Influence of obesity and menopausal status on serum leptin, cholecystokinin, galanin and neuropeptide Y levels.

Obesity occurs in 60% of women after menopause and is characterized by an excess of adipose tissue that depends on several orexigenic (neuropeptide Y (NPY) stimulates carbohydrate ingestion, galanin stimulates fat intake) and anorectic (leptin, cholecystokinin (CCK)) factors. Both leptin and insulin can reduce hypothalamic NPY production and secretion. Behavior related to the consumption of food is probably attributed to the NPY-galanin signalling route. We investigated basal levels of serum leptin, CCK, galanin and NPY in 16 non-obese premenopausal women, in 15 obese premenopausal women (body mass index (BMI) 34.6 +/- 1.3 SD) and in ten obese postmenopausal women (BMI 34.7 +/- 1.5 SD) to determine the relationship between obesity, menopause and these neuropeptides. Obese premenopausal women had three-fold elevations of serum leptin (32.1 +/- 3.2 ng/ml) in comparison to non-obese premenopausal women (10.3 +/- 1.5 ng/ml), but similar levels to those in obese postmenopausal women (35.3 +/- 4.1 ng/ml). In all 44 patients and in both sub-groups of premenopausal and postmenopausal women, serum leptin exhibited a strong positive correlation with BMI (r = 0.8692, p < 0.0001; r = 0.8803, p = 0.0001; r = 0.8184, p = 0.0001, respectively). Serum galanin values showed a statistically significant increment in the obese postmenopausal group (51.1 +/- 8.1 pg/ml) compared to both premenopausal groups: the non-obese (34.9 +/- 5.8 pg/ml) and the obese (36.0 +/- 5.5 pg/ml). Non-obese menstruating women demonstrated NPY levels (175.0 +/- 12.8 pg/ml) significantly higher than those of obese premenopausal women (126.0 +/- 12.1 pg/ml) and obese postmenopausal women (138.1 +/- 15.4 pg/ml). CCK values showed no differences between non-obese and obese pre- and postmenopausal groups. Basal insulin values were elevated in both obese groups compared to non-obese premenopausal women. Significantly increased leptin and galanin levels in postmenopausal obese women coupled with decreased NPY levels revealed some changes in the neuropeptides regulating eating behavior, which may be the reason for the onset of postmenopausal obesity.     

Relationships between serum leptin level and regional bone mineral density, bone metabolic markers in healthy women

BACKGROUND: Leptin might affect bone metabolism. This study was performed to investigate the relationship of leptin to bone metabolism in detail in premenopausal and postmenopausal healthy women. METHODS: The relationships between serum leptin level and bone mineral density of several regional sites of the body as well as whole body, along with bone metabolic markers, were examined in 47 premenopausal and 29 postmenopausal healthy women. RESULTS: Serum leptin level was weakly correlated with bone mineral density of pelvis (Pearson's correlation coefficient r=0.39, p<0.05) and left leg (r=0.41, p<0.01) in the premenopausal women, although the correlation decreased after adjustment for BMI. There was no significant relationship between serum leptin level and whole body bone mineral density both in the premenopausal and postmenopausal women. Serum leptin level was correlated with serum alkaline phosphatase (r=0.56, p<0.001) and urinary deoxypyridinoline/cr (r=-0.32, p<0.05) by Pearson's correlation test in the premenopausal women; the relationships were maintained even after adjustment for BMI (r=0.50 and -0.48, respectively). CONCLUSIONS: Leptin is not a key regulator of bone metabolism, although it may have some effects on bone metabolic markers and BMD regionally in premenopausal women.     

Breast cancer size in postmenopausal women is correlated with body mass index and androgen serum levels.

Our objective was to investigate the effects of age, weight, body mass index (BMI), sex steroid receptor status and serum parameters such as estradiol, testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEAS) and leptin on the size of a malignant breast tumor. A total of 62 premenopausal (median age 44.0 years) and 151 postmenopausal (median age 59.1 years) Caucasian women undergoing lumpectomy or mastectomy for invasive breast cancer were examined. Patient parameters (age, body weight, BMI), tumor parameters (tumor size, estrogen and progesterone receptor status) and serum parameters (estradiol, testosterone, androstenedione, DHEAS and leptin) were measured. An increase of BMI and DHEAS levels was associated with larger tumors by partial correlation (rp) analysis (rp = 0.418, p = 0.008; and rp = 0.329, p = 0.041, respectively), whereas higher androstenedione levels corresponded with smaller tumors. Furthermore, BMI, androstenedione and DHEAS levels were correlated: an increase in DHEAS was associated with higher androstenedione serum concentrations (rp = 0.603, p < 0.001), but was also associated with a lower BMI (rp = -0.378, p < 0.001). BMI and androstenedione serum concentrations were also associated (rp = 0.242, p = 0.009), thus closing a circle of mutual interactions. We conclude that, although breast cancer progression is characterized by autonomous growth that has become independent of growth regulatory mechanisms, tumor size at the time of detection is influenced by a complex system of counter-regulatory feedback mechanisms that might represent the body's physiological attempt to control the size of a malignant tumor.     

Effects of sex steroid hormones and menopause on serum leptin concentrations

Leptin is a protein secreted by adipocytes; its circulating levels are correlated to fat mass and it acts on the hypothalamic centers regulating body weight. Leptin may also play an important role in regulating reproductive function. Indeed, ob/ob mice, lacking leptin due to a genetic mutation, are obese and infertile; administration of recombinant leptin to these animals reduces body weight and restores fertility. A sexual dimorphism in serum leptin levels has also been observed, with higher concentrations in women. Studies in vitro seem to indicate that estrogens stimulate leptin secretion, while in vivo studies are extremely discordant. In humans, several studies showed increased, unmodified and decreased leptin levels after the menopause. Furthermore, hormonal replacement therapy (HRT) after the menopause was reported to result in unmodified, increased or decreased leptin levels. It is likely that the effects of postmenopausal hypoestrogenism on leptin levels are masked by the postmenopausal changes in body composition. Indeed, after menopause, there is an increase in body weight, body mass index (BMI) and fat mass with a centralization of fat distribution. Administration of HRT may stop these changes and even restore a premenopausal pattern, leading then to decreased leptin levels.     

Effects of sex steroid hormones and menopause on serum leptin concentrations.

Leptin is a protein secreted by adipocytes; its circulating levels are correlated to fat mass and it acts on the hypothalamic centers regulating body weight. Leptin may also play an important role in regulating reproductive function. Indeed, ob/ob mice, lacking leptin due to a genetic mutation, are obese and infertile; administration of recombinant leptin to these animals reduces body weight and restores fertility. A sexual dimorphism in serum leptin levels has also been observed, with higher concentrations in women. Studies in vitro seem to indicate that estrogens stimulate leptin secretion, while in vivo studies are extremely discordant. In humans, several studies showed increased, unmodified and decreased leptin levels after the menopause. Furthermore, hormonal replacement therapy (HRT) after the menopause was reported to result in unmodified, increased or decreased leptin levels. It is likely that the effects of postmenopausal hypoestrogenism on leptin levels are masked by the postmenopausal changes in body composition. Indeed, after menopause, there is an increase in body weight, body mass index (BMI) and fat mass with a centralization of fat distribution. Administration of HRT may stop these changes and even restore a premenopausal pattern, leading then to decreased leptin levels.     

Serum leptin concentrations in women during gonadotropin stimulation cycles

OBJECTIVE: To determine whether elevated follicular steroid levels during gonadotropin stimulation cycles are associated with altered circulating leptin concentrations. STUDY DESIGN: Sequential serum samples were collected from women (N = 37) undergoing luteal phase GnRH agonist + FSH treatment cycles prior to oocyte retrieval for in vitro fertilization. Leptin concentrations in serum were measured by radioimmunoassay and compared with serum estradiol, testosterone and dehydroepiandrosterone sulfate (DHEAS) levels. RESULTS: Serum leptin concentrations during stimulated cycles were variable between patients and correlated positively (r = .556, P < .01) with body mass index. Serum leptin levels correlated positively (r = .185, P < .05) with estradiol concentrations across all days. Mean serum leptin concentrations on the day gonadotropin treatment began (baseline, 12.9 +/- 2.0 ng/mL) were lower (P < .0001) than on the day peak estradiol levels were reached (18.4 +/- 2.3 ng/mL). Serum leptin concentrations also correlated with DHEAS levels (r = .214, P < .05) but did not correlate with testosterone or the estradiol:testosterone ratio. CONCLUSION: Gonadotropin stimulation in women is associated with elevated leptin levels, consistent with an interaction between the reproductive axis and leptin secretion and/or clearance.     

Association between metabolic syndrome and serum leptin levels in postmenopausal women

Menopausal status is associated with weight gain, increased central fat mass, abnormal lipid metabolism, insulin resistance and susceptibility to metabolic syndrome (MetS). Leptin is synthesised and secreted by adipocytes. Serum leptin levels are highly correlated with fat mass. We determined the association between MetS and serum leptin levels in 153 postmenopausal women. The difference in serum leptin level between MetS and non-MetS groups showed a statistical significance after adjusting for body mass index (BMI; 19.9 ± 9.5 vs 12.1 ± 5.9 ng/ml, p = 0.013). The indicator of abdominal obesity, waist-to-hip ratio (WHR) and visceral fat area (VFA), had a positive correlation with serum leptin level in non-obese subjects after adjusting for BMI (p = 0.017, p < 0.001, respectively). Of the components of MetS, abdominal obesity and the number of MetS components had a positive correlation with serum leptin level (p < 0.05, p < 0.001, respectively).     

Serum leptin concentrations in women taking oral contraceptives

OBJECTIVES: To investigate serum leptin concentrations in women taking oral contraceptives containing the same gestagen and different doses of ethinyl estradiol. STUDY DESIGN: 30 women received tablets containing 20 microg of ethinyl estradiol (EE) and 150 microg of desogestrel (DSG) (Mercilon) whereas another group of 30 women received 30 microg of EE and 150 microg of DSG (Marvelon). Serum leptin concentrations were estimated using a Leptin RIA kit (Linco Research USA) after an overnight fast on the first day of the cycle prior to the onset of therapy as well as after the 3rd and 6th treated cycles. RESULTS: In both groups a positive correlation between serum leptin and body mass index (BMI) was found (r=0.56; P<0.001 and r=0.67; P<0.001). The initial serum leptin concentration in the Mercilon group was 7.62+/-8.46 ng/ml. This value was not statistically different from values after 3 months (9.31 8.23 ng/ml) and after 6 months (10.53+/-8.03 ng/ml) of treatment. Very similar results were found in patients receiving Marvelon: 8.81+/-6.56 ng/ml initially; 11.62+/-11.16 ng/ml at 3 months, and 10.38+/-7.32 ng/ml at 6 months. The statistical analysis did not reveal any significant difference at each investigated time point in either study group. CONCLUSIONS: Modern low dose OC containing third generation gestagen and low dose of ethinyl estradiol, does not have any influence on serum leptin or BMI, and therefore does not exert a significant influence on body energy metabolism.     

Correlation of Kupperman's index with estrogen and androgen levels, according to weight and body fat distribution in postmenopausal women from Mexico City

OBJECTIVES: To establish the differences in Kupperman's index (KI) and hormone levels according to weight and body fat distribution in postmenopausal women, since obesity and fat distribution affect hormone levels. MATERIAL AND METHODS: One hundred and twenty-five postmenopausal women were studied and divided according to body mass index (BMI) and waist-hip ratio (WHR): normal weight (BMI < or = 27), obesity (BMI > 27); lower-level body fat distribution (WHR < or = 0.85) and upper-level body fat distribution (WHR >0.85). Afterwards four subgroups were created: (I) BMI < or = 27 and WHR < or = 0.85, (II) BMI < or = 27 and WHR > 0.85, (III) BMI > 27 and WHR < or = 0.85, and (IV) BMI >27 and WHR > 0.85. Climacteric symptoms were analyzed with Kupperman's index. Estrone, estradiol, testosterone, androstenedione, and dehydroepiandrosterone sulfate determinations were done by radioimmunoassay and verified by chemoluminescence. The androstenedione-estrone and testosterone-estradiol ratios were calculated. Statistical analysis was by Student's t test for independent samples, plus Pearson's correlation analysis. RESULTS: Average age was 53.0 +/- 6.5 years, time since menopause 74.2 +/- 64.3 months. When comparing those with lower-level body fat distribution and those with upper-level body fat distribution, the A levels were significantly lower (P < 0.04) in those with upper-level distribution. Kupperman's index was significantly lower in subgroup I when compared with subgroups III and IV. The androstenedione level was lower in subgroup IV compared with subgroup III. In the whole sample, there was a correlation of the WHR with testosterone (0.297, P < .004) and the testosterone-estradiol ratio (0.209, P < .04). CONCLUSION: It was shown that the testosterone-estradiol ratio has a better correlation with the symptoms, so it can be used to evaluate climacteric patients when they complain of menopausal symptoms.     

孕妇血清瘦素水平的测定

目的　探讨孕妇血清瘦素水平的变化及其与妊娠的关系。方法　采用放射免疫测定法 ,测定 2 5 1例孕妇 (观察组 )和 35例年龄、体重指数相近的正常非孕妇女 (对照组 )的血清瘦素水平 ,并将瘦素水平与孕妇的孕周、体重、体重指数、腹围、子宫底高度、血压等的关系进行了相关分析。结果　观察组瘦素水平为 (15 .1± 7.4) μg/L ,对照组瘦素水平为 (9.1± 4.9) μg/L ,两组比较 ,差异极有显著性 (P <0 .0 0 1)。相关分析显示 ,孕妇血清瘦素水平与其体重 (r =0 .5 2 9)、体重指数 (r =0 .5 5 1)、腹围 (r=0 .5 6 4)、子宫底高度 (r =0 .15 1)、收缩压 (r =0 .134 )、舒张压 (r=0 .2 5 1)均有相关性。妊娠期间 ,血清瘦素水平虽然逐渐上升 ,但直到孕 30周 ,统计学上尚无明显差异。结论　监测孕妇瘦素水平变化 ,对妊娠并发症 (如妊娠高血压综合征 )的临床观察可能有一定的意义     

Body composition estimated by bioimpedance analysis in Sicilian climacteric women

AIM: The aim of this study was to evaluate the effects of menopause transition on body weight, and body composition in a Sicilian climateric population. METHODS: Two hundred and nine (60 pre- and one 149 postmenopausal) untreated, healthy women were selected. Body composition was estimated by BIA101 of AKERN SRL. Body Mass Index (BMI), waist and hip circumferences were also measured. RESULTS: The mean BMI of the study population was 29.4+/-0.7. There was no significative difference between pre- and postmenopausal subjects regarding BMI (chi-squared=9.25; P=0.16), its class distribution, fat mass (FM), TBW and waist-to-hip ratio (WHR). The FM was significantly more represented in pre- than in postmenopausal women (47.43+/-1.33 vs 45.02+/-0.81 kg) (P<0.01). Linear regression analysis showed a positive correlation between BMI and fat free mass (FM) percentage (chi-squares=0.7045) nevertheless among the subjects aged=or>55 years, in 57% of the normoweight the body fat (BF) percentage was undesirably high. CONCLUSION: Climacteric changes and aging process are related to changes in body weight and fat distribution; even subjects apparently 'normo-weight' (BMI below 25) were 'over-fat', because revealed undesirably high BF%. Further investigation in larger population is needed to define whether BMI or BF% better predicts the risk of obesity-related diseases in climateric Sicilian women.     

The contribution of menopause to changes in body-fat distribution.

OBJECTIVE: To investigate whether menopause contributes to changes in body-fat distribution, irrespective of aging or obesity. METHODS: The subjects were 545 premenopausal (aged 16-55 years; mean +/- standard deviation, 37.7 +/- 9.1 years) and 219 postmenopausal (aged 45-65 years, 58.0 +/- 5.0 years) women. Baseline characteristics included age, body mass index (BMI), and menopausal status (premenopause or postmenopause). The ratio of trunk fat to leg fat (trunk-leg ratio) was estimated by dual-energy X-ray absorptiometry. The trunk-leg ratio and baseline characteristics were compared between the 2 groups. In all subjects (n = 764), possible correlations between the trunk-leg ratio and the baseline characteristics were determined using univariate and multivariate analysis. In postmenopausal women, the relationship of the trunk-leg ratio to YSM or age after adjusting for BMI was investigated. RESULTS: The trunk-leg ratio and BMI were significantly higher in postmenopausal women than in premenopausal women. In all subjects, age and BMI were positively correlated with the trunk-leg ratio (r = 0.445 and 0.587, respectively, p < 0.0001). Menopause was also positively correlated with the trunk-leg ratio on univariate regression analysis (standardized regression coefficient = 0.369, p < 0.0001). On multiple regression analysis, age, BMI, and menopause were independently correlated with the trunk-leg ratio (p < 0.05). In postmenopausal women, age and YSM were positively correlated with the trunk-leg ratio, independent of the BMI (p < 0.01). CONCLUSIONS: Menopause contributes to a change in body-fat distribution, irrespective of aging or obesity.     

Circulating leptin levels during ovulation induction: relation to adiposity and ovarian morphology

OBJECTIVE: To assess serum leptin levels based on body habitus and ovarian morphology during controlled ovarian hyperstimulation. Design: Prospective analysis. SETTING: University IVF program. PATIENT(s): Women undergoing IVF-ET were divided into two groups, obese ovulatory women (n = 6; mean (+/-SD) body mass index, 30.1 +/- 0.6 kg/m(2)) and lean ovulatory women (n = 20); mean (+/- SD) body mass index 22.0 +/- 0.2 kg/m(2)). Lean women were categorized further according to whether they had polycystic-appearing ovaries (n = 8) or normal-appearing ovaries (n = 12). INTERVENTION(s): Controlled ovarian hyperstimulation and IVF. MAIN OUTCOME MEASURE(s): Serum estradiol, testosterone, and leptin. RESULT(s): Mean (+/- SD) leptin levels were significantly higher before and after GnRH agonist down-regulation in obese women (41.7 +/- 5.2 pg/mL and 36.1 +/- 5.8 pg/mL, respectively) compared with lean women (8.4 +/- 1.0 pg/mL and 6.9 +/- 1.1 pg/mL, respectively). Mean (+/- SD) leptin levels increased significantly in both groups (54.5 +/- 5.1 pg/mL and 11.7 +/- 1.2 pg/mL, respectively), and the mean (+/-SD) percentage increase was similar (55% +/- 18% and 54.8% +/- 17%, respectively). Mean (+/-SD) leptin levels were similar in women with polycystic-appearing and normal-appearing ovaries before controlled ovarian hyperstimulation, but increased significantly in women with polycystic-appearing ovaries afterward (14.7 +/- 1.8 pg/mL and 9.3 +/- 1.0 pg/mL, respectively). CONCLUSION(s): Significant increases in leptin levels occur during controlled ovarian hyperstimulation, suggesting that leptin plays a role in follicular growth and maturation. The exaggerated response in women with polycystic-appearing ovaries reflects either a greater number of recruited follicles or a predisposition of adipocytes to leptin production.     

Leptin as a trigger for puberty in girls

The influence of leptin on the serum levels of follicle stimulating hormone (FSH) and estradiol in girls during puberty was longitudinally studied. Two hundred and twenty-seven healthy girls aged from 8.8 to 15.4 years were included in the study. After physical examination, girls were divided into four groups according to pubertal development. Body fat was assessed using body mass index and the sum of three skin folds: at the triceps site, subscapular site and on abdomen. Serum concentration of leptin, FSH and estradiol were assessed by RIA methods. RESULTS: The mean serum concentration of leptin, FSH and estradiol increase progressively throughout puberty. Leptin strongly correlates with the thicknesses of the skin folds and BMI but small significant positive correlations were found between leptin and FSH as well between leptin and estradiol.     

Does tibolone affect serum leptin levels and body weight in postmenopausal women?

Objectives Leptin has a significant role in body weight regulation and energy balance. We examined the effect of tibolone on the body weight and serum leptin levels in postmenopausal women.Study design Twenty women (aged 43–60 years) participated in this prospective study. All women in this study protocol received 2.5 mg/day of tibolone. Absolute and body mass index (BMI)-corrected serum leptin concentrations and BMI values were measured at baseline, after 3 months, and after 6 months of the tibolone therapy.Results Tibolone did not affect absolute and BMI-corrected serum leptin levels, and BMI values during the treatment. A significant linear correlation between BMI values and serum leptin levels was observed (p<0.05, r=0.67).Conclusions Tibolone seems not to affect serum leptin levels, body weight and BMI values of postmenopausal women. There is a significant correlation between serum leptin levels and BMI values.     

The utility of serum leptin and follicular fluid leptin, estradiol, and progesterone levels during an in vitro fertilization cycle

PURPOSE: To prospectively evaluate serum and follicular fluid leptin, estradiol, and progesterone levels during in vitro fertilization. METHODS: Prospective observational study measuring serum levels at six points during the IVF cycle and follicular fluid at the time of retrieval. RESULTS: Serum leptin and estradiol levels both significantly increased for the individual patients during the IVF stimulation process. None of the leptin levels differed based on pregnancy outcome. BMI significantly correlated with all leptin levels. Follicular fluid estradiol correlated with serum estradiol only in pregnant patients (r = 0.97, p<0.01) and was unrelated in non-pregnant patients (r=-0.15, p=0.81). CONCLUSION: Serum and follicular leptin levels are highly correlated. Leptin levels increase during the IVF cycle and vary between patients based on maternal BMI, but do not correlate with other serum hormone levels or pregnancy outcome. Pregnancy outcome success was reflected in the relationship between follicular fluid and serum levels of estradiol, independent of leptin levels.     

Leptin levels in serum depending on Body Mass Index in patients with endometrial hyperplasia and cancer

Leptin levels in serum depending on Body Mass Index (BMI) in patients with endometrial hyperplasia and cancer. OBJECTIVES: Concentrations of leptin, a hormone secreted by white adipose tissue, correlate strongly with body mass. Leptin interacts with several other hormones, modifies the activities of some enzymes and proinflammatory cytokines, participates in hematopoiesis, thermogenesis, and angiogenesis, and is involved in the control of carbohydrate and lipid metabolism. This study was undertaken to determine whether serum concentrations of leptin in obese patients with endometrial hyperplasia and cancer deviate from values in patients with normal endometrium. STUDY DESIGN: We enrolled 86 obese postmenopausal women, including 40 with endometrial cancer and hyperplasia and 46 with normal endometrium. Depending on BMI, three subgroups were formed: I<30; II = 30-40; III > 40. Leptin concentrations were measured with immunoenzymatic test kits from IBL. Statistical comparison was done with the chi square (chi(2)) test and Statistica software package. RESULTS: Mean serum concentration of leptin in endometrial cancer and hyperplasia was 16737.1 pg/ml as opposed to 9048.7 pg/ml in patients without endometrial pathology (p<0.0001). Significantly, higher concentrations of leptin were noted in every BMI subgroup of patients with endometrial pathology in comparison to controls (p<0.005). CONCLUSIONS: Leptin appears to participate in proliferative processes of the endometrium. Obesity is an important risk factor in endometrial cancer.     

Effects of bilateral ovariectomy and estrogen replacement therapy on serum leptin,sex hormone binding globulin and insulin like growth factor-I levels

Studies evaluating the effect of estrogen replacement therapy (ERT) on leptin levels are contradictory. The aim of this study was to investigate effects of bilateral ovariectomy and ERT on serum leptin levels and anthropometric measurements as well as interaction among leptin, sex hormone binding globulin (SHBG), and insulin like growth factor-I (IGF-I) in premenopausal women after bilateral ovariectomy. Twenty-four premenopausal women who undergo bilateral overiectomy were divided into two groups based on whether they received hormonal treatment postoperatively. The studied parameters were evaluated in both groups preoperatively and during the fourth and eighth weeks postoperatively. Serum leptin, testosterone, prolactin, insulin, IGF-1 levels, BMI, HOMA-IR, and waist-to-hip ratio values did not change in both groups at all times. In the estradiol group, serum SHBG concentrations were significantly higher on weeks 8 compared with control group and basal values (p?=?0.03 and 0.014, respectively). Leptin levels showed a positive linear correlation with BMI in all groups and at all times evaluated (r?=?0.80, p?<?0.01 for controls and r?=?0.62, p?<?0.01 for women treated with 17β-estradiol) and with insulin in estradiol group on weeks 4 (r?=?0.755, p?<?0.05). No correlation was found between leptin and estradiol, testosterone, prolactin, SHBG, IGF-1 levels, and anthropometric variables at all times. Leptin levels do not show modification 8 weeks after bilateral ovariectomy and under ERT, suggesting that estrogens do not have a stimulatory action on leptin in humans. Although needing confirmation by a longer study, our findings suggest that IGF-I system and SHBG did not regulate leptin and vice versa and ERT do not have any effect on leptin, SHBG, and IGF-I.     

多囊卵巢综合征患者血循环中瘦素水平及其相关因素的临床研究

目的 :探讨多囊卵巢综合征 (PCOS)患者血循环中瘦素水平与其它内分泌、代谢指标之间的关系 ,进一步研究瘦素的作用规律。方法 :PCOS患者 82例 ,行葡萄糖耐量试验 (OGTT)、胰岛素释放试验 ,测定 5个时点的血糖、胰岛素以及C 肽 (C P)浓度 ;测定空腹血瘦素、性激素及促性腺激素浓度 ;同时测定患者的体重指数 (BMI)、腰臀比例(WHR) ,观察胰岛素增敏剂治疗对瘦素的影响。瘦素和胰岛素用放免法测定 ,C 肽和性激素用发光免疫法测定。结果 :肥胖组瘦素水平显著高于消瘦组 (P =0 .0 0 0 1 ) ,瘦素水平与体重指数呈高度正相关 (P =0 .0 0 0 1 ) ;与腰臀比例、空腹、60min、1 2 0min胰岛素浓度呈显著正相关 (P分别为 0 .0 1 96、0 .0 3 0 8、0 .0 0 0 6、0 .0 0 1 4) ;与OGTT各时点的血糖、C 肽浓度以及血糖、胰岛素、C 肽曲线下面积之间无显著相关性 (P >0 .0 5 )。二甲双胍、文迪雅对瘦素水平无显著影响。结论 :PCOS患者的瘦素浓度与体内脂肪含量及分布密切相关。PCOS患者可能同时存在瘦素抵抗和胰岛素抵抗。用改善胰岛素敏感性药物治疗对瘦素水平无显著影响。     

Influence of NaMFP therapy on plasma leptin concentration in postmenopausal women

OBJECTIVE: To investigate the effect of a low dose of fluoride on the plasma leptin concentration in postmenopausal women. STUDY DESIGN: One hundred one healthy, postmenopausal women participated in this comparative study. To evaluate the influence of NaMFP treatment and body mass index (BMI) on leptin concentrations, patients were allocated to one of four groups: postmenopausal women (1) on NaMFP with BMI < 25 (n = 29), (2) on NaMFP with BMI > or = 25 (n = 26), (3) not on NaMFP with BMI > or = 25 (n = 24) and (4) not on NaMFP with BMI < 25 (n = 22). Plasma leptin levels were measured before and 12 months after the initiation of NaMFP or, in groups 3 and 4, after the start of the study. Ninety-eight women completed the study. RESULTS: There were significant differences in leptin concentrations at baseline and 12 months between NaMFP users with BMI > or = 25 and BMI < 25 and between women not taking NaMFP with BMI > or = 25 and BMI < 25 (group 2 versus 1 and 3 versus 4). After controlling for BMI, the use of NaMFP was not found to be related to the leptin value (group 1 versus 4 and group 2 versus 3). Although plasma leptin concentrations tended to be decreased slightly at 12 months in NaMFP users, this decrease was not statistically significant (P = .065). CONCLUSION: Leptin concentrations are significantly higher in obese, postmenopausal women than in nonobese, postmenopausal women. Plasma leptin concentrations are slightly but nonsignificantly influenced by long-term, low-dose fluoride treatment. Further studies are needed to elucidate the role of NaMFP on plasma leptin concentrations.