HBV感染免疫耐受期孕妇分娩前后临床指标及细胞因子水平变化特征

[摘要]　目的　分析HBV感染免疫耐受期孕妇分娩前后临床指标及细胞因子水平的变化规律,比较分娩后不同ALT水平组孕妇血清细胞因子水平差异。方法　选择2015年1月—2017年12月就诊于首都医科大学附属北京佑安医院的HBV感染免疫耐受期孕妇52例,妊娠28周给予替比夫定（telbivudine, LdT）抗病毒干预,分别于LdT干预前（基线）、分娩前（2周）及分娩后（6周）进行生化、血清学及病毒学检测,同步留取相应时间点外周血标本进行细胞因子检测,并分析分娩前后临床指标及细胞因子水平的变化特征。结果　52例患者分娩后6周ALT水平均值明显高于LdT干预前和分娩前,其中ALT≥2倍正常值上限（upper limit of normal, ULN）者达28.8%（15/52例）;与LdT干预前相比,分娩前HBV DNA水平显著下降,平均降幅达（3.68±0.79） lg IU/ml;HBsAg和HBeAg水平在分娩前后无明显变化。与分娩后ALT＜2倍ULN组相比,ALT≥2倍ULN组的IFN-γ水平在LdT干预前呈低水平表达,分娩后呈高水平表达,差异均有统计学意义（Z=2.284,P=0.022;Z=2.223,P=0.026）;2组间IL-2、IL-4、IL-6、IL-10、TNF-α在LdT干预前、分娩前及分娩后均无明显差异。结论　HBV感染免疫耐受期孕妇分娩后部分患者ALT明显升高,结合分娩前后细胞因子的动态变化,提示分娩后可能出现免疫功能增强并打破机体对HBV的免疫耐受,这或许有利于分娩后的抗病毒治疗,但仍须要进一步深入的研究。     

Soluble leptin receptor levels in patients with anorexia nervosa

OBJECTIVE: To examine whether changes of serum soluble leptin receptor levels (S-LEPR) can modify leptin half-life and its tissue effects. The aim of our study was to measure S-LEPR levels in patients with anorexia nervosa (AN) before and 6 weeks after partial refeeding. METHODS: Anthropometric variables, serum leptin, S-LEPR, insulin, cortisol and TNF-alpha were measured in 15 AN patients before and after partial refeeding and 15 healthy control women. RESULTS: S-LEPR levels in AN patients were significantly higher than in healthy subjects (26.8 +/- 8.1 vs. 16.36+/-2.6U/mL, p < 0.01) and were not affected by partial refeeding (26.8 +/- 8.1 vs. 24.2 +/- 6.1 U/mL). In contrast, body mass index (BMI), body fat content, and serum leptin levels in AN patients increased significantly after partial refeeding. Except for the inverse relationship of S-LEPR levels to BMI and body fat content no clear relationship of this parameter to serum leptin, cortisol, insulin or TNF-alpha was found. CONCLUSION: S-LEPR levels are significantly increased in AN patients and this increase is unaffected by partial refeeding. The possibility of etiological role of increased S-LEPR levels in AN patients by affecting leptin central and/or peripherial effects should be further elucidated.     

Decreased soluble leptin receptor levels in women with polycystic ovary syndrome

OBJECTIVE: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and a high incidence of obesity. Leptin, the product of the ob gene, is involved in the regulation of energy balance and obesity and circulates in both free and bound forms. The soluble leptin receptor (sOB-R) is the most important leptin-binding protein, thus influencing the biologically active free leptin level. DESIGN: We assessed the correlation of metabolic and endocrine parameters with leptin and sOB-R levels in 122 PCOS women (aged 27 +/- 5.7 years) and 81 healthy controls (aged 25 +/- 4.0 years). METHODS: Leptin and sOB-R levels were measured using ELISA kits. In addition, anthropometric variables, body fat and endocrine parameters were evaluated and a glucose tolerance test performed to assess indices of insulin resistance and glucose metabolism. RESULTS: In PCOS patients, no correlation was found between leptin or sOB-R and parameters of hyper-androgenism. However, as expected, body mass index (BMI), body fat, waist circumference and indices of insulin resistance were significantly correlated with leptin in PCOS subjects and controls. In a subgroup analysis of lean, overweight and obese PCOS patients, significant differences were found in leptin (29.7 +/- 20.7 vs 45.4 +/- 25.0 vs 67.7 +/- 28.8 ng/ml, P < 0.0001) and sOB-R (8.0 +/- 3.4 vs 6.4 +/- 2.5 vs 5.7 +/- 2.3 ng/ml, P < 0.05). Compared with BMI-matched controls, lean PCOS patients had lower sOB-R levels (8.0 +/- 3.4 vs 12.7 +/- 4.7 ng/ml, P < 0.0001) and higher free leptin indices (4.5 +/- 3.9 vs 2.8 +/- 2.2, P = 0.0285). CONCLUSION: Taking into account that low sOB-R levels supposedly compensate diminished leptin action, PCOS per se might cause leptin resistance.     

Circulating levels of inhibin in pregnant women at term: simultaneous disappearance with oestradiol and progesterone after delivery

Circulating levels of immunoreactive inhibin (ir-inhibin) and its disappearance after delivery of the placenta were determined in seven pregnant women at term. Serum oestradiol (E2) and progesterone (P4) levels were measured simultaneously and served as comparisons. Fetal contributions of ir-inhibin were assessed by determining concentrations in the umbilical artery (UA) and vein (UV). Relative changes in circulating levels of ir-inhibin, E2, and P4 were compared to levels found in nonpregnant women during the early follicular phase (EFP) and mid-luteal phase (MLP) of the normal menstrual cycle. In pregnant women, ir-inhibin levels at delivery were 15- and 3-fold higher than EFP and MLP values respectively. The disappearance of all three hormones after removal of the placenta followed a bi-exponential curve with an initial, rapid component and a second, slower component. There was a highly significant positive correlation between the disappearance curves of all three placental hormones (r = 0.97, P less than 0.0001). Concentrations of ir-inhibin in the cord blood were about half that in maternal serum and without significant difference between levels in UA and UV.     

Soluble thrombomodulin and vascular adhesion molecule-1 are associated to leptin plasma levels in obese women

Recent studies have suggested that leptin, a plasma protein secreted by adipocytes, may play a role in artherothrombosis. In this study, we tested the hypothesis that leptin contributes to in vivo endothelial dysfunction in obese subjects. A cross-sectional comparison of plasma leptin, soluble thrombomodulin (sTM) and soluble vascular adhesion molecule-1 (VCAM-1) was carried out in 35 obese women (age 48+/-13) selected with a body mass index (BMI) > or =30kg/m(2) and 25 normal weight women (age 50+/-11, BMI < 25). An additional study was conducted to determine the short-term effects of weight loss induced by caloric restriction. Plasma levels of leptin, sTM and sVCAM-1 were measured before and after weight loss. Obese women had higher levels of leptin (35+/-22 versus 22+/-19, P<0.01), sTM (4.8+/-1.8 versus 1.9+/-1.5, P<0.001) and sVCAM-1 (726+/-109 versus 583+/-50, P<0.001) than non-obese women. sTM and sVCAM-1 concentrations had a positive correlation with BMI (sTM, r=0.70, P<0.001; sVCAM-1, r=0.60, P<0.001), waist circumference (sTM, r=0.66, P<0.001; sVCAM-1, r=0.37, P<0.01) and leptin levels (sTM, r=0.53, P<0.001; sVCAM-1, r=0.42, P<0.005). At multiple regression analysis leptin predicted sTM and sVCAM-1 independently of obesity measures and other covariates. Twenty-nine obese patients who completed the program of weight reduction showed a significant decrease in leptin, sTM, and sVCAM-1 levels. The magnitude of decrease of sTM and sVCAM-1 was related to the magnitude of reduction in leptin levels. Therefore, our results show that obesity is associated with enhanced levels of atherosclerosis markers. These abnormalities are related to abdominal obesity possibly mediated by leptin levels, and are reversible with weight loss.     

Circulating soluble leptin receptor, leptin, and insulin resistance before and after weight loss in obese children

OBJECTIVE: To study the relationships between leptin, soluble leptin receptor (sOB-R), and insulin resistance in obese children before and after weight reduction. METHODS: We determined fasting serum leptin, sOB-R, and insulin resistance index (Homeostasis model assessment (HOMA)) in 36 obese children at baseline and 1 y later and compared them to 72 lean children matched for age, gender, and pubertal stage. The changes of leptin (Deltaleptin) and sOB-R (DeltasOB-R) over the 1 y period were correlated to the changes of HOMA (DeltaHOMA), the changes of weight status, and the changes of percentage body fat (Delta%BF) based on skinfold measurements. Multiple linear regression analyses were conducted for the dependent variables Deltaleptin and DeltasOB-R, including DeltaBMI and DeltaHOMA as independent variables adjusted for age, gender, and pubertal stage. Changes of leptin and sOB-R levels were analyzed in 11 obese children after they had lost weight substantially (decrease SDS-BMI>0.5) and compared to 11 obese children without substantial weight loss matched for age, gender, and pubertal stage. RESULTS: Obese children showed significantly (P<0.001) higher leptin and lower sOB-R levels. Deltaleptin correlated significantly to DeltaSDS-BMI (r=0.28, P<0.05), Delta%BF (r=0.44, P<0.05), and DeltaHOMA (r=0.42, P<0.01), while DeltasOB-R correlated significantly to DeltaSDS-BMI (r=-0.42, P<0.01) and Delta%BF (r=-0.47, P<0.01), but not to DeltaHOMA. In contrast to DeltasOB-R, Deltaleptin correlated significantly to DeltaHOMA (P=0.02) in multiple linear regression analysis. Substantial weight loss led to a significant increase in sOB-R (P=0.02) and to a decrease in HOMA (P=0.02). In children without substantial weight loss, there were no changes in sOB-R, while HOMA (P=0.04) and leptin (P=0.02) increased significantly. CONCLUSIONS: The decrease of sOB-R and the increase of leptin levels in obese children normalized after weight loss. Therefore, these changes are consequences rather than the cause of overweight. In contrast to sOB-R, leptin levels are associated with insulin resistance.     

Homocysteine, folate and cobalamin levels in hypothyroid women before and after treatment

Hypothyroidism may result in accelerated atherosclerosis. Hyperhomocysteinaemia is an independent risk factor for premature atherosclerotic vascular disease. The aim of the present study was to assess plasma total homocysteine (tHcy), folate and cobalamin concentrations in hypothyroid patients before and after treatment. Thirty-one hypothyroid and thirty health young women were studied. The hypothyroid patients were investigated in the untreated state and again after restoration of euthyroidism. The levels of homocysteine, folate, cobalamin and thyroid stimulating hormone (TSH), free thyroxine (fT(4)), free triiodothyronine (fT(3)) and renal function were measured before and after treatment. In hypothyroidism tHcy was higher but not statistically significant than in control group. Serum level of folate was higher and serum cobalamin was lower in the hypothyroid state. Following L-thyroxine therapy tHcy significantly decreased as well as the concentration of cobalamin. Level of folate remained unchanged. Univariate analysis in hypothyroid group indicated that tHcy negative correlated with creatinine clearance, fT(3), fT(4), cobalamin and positive with TSH. In multivariate analysis tHcy correlated with creatinine clearance, cobalamin and fT(4). Thyroid status influences the plasma tHcy. Free triiodothyronine and next free thyroxine have the greatest negative influence. This would account for hyperhomocysteinemia in the hypothyroid state and premature atherogenesis.     

High leptin levels in women developing postpartum thyroiditis

BACKGROUND: There is experimental evidence that leptin is required for the development of T helper 1 (Th1)-mediated autoimmune diseases. However, to our knowledge, there are no studies demonstrating such a role in human autoimmune thyroid disease. OBJECTIVE: In the present study we have retrospectively examined patients developing postpartum thyroiditis (PPT), as a model of autoimmune disease, for changes in serum leptin levels during the postpartum period. MATERIALS AND METHODS: The study group included 61 women in the first month postpartum who were positive for thyroid peroxidase antibodies (TPOAb+ve). Twenty TPOAb-negative (-ve), age and body mass index (BMI)-matched, postpartum women were enrolled as the control group. All subjects were evaluated for BMI, serum leptin values, thyroid function [serum free-triiodiothyronine (FT3), free-thyroxine (FT4), thyrotropin (TSH)] and autoimmunity [TPOAb levels and complement activity index (C3 index)] at 4, 12, 16, 20 and 24 weeks' postpartum. During the postpartum period, 32 of 61 TPOAb+ve women (52.4%) showed one or more episodes of thyroid dysfunction (PPTD group), whereas the remaining 29 TPOAb+ve women remained euthyroid throughout the study period (PPTE group). None of the control group developed thyroid dysfunction. RESULTS: Four weeks postpartum, TPOAb+ve women showed higher serum leptin values than TPOAb-ve women, despite comparable BMI. At this time, PPTE and PPTD patients showed no significant differences in leptin levels or leptin/BMI ratio. Throughout the postpartum period, PPTD patients maintained significantly higher leptin values and leptin/BMI ratio compared to the healthy women. In PPTE women, however, a significant reduction in leptin levels and leptin/BMI ratio was seen at 12 weeks' postpartum. This decrease was transient and correlated negatively with the variation in C3 index at the same time. No significant correlation was found between serum leptin variations and FT4 or TSH levels. CONCLUSIONS: This study has demonstrated that women developing postpartum thyroiditis have higher leptin values compared to the healthy women. The higher levels were maintained for 6 months postpartum. This result would suggest an involvement of leptin in the pathogenesis of postpartum thyroid disease, although further studies are needed to characterize the reciprocal effects of leptin, immune system and thyroid hormones during the course of this disease.     

Serum leptin levels in patients with acromegaly before and after correction of hypersomatotropism by trans-sphenoidal surgery

It has been shown that GH excess is associated with decreased leptin levels and decreased body fat mass. Reports regarding the effect of GH on serum leptin levels are inconsistent. We studied leptin secretion in 20 acromegalics before and 2 months after trans-sphenoidal surgery and in 20 gender-, age-, and body mass index (BMI)-matched control subjects. The mean 8-h leptin concentration for each subject was measured from a pool formed of samples collected hourly beginning at 2200 h until 0600 h the next morning. In a subgroup of 10 acromegalics, leptin pulsatility was assessed for the same period of time in 10-min sampling intervals. Basal GH, insulin-like growth factor-I (IGF-I), insulin, glucose, and lipids levels were measured. Area under the curve for insulin (AUCins) during oral glucose tolerance test was calculated. Control subjects and acromegalics had similar BMI, but patients with active acromegaly had significantly lower mean leptin level (mean +/- SEM; in men, 2.6+/-0.4 vs. 7.1+/-1.1 microg/L, P = 0.003; in women, 16.0+/-3.4 vs. 23.5+/-3.1 microg/L; P = 0.036). Mean 8-h leptin correlated with BMI (r = 0.57, P = 0.007, in controls; r = 0.70, P = 0.001, in patients). In stepwise regression analysis with mean 8-h leptin as a dependent variable, BMI (P<0.001) and gender (P = 0.01) in acromegalics entered the equation, whereas in control subjects gender, free fatty acids, insulin, and age accounted for 99.3% in leptin variability. After surgery, BMI did not change significantly; and glucose (P = 0.014), GH (P<0.001), and IGF-I (P<0.001) levels together with AUCins (P = 0.002) decreased, whereas mean leptin concentration rose significantly and attained normal levels (4.1+/-0.8 microg/L, P = 0.028) in acromegalic men and (23.6+/-4.7 microg/L, P = 0.003) in acromegalic women. Correlation between leptin level and BMI was preserved after surgery (r = 0.62, P = 0.005). In stepwise regression analysis, free fatty acids (P = 0.04) contributed to 26.8% of the variance in corrected-leptin (for BMI and gender). Leptin concentration peak height and interpeak nadir level rose significantly (P = 0.033 and P = 0.037) after surgery by Cluster analysis, without significant changes in leptin pulse frequency and incremental peak amplitude. Nocturnal rise of leptin (mathematically described by a cubic curve) was characterized by an acrophase just after midnight, before and after surgery. The amplitude and the average leptin concentration of the cubic fit increased significantly after surgery (P = 0.028 and P< 0.001). In conclusion in acromegalic patients: 1) leptin secretion maintains the pulsatility and nocturnal rise; 2) the gender-based leptin differences are preserved; 3) GH-IGF-I normalization leads to a rise in leptin that is not related to changes in BMI; and 4) the possible role of rise in leptin levels when assessing clinical and metabolic outcome of therapy in acromegalic patients deserves additional studies.     

Soluble leptin receptor and insulin resistance as determinant of sleep apnea

OBJECTIVE: To investigate the possible associations between sleep apnea syndrome, hyperinsulinemia/insulin resistance and hyperleptinemia in subjects with different degrees of body mass index. DESIGN: To test for the presence or absence of sleep apnea syndrome in association with hyperinsulinemia/insulin resistance and hyperleptinemia. SUBJECTS: Twenty subjects with different body mass index (mean BMI 30.9+/-4.2). MEASUREMENTS: Insulin action and plasma soluble leptin receptor were measured by euglycemic hyperinsulinemic glucose clamp and by ELISA method, respectively. Occurrence of sleep apnea syndrome was assessed by clinical and nocturnal monitoring using a validated sleep apnea recorder. RESULTS: The apnea/hypopnea index (AHI) was positively correlated with plasma soluble leptin receptor (0.76; P<0.001) and negatively with the degree of insulin-mediated glucose uptake (r=-0.73; P<0.001). In a multivariate analysis AHI was associated with plasma soluble leptin receptor and insulin mediated glucose uptake independently of age, gender, BMI, plasma leptin levels and PaCO(2). CONCLUSION: Sleep apnea syndrome is associated with plasma soluble leptin receptor and insulin resistance independently of BMI.     

Serum allopregnanolone levels in pregnant women: changes during pregnancy, at delivery, and in hypertensive patients

Allopregnanolone is a neuroactive steroid measurable in peripheral circulation. The aim of the present study was to investigate the presence and the possible changes in serum allopregnanolone and progesterone levels in pregnant women during gestation, at delivery, and in patients with chronic hypertension, with or without superimposed preeclampsia. We also evaluated allopregnanolone in cord blood. Three groups of pregnant women were studied: 1) healthy controls followed longitudinally throughout gestation (n = 14); 2) at vaginal or cesarean delivery (n = 66); and 3) with chronic hypertension (n = 12), with (n = 7) or without (n = 5) superimposed preeclampsia. Allopregnanolone and progesterone levels were measured in maternal and cord serum by RIA. In healthy pregnant women, serum allopregnanolone and progesterone levels progressively increased throughout gestation. Whereas no changes were found at vaginal delivery, serum allopregnanolone and progesterone levels were significantly lower at delivery by emergency cesarean section (P < 0.01). Umbilical cord serum allopregnanolone and progesterone levels in emergency cesarean were significantly lower than those found at vaginal delivery (P < 0.01). Patients with chronic hypertension, with or without superimposed severe preeclampsia, showed serum allopregnanolone levels significantly higher than those of healthy women at the same gestational age (P < 0.01). In conclusion, maternal serum allopregnanolone levels increased during normal gestation were lower in women who underwent emergency cesarean and higher in patients with chronic hypertension, with or without preeclampsia. Because allopregnanolone is active on the central nervous system and in the control of systemic blood pressure, an involvement of this neurosteroid in the adaptive processes induced by pregnancy is suggested.     

Serum leptin levels in women with systemic lupus erythematosus

The purpose of this study was to evaluate serum leptin levels in systemic lupus erythematosus (SLE). Forty-one women with SLE were compared with 23 healthy women of similar age and body mass index (BMI). Clinical characteristics and Mexican systemic lupus erythematosus disease activity index (Mex-SLEDAI) score were assessed. Serum leptin levels (ng/dl) were measured by enzyme-linked immunosorbent assay (ELISA). Comparisons of leptin levels were made with the Mann-Whitney U-test. In a multiple regression analysis, those factors that could influence the leptin levels were adjusted. Patients with SLE had higher leptin levels than the control group (SLE median 31 vs control median 15, P=0.023). After adjusting by other variables, the serum leptin levels remained higher in SLE than in controls (P=0.02). Patients with SLE had no association between leptin levels and Mex-SLEDAI score, age, duration of disease, or prednisone doses. Those with SLE had higher leptin levels than controls. Further longitudinal studies are required to evaluate the role of this hormone in the exacerbations of SLE.     

Serum leptin levels in patients with primary hyperaldosteronism before and after treatment: relationships to insulin sensitivity

BACKGROUND: Leptin is a protein hormone produced predominantly by adipocytes that plays a role in food intake regulation and a series of other physiological processes including blood pressure regulation. OBJECTIVES: The aim of our study was to compare serum leptin levels in patients with primary hyperaldosteronism (PA) with those of healthy subjects and to explore the relationship of serum leptin levels and the parameters of insulin action in these patients before and after surgical or pharmacological treatment. METHODS: Serum potassium, leptin, aldosterone, insulin levels and plasma renin activity were measured and hyperinsulinaemic euglycaemic clamp was performed in 11 patients with PA and 11 healthy age-, gender- and body mass index (BMI)-matched subjects. In eight of 11 patients the same measurements were repeated at least 6 months after surgical or pharmacological treatment. RESULTS: The basal serum leptin levels in PA patients did not significantly differ from those of healthy subjects (mean+/-s.e.m. 8.4+/-1.9 vs 11.2+/-1.8 ng/ml, P=0.30), although their insulin sensitivity was significantly impaired (PA patients vs control subjects: glucose disposal rate in the last 20 min of clamp (M) 18.7+/-1.8 vs 30.6+/-3.3 micromol/kg/min, metabolic clearance rate of glucose (MCR(g)) 3.9+/-0.5 vs 7.2+/-1.1 ml/kg/min, P<0.05). The surgical or pharmacological treatment of PA patients increased significantly their serum leptin levels (10.9+/-3.7 vs 8.4+/-1.9 ng/ml, P<0.05) and simultaneously improved their insulin sensitivity. Basal serum leptin levels in both groups correlated positively with BMI and serum insulin levels. The inverse relationship between serum leptin levels and the insulin sensitivity parameters was found in both PA patients before treatment and healthy subjects. These relationships disappeared after treatment of PA patients except for those between serum leptin levels and MCR(g). CONCLUSION: Basal serum leptin levels in untreated patients with PA do not significantly differ from those of healthy subjects, but increase significantly after surgical or pharmacological treatment. The increase in serum leptin levels is paradoxically accompanied by the improvement of insulin sensitivity in these patients.     

Determinants of serum leptin levels in healthy postmenopausal women

The aim of this study was to evaluate factors that influence leptin levels in postmenopausal women. One hundred and forty-four postmenopausal women were evaluated cross-sectionally. In every woman a complete medical history was obtained, body mass index (BMI) was recorded and morning fasting blood was obtained for the determination of serum leptin, follicle stimulating hormone (FSH), estradiol, testosterone, delta4androstendione, dehydroepiandrosterone sulphate (DHEAS) and insulin. In univariate analysis, age, BMI and insulin were positively correlated with serum leptin, while DHEAS showed a negative association with leptin concentrations (age r=0.21, p=0.005, BMI r=0.41, p=0.0001, insulin r=0.20, p=0.008, DHEAS r=-0.28, p=0.0001). In stepwise multivariate regression analysis serum leptin could be best predicted from BMI, serum insulin and serum DHEAS [leptin= (1.41 * BMI) - (0.01 * DHEAS) + (3.26 * insulin) - 26.3; model r2=0.24, p=0.001]. In conclusion, BMI and serum insulin have a positive while serum DHEAS has a negative impact on serum leptin. Neither endogenous estradiol, nor endogenous testosterone are associated with leptin levels. Further studies are needed to elucidate the role of leptin in determining body weight and composition in postmenopausal women.     

高血压患者血浆瘦素及其可溶性瘦素受体水平的相关性研究

目的:探讨原发性高血压患者血浆瘦素及其可溶性瘦素受体水平的变化及其在高血压发生、发展中的作用。方法:选择2008-10-2009-07在我科住院的原发性高血压患者180例,男女各90例,门诊60例体检正常者作为对照组。采用酶联免疫法测定瘦素及其可溶性瘦素受体浓度,同时测定空腹血糖、三酰甘油、高密度脂蛋白、低密度脂蛋白、体质指数、腰臀比等指标,分析血浆瘦素及其可溶性瘦素受体与原发性高血压的关系。结果:高血压组患者血浆瘦素水平明显高于对照组(12.217±6.10∶8.89±5.27,P0.01),可溶性瘦素受体水平低于对照组(124.08±62.12∶164.23±69.60,P0.01)。且与正常对照组相比,随着血压水平的升高,血浆瘦素水平也明显升高,可溶性瘦素受体水平呈下降趋势。结论:原发性高血压患者的血浆瘦素浓度升高,可溶性瘦素受体浓度下降,与血压之间具有一定的相关性,说明瘦素抵抗与高血压的发生和发展密切相关。     

Role of serum leptin levels and leptin receptor gene polymorphisms in systemic lupus erythematosus

Clinical Rheumatology - Serum leptin and leptin receptor gene polymorphisms may play a role in the etiopathogenesis of SLE. This study was undertaken to explore the relationship between serum...     

The changes of serum leptin and soluble leptin receptor levels in patients undergoing mobilization of peripheral blood stem cells before autologous stem cells transplantation

BACKGROUND AND OBJECTIVES: Leptin was demonstrated to stimulate the proliferation of hematopoietic stem cells in vitro, but there is scarce information concerning serum leptin levels in patients with hematological diseases. The aim of our study was to measure serum leptin levels in patients undergoing mobilization of peripheral blood stem cells (PBSC) before autologous stem cell transplantation (ASCT). DESIGN AND METHODS: Eighteen patients indicated for ASCT were included in the study. The blood samples were obtained before the initiation of mobilization chemotherapy, at the phase of maximal leukopenia and on the second day of stem cell harvest. Serum leptin levels, soluble leptin receptor, cortisol, insulin, tumor necrosis factor alpha (TNFalpha), and interleukin-1 receptor antagonist (IL-1ra) levels were measured in the withdrawn samples. RESULTS: The basal values of parameters measured except for higher levels of IL-1ra in mobilized group did not differ significantly from those of a control group of healthy subjects. Serum leptin levels decreased significantly at the leukopenia phase and remained suppressed in the stem cell harvest phase (means +/- standard error means (SEM): 12.2 +/- 2.4 vs. 7.7 +/- 1.5 vs. 9.3 +/- 1.9 ng mL(-1)). No significant changes were found in soluble leptin receptor, insulin, cortisol, and TNFalpha levels throughout three measurements, while IL-1ra levels increased significantly in the SC harvest phase compared to the previous two measurements. INTERPRETATION AND CONCLUSIONS: As no metabolic variations explaining suppressed leptin levels were found, this suppression could be the result either of G-CSF administration or increased leptin consumption by activated stem cells.     

Serum leptin levels in acromegalic patients before and during somatostatin analogs therapy

GH excess is characterized by alterations of body composition such as decreased body fat mass; however, scant data are present regarding its effect on serum leptin levels. To better elucidate this topic, leptin secretion was studied in 20 acromegalic patients, before and after 6 months of treatment with somatostatin analogs (SR-lanreotide 30 mg and octreotide LAR). Basal GH, IGF-I, insulin, blood glucose and lipid levels were measured and the area under the curve (AUC) for insulin and glucose and oral glucose insulin sensitivity (OGIS) during oral glucose tolerance test (OGTT) were calculated. After 6 months of somatostatin analogs therapy, a significant reduction in GH and IGF-I plasma levels was observed (p<0.0005, both) with a significant increase of leptin levels (7.4+/-1.3 vs 13.2+/-1.6 ng/ml; p<0.05). Interestingly, the typical correlation of leptin with body mass index (BMI) was not present in active acromegaly, whereas it was restored after somatostatin analogs treatment; moreover, the gender difference in leptin secretion between men and women was preserved in active and controlled acromegaly. In conclusion, the gender-based leptin differences are preserved and leptin secretion/BMI ratio is normalized in acromegalic patients after somatostatin analogs therapy.