calcium to another group of six normal men raised serum calcium concentrations above 11 mg/100 ml. This did not alter glucose or insulin curves during oral glucose tolerance but markedly accentuated insulin responses to tolbutamide and potentiated its hypoglycemic effect. When highly purified parathormone was incubated with isolated pancreatic islets of male rats, glucose-stimulated insulin secretion was unaffected.These findings suggest that chronic hypercalcemia of hyperparathyroidism sustains a form of endogenous insulin resistance that necessitates augmented insulin secretion to maintain plasma glucose homeostasis. This state is insufficient to oppose tolbutamide-induced hypoglycemia because of an additional direct, selective enhancement of hypercalcemia on pancreatic beta cell responsiveness to the sulfonylurea. The possible direct role of parathormone in these events has not been established.     

Ageing and the response of plasma insulin, glucose and C-peptide concentrations to intravenous glucose in postmenopausal women.

1. Eighty-six apparently healthy postmenopausal women not receiving hormone replacement therapy were given an intravenous glucose tolerance test. Plasma glucose, insulin and C-peptide concentrations were determined in fasting and post-glucose challenge samples. 2. Using a multivariate regression model, with predictor variables of chronological age, menopausal age and body mass index, neither chronological age nor menopausal age correlated with fasting or post-challenge plasma glucose or C-peptide concentrations. In contrast, menopausal age was positively associated with fasting plasma insulin concentration (P = 0.038, model r2 = 0.107), insulin area (P = 0.01, model r2 = 0.236) and incremental insulin area (P = 0.024, model r2 = 0.243). This relationship could not be explained by differences in lifestyle variables of alcohol consumption, physical activity, previous duration of oral contraceptive usage, history of cigarette smoking or body mass index. 3. Our findings suggest that loss of ovarian function is associated with hyperinsulinaemia, possibly via alterations in the clearance of circulating insulin from the plasma. The hyperinsulinaemia observed may contribute to the increased risk of cardiovascular disease seen in postmenopausal women.     

Studies of glucose intolerance in cirrhosis of the liver

Patients with hepatic cirrhosis often have demonstrable glucose intolerance. We studied 21 patients with cirrhosis of the liver. Oral glucose tolerance tests (OGTT), intravenous arginine stimulation tests (IVAST), and intravenous insulin tolerance tests (IVITT) were performed, and timed blood samples were obtained for the assay of glucose immunoreactive insulin (IRI), C-peptide (C-P), and immunoreactive glucagon (IRG). The 125I-insulin binding to circulating monocytes was studied in some of the patients. All results were compared to those of similar studies performed on healthy controls. During OGTT significant glucose intolerance was demonstrable in the patients with cirrhosis (2 hr plasma glucose 198.8 +/- 14.3 mg/dl in cirrhosis and 116.4 +/- 4.2 in controls; p less than 0.001). Two-hour plasma IRI, C-P, and IRG were significantly higher in the cirrhotic patients than in controls (p less than 0.001; less than 0.001; less than 0.025). In response to IVAST, the patients with cirrhosis showed a greater first-phase insulin secretion and controls had a slightly better second-phase insulin release. Plasma IRG rose from a basal value of 446 pg/ml to 1100 in the patients with cirrhosis and from 171 pg/ml to 494 in controls. After intravenous insulin administration, there was only a 40% decline in plasma glucose concentration from basal values in the patients with cirrhosis whereas the controls showed a 60% decline, demonstrating that the patients with cirrhosis had significant insulin resistance. Moreover, the half-life of insulin was prolonged in the patients with cirrhosis (t 1/2 = 15.5 min in cirrhosis and 10.3 in controls; p less than 0.001); and the ratio of C-P to insulin during OGTT was also reduced, indicating that the patients with cirrhosis have reduced hepatic clearance of insulin. The specific binding of 125I-insulin to circulating monocytes was 2.7% in cirrhosis, 2% in obese controls, and 4% in lean controls. There was a significant negative correlation between the fasting plasma insulin values and the specific binding of insulin. In conclusion, patients with hepatic cirrhosis have significant glucose intolerance characterized by hyperinsulinemia, hyperglucagonemia, insulin resistance, and down-regulation of insulin receptors. Although hyperinsulinemia is probably caused by reduced hepatic clearance of insulin, hyperglucagonemia is primarily due to increased pancreatic secretion.     

Reproducibility of beta-cell function estimates in non-insulin-dependent diabetes mellitus

We evaluated the reproducibility of different estimates of endogenous insulin secretion in 30 patients with non-insulin-dependent diabetes mellitus (NIDDM). Fasting blood glucose concentration was similar on the 2 days of study. The coefficients of variation of fasting plasma C-peptide, plasma C-peptide 6 min after the injection of 1 mg i.v. glucagon, and the increment in plasma C-peptide after glucagon were 16.0, 14.8 and 24.1%, respectively. The coefficients of variation of the corresponding plasma insulin values were 19.2, 24.8, and 34.8%, respectively. The coefficient of variation of 24-h urinary C-peptide excretion was 22.1%. Because fasting plasma C-peptide correlated closely with plasma C-peptide 6 min after glucagon (test 1: r = .70, P less than .01; test 2: r = .76, P less than .01), it seems that these two values can be used equally well as assessment of beta-cell function in NIDDM. In conclusion, fasting plasma insulin, fasting plasma C-peptide, and plasma C-peptide 6 min after glucagon stimulation showed a similar and acceptable degree of reproducibility. Plasma insulin 6 min after glucagon and increments in plasma insulin and C-peptide, as well as urinary C-peptide, seem to be less reproducible.     

妊娠期糖尿病患者血清Betatrophin含量检测及其与机体糖脂代谢紊乱的关系

目的 探讨妊娠期糖尿病(GDM)患者血清Betatrophin含量与机体糖脂代谢紊乱的关系.方法 前瞻性选取2018年12月至2020年1月在庆阳市人民医院进行糖耐量筛查并确诊为GDM的孕妇117例作为GDM组,同期在本院进行糖耐量筛查的健康孕妇100例作为正常对照组.比较2组孕妇的血清Betatrophin含量、外周...     

Insulin resistance and enhanced protein glycation in men with prehypertension.

BACKGROUND: Insulin resistance and hyperinsulinemia have been reported among patients with hypertension. However, little is known about insulin sensitivity in subjects with prehypertension. The aim of this study was to assess whether the metabolic characteristics of insulin resistance syndrome are present in prehypertensive subjects. METHODS: Plasma fasting glucose, lipid profile, glycated hemoglobin, fructosamine and insulin concentrations were evaluated in 35 prehypertensive subjects and in 30 healthy controls. RESULTS: Prehypertensive subjects had significantly higher levels of plasma insulin and triglycerides compared with normotensive subjects. The level of high-density lipoprotein cholesterol was significantly lower in prehypertensive subjects compared with controls. There was no significant difference in total cholesterol and low-density lipoprotein cholesterol levels. The levels of glycated hemoglobin and fructosamine were also significantly higher in prehypertensive subjects compared with controls. Plasma insulin levels were positively correlated with systolic and diastolic blood pressure in prehypertensive subjects. Similarly, plasma insulin was significantly positively correlated with triglyceride and negatively correlated with high-density lipoprotein cholesterol. CONCLUSIONS: The present study indicates that prehypertensive non-diabetic subjects have higher insulin resistance and protein glycation compared to normotensive subjects, which may contribute to the pathogenesis of prehypertension.     

No glycemic benefit from guar administration in NIDDM

A randomized crossover study of 5-g guar minitablets against placebo, given three times per day with main meals for 8 wk, was done in 29 non-insulin-dependent diabetes mellitus (NIDDM) patients who had near-normal fasting plasma glucose concentrations on treatment with diet alone, additional sulfonylurea, or ultralente insulin. Guar did not reduce the excessive postprandial glycemic excursion, glycosylated hemoglobin values, basal plasma glucose concentrations, basal or incremental plasma C-peptide values, or body weight. There were few side effects with either guar or placebo therapy. Mean low-density lipoprotein cholesterol levels were significantly reduced (P less than .001) by guar administration (116 +/- 23 vs. 104 +/- 19 mg/dl). Guar additives did not improve the excessive postprandial glycemia found in NIDDM patients in whom near-normal fasting plasma glucose levels had been obtained.     

Alterations of serum lipids in breast cancer: effects of disease activity, treatment, and hormonal factors.

Fasting venous blood collected from 83 patients with breast cancer was analyzed for triglycerides; total, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol; tumor necrosis factor (TNF alpha); glucose; creatinine; insulin; glucagon; growth hormone; cortisol; and thyrotropin. Patients with stage IV disease had significantly higher (P less than 0.05) triglyceride concentrations and significantly lower (P less than 0.05) concentrations of total and HDL cholesterol than did patients with less advanced disease or age-matched controls. Furthermore, LDL cholesterol concentrations in patients with boney metastases were significantly lower (P less than 0.05) than concentrations in patients with liver or liver plus boney metastases or in controls. These results could not be attributed to smoking habits, alcohol consumption, or treatment. We observed no correlations between serum concentrations of lipid and concentrations of TNF alpha, insulin, glucose, creatinine, cortisol, growth hormone, or thyrotropin. However, there was a significant (P less than 0.05) negative correlation between total cholesterol and glucagon and between LDL cholesterol and glucagon for patients with stage II, III, and IV disease, suggesting that glucagon may reduce LDL cholesterol concentrations by an as-yet-unidentified mechanism.     

Different mechanisms for impaired fasting glucose and impaired postprandial glucose tolerance in humans

OBJECTIVE: To compare the pathophysiology of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) in a more comprehensive and standardized fashion than has hitherto been done. RESEARCH DESIGN AND METHODS: We studied 21 individuals with isolated IFG (IFG/normal glucose tolerance [NGT]), 61 individuals with isolated IGT (normal fasting glucose [NFG]/IGT), and 240 healthy control subjects (NFG/NGT) by hyperglycemic clamps to determine first- and second-phase insulin release and insulin sensitivity. Homeostasis model assessment (HOMA) indexes of beta-cell function (HOMA-%B) and insulin resistance (HOMA-IR) were calculated from fasting plasma insulin and glucose concentrations. RESULTS: Compared with NFG/NGT, IFG/NGT had similar fasting insulin concentrations despite hyperglycemia; therefore, HOMA-IR was increased approximately 30% (P < 0.05), but clamp-determined insulin sensitivity was normal (P > 0.8). HOMA-%B and first-phase insulin responses were reduced approximately 35% (P < 0.002) and approximately 30% (P < 0.02), respectively, but second-phase insulin responses were normal (P > 0.5). NFG/IGT had normal HOMA-IR but approximately 15% decreased clamp-determined insulin sensitivity (P < 0.03). Furthermore, HOMA-%B was normal but both first-phase (P < 0.0003) and second-phase (P < 0.0001) insulin responses were reduced approximately 30%. IFG/NGT differed from NFG/IGT by having approximately 40% lower HOMA-%B (P < 0.012) and approximately 50% greater second-phase insulin responses (P < 0.005). CONCLUSIONS: Since first-phase insulin responses were similarly reduced in IFG/NGT and NFG/IGT, we conclude that IFG is due to impaired basal insulin secretion and preferential resistance of glucose production to suppression by insulin, as reflected by fasting hyperglycemia despite normal plasma insulin concentrations and increased HOMA-IR, whereas IGT mainly results from reduced second-phase insulin release and peripheral insulin resistance, as reflected by reduced clamp-determined insulin sensitivity.     

Insulin and C-peptide secretion in non-insulin-dependent diabetes mellitus and its response to dietary therapy

We studied insulin and C-peptide levels in patients with non-insulin-dependentdiabetes mellitus (NIDDM) during standard oral or intravenousglucose tolerance tests (GTT) at the time of diagnosis and after3 months dietary therapy. On the second occasion they also hadan ‘augmented’ GTT, in which slow intravenous infusionof glucose raised basal plasma glucose to a level similar tothat at the time of diagnosis. Eight patients had oral tests,and seven patients intravenous tests. In both groups, dietarytherapy significantly reduced fasting and peak plasma glucose(p<0.05 for oral; p<0.01 for intravenous GTT). Serum insulinlevels during conventional oral GTT were not significantly differentafter dietary therapy compared to diagnosis, but were significantlyhigher during the ‘augmented’ oral GTT (p<0.05).In those patients who underwent intravenous GTT, there was asignificant increase in both the total amount of insulin secreted(0–60 min) and in first-phase insulin secretion (0–10min) during the ‘augmented’ test compared to diagnosis(p<0.01), but first-phase insulin secretion during the conventionalintravenous GTT was unchanged. Serum C-peptide responses werealso greater during ‘augmented’ tests (p<0.05),similar in pattern to serum insulin. There is a relative deficiencyin insulin secretion in untreated NIDDM, which can be reversedby dietary therapy. It is essential to study insulin and C-peptidesecretion in controlled ‘fasting’ glucose conditions.     

α2-HS糖蛋白与妊娠期糖尿病关系的研究

目的观察不同程度糖代谢异常孕妇血清α2-HS糖蛋白(AHSG)浓度的变化并探讨其与血糖、血脂代谢及胰岛素抵抗的关系。方法根据75 g口服葡萄糖耐量(OGTT)结果将135名孕周为36～41周的孕妇分为3组:妊娠期糖尿病(GDM)组(45例)、糖耐量异常(GIGT)组(45例)、正常糖耐量(NGT)组(45例)。检测各组血清AHSG、空腹血糖(FPG)、空腹胰岛素(FINS)、空腹血脂([总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)]水平并计算体重指数(BMI)、胰岛素抵抗指数(HOMA-IR)、胰岛β细胞功能指数(HOMA-β)。结果 GDM组、GIGT组、NGT组的AHSG浓度分别为150.2±20.0、131.9±16.0(、124.0±15.0)μg/L,3组之间差异均有统计学意义(P<0.05)。GDM组FPG、TG、LDL-C、FINS水平均高于NGT组(P<0.05、P<0.01),HDL-C水平低于NGT组(P<0.05);GDM组TG、FINS水平高于GIGT组(P均<0.05、P<0.01);GIGT组TG、LDL-C、FINS高于NGT组(P<0.05、P<0.01);3组之间TC水平差异无统计学意义(P>0.05)。NGT组、GIGT组、GDM组HOMA-IR逐渐升高、HOMA-β逐渐下降3,组之间差异均有统计学意义(P<0.05)。AHSG浓度与BMI、TG、FINS、HOMA-IR呈正相关[相关系数(r)分别为0.406、0.503、0.533、0.612,P均<0.05],与HDL-C、HOMA-β呈负相关(r分别为-0.321、-0.589,P均<0.05),与FPG、TC无相关性(r分别为0.0580、.095,P均>0.05)。结论 AHSG在GDM患者的血糖、血脂代谢中发挥重要作用。AHSG参与了胰岛素抵抗、加重了β细胞损害,与GDM的发病关系密切。     

Effects of sympatholytic therapy with moxonidine on serum adiponectin levels in hypertensive women

We examined whether moxonidine influences lipid profile, insulin resistance, adiponectin levels, renal function and microalbuminuria in women with essential hypertension in a study of 55 non-diabetic hypertensive patients and 53 normotensive women. Hypertensive patients received moxonidine for 12 weeks. At baseline the hypertensive group had significantly higher mean blood pressure, low-density lipoprotein cholesterol, triglycerides, total cholesterol, fasting glucose, urinary albumin excretion and homeostasis model assessment of insulin resistance (HOMA-IR), together with significantly lower mean high-density lipoprotein cholesterol, creatinine clearance and serum adiponectin than the normotensive group. Moxonidine significantly decreased blood pressure, fasting glucose, triglycerides, total cholesterol, HOMA-IR and albumin excretion, but significantly increased serum adiponectin. The change in adiponectin level was negatively correlated with the change in HOMA-IR. Moxonidine treatment may improve unfavourable metabolic status related to insulin resistance by increasing adiponectin levels in patients with essential hypertension. Since it can improve adiponectin levels, it may be used in the antihypertensive treatment of patients at high risk of diabetes and cardiovascular disease.