Metabolic Syndrome and Insulin Resistance Are Associated with Chronic Kidney Disease in Nondiabetic Adults with Abdominal Obesity

Aims: we investigate whether insulin resistance is associated with an increased prevalence for chronic kidney disease irrespective of the concurrent presence of metabolic syndrome. Methods: 1638 patients with abdominal obesity were selected. Metabolic syndrome and abdominal obesity were defined according to the International Diabetes Federation criteria. Insulin resistance was defined by Homeostasis Model Assessment Index >P75. Chronic kidney disease was defined by the presence of a low estimated glomerular filtration rate (Results: metabolic syndrome was present in 1030 (62.9%) patients and insulin resistance in 787 (48%). Conversely 61% of those with metabolic syndrome were insulin resistant and 79% of those with insulin resistance had metabolic syndrome. Chronic kidney disease was present in 18%. In multivariate analysis, chronic kidney disease was increased in subjects with insulin resistance (odds ratio [OR] = 1.350;CI 95%: 1.021 - 1.785;p = 0.035) and in those with metabolic syndrome (OR = 1.417;CI 95%: 1.045 - 1.922;p = 0.025). Conclusions: Metabolic syndrome and insulin resistance were significant and independently associated with chronic kidney disease in nondiabetic adults with abdominal obesity.

Insulin resistance as the molecular link between diabetes and Alzheimer's disease

Diabetes mellitus(DM)and Alzheimer's disease(AD)are two major health concerns that have seen a rising prevalence worldwide.Recent studies have indicated a possible link between DM and an increased risk of developing AD.Insulin,while primarily known for its role in regulating blood sugar,also plays a vital role in protecting brain functions.Insulin resistance(IR),especially prevalent in type 2 diabetes,is believed to play a significant role in AD's development.When insulin signalling becomes dysfunctional,it can negatively affect various brain functions,making individuals more susceptible to AD's defining features,such as the buildup of beta-amyloid plaques and tau protein tangles.Emerging research suggests that addressing insulin-related issues might help reduce or even reverse the brain changes linked to AD.This review aims to explore the relationship between DM and AD,with a focus on the role of IR.It also explores the molecular mechanisms by which IR might lead to brain changes and assesses current treatments that target IR.Understanding IR's role in the connection between DM and AD offers new possibilities for treatments and highlights the importance of continued research in this interdisciplinary field.

Assessing the impact of concurrent high-fructose and highsaturated fat diets on pediatric metabolic syndrome:A review

High-saturated fat(HF)or high-fructose(HFr)consumption in children predispose them to metabolic syndrome(MetS).In rodent models of MetS,diets containing individually HF or HFr lead to a variable degree of MetS.Nevertheless,simultaneous intake of HF plus HFr have synergistic effects,worsening MetS outcomes.In children,the effects of HF or HFr intake usually have been addressed individually.Therefore,we have reviewed the outcomes of HF or HFr diets in children,and we compare them with the effects reported in rodents.In humans,HFr intake causes increased lipogenesis,hypertriglyceridemia,obesity and insulin resistance.On the other hand,HF diets promote low grade-inflammation,obesity,insulin resistance.Despite the deleterious effects of simultaneous HF plus HFr intake on MetS development in rodents,there is little information about the combined effects of HF plus HFr intake in children.The aim of this review is to warn about this issue,as individually addressing the effects produced by HF or HFr may underestimate the severity of the outcomes of Western diet intake in the pediatric population.We consider that this is an alarming issue that needs to be assessed,as the simultaneous intake of HF plus HFr is common on fast food menus.

Nutrition, insulin resistance and dysfunctional adipose tissue determine the different components of metabolic syndrome

Obesity is an excessive accumulation of body fat that may be harmful to health. Today, obesity is a major public health problem, affecting in greater or lesser proportion all demographic groups. Obesity is estimated by body mass index(BMI) in a clinical setting, but BMI reports neither body composition nor the location of excess body fat. Deaths from cardiovascular diseases, cancer and diabetes accounted for approximately 65% of all deaths, and adiposity and mainly abdominal adiposity are associated with all these disorders. Adipose tissue could expand to inflexibility levels. Then, adiposity is associated with a state of low-grade chronic inflammation, with increased tumor necrosis factor-α and interleukin-6 release, which interfere with adipose cell differentiation, and the action pattern of adiponectin and leptin until the adipose tissue begins to be dysfunctional. In this state the subject presents insulin resistance and hyperinsulinemia, probably the first step of a dysfunctional metabolic system. Subsequent to central obesity, insulin resistance, hyperglycemia, hypertriglyceridemia, hypoalphalipoproteinemia, hypertension and fatty liver are grouped in the so-called metabolic syndrome(MetS). In subjects with MetS an energy balance is critical to maintain a healthy body weight, mainly limiting the intake of high energy density foods(fat). However, high-carbohydrate rich(CHO) diets increase postprandial peaks of insulin and glucose. Triglyceride-rich lipoproteins are also increased, which interferes with reverse cholesterol transport lowering highdensity lipoprotein cholesterol. In addition, CHO-rich diets could move fat from peripheral to central deposits and reduce adiponectin activity in peripheral adipose tissue. All these are improved with monounsaturated fatty acid-rich diets. Lastly, increased portions of ω-3 and ω-6 fatty acids also decrease triglyceride levels, and complement the healthy diet that is recommended in patients with MetS.

Low serum amylase and obesity, diabetes and metabolic syndrome: A novel interpretation

For the last decade, low serum amylase(hypoamylasemia) has been reported in certain common cardiometabolic conditions such as obesity, diabetes(regardless of type), and metabolic syndrome, all of which appear to have a common etiology of insufficient insulin action due to insulin resistance and/or diminished insulin secretion. Some clinical studies have shown that salivary amylase may be preferentially decreased in obese individuals, whereas others have revealed that pancreatic amylase may be preferentially decreased in diabetic subjects with insulin dependence. Despite this accumulated evidence, the clinical relevance of serum, salivary, and pancreatic amylase and the underlying mechanisms have not been fully elucidated. In recent years, copy number variations(CNVs) in the salivary amylase gene(AMY1), which range more broadly than the pancreatic amylase gene(AMY2A and AMY2B), have been shown to be well correlated with salivary and serum amylase levels. In addition, low CNV of AMY1, indicating low salivary amylase, was associated with insulin resistance, obesity, low taste perception/satiety, and postprandial hyperglycemia through impaired insulin secretion at early cephalic phase. In most populations, insulin-dependent diabetes is less prevalent(minor contribution) compared with insulin-independent diabetes, and obesity is highly prevalent compared with low body weight. Therefore, obesity as a condition that elicits cardiometabolic diseases relating to insulin resistance(major contribution) may be a common determinant for low serum amylase in a general population. In this review, the novel interpretation of low serum, salivary, and pancreas amylase is discussed in terms of major contributions of obesity, diabetes, and metabolic syndrome.

Relationship between insulin resistance, obesity and serum prostate-specific antigen levels in healthy men

The purpose of this study was to determine the relationship between insulin resistance, obesity and serum prostate-specific antigen （PSA） levels in healthy men with serum PSA level below 4 ng mL-1. The men included in the study cohort were 11 827 healthy male employees of the Korea Hydro and Nuclear Power Co., LTD who had undergone medical checkups including fasting glucose, fasting insulin and serum PSA between January 2003 and December 2008. Insulin resistance was calculated by homeostasis model assessment （HOMA [fasting glucose × fasting insulin]/22.5） and quantitative insulin sensitivity check index （QUICK/; 1/[log （fasting insulin） ＋ log （fasting glucose）]）. Age-adjusted body mass index （BMI） was significantly increased according to increasing quartile of insulin resistance as determined by HOMA and QUICKI, respectively, in analysis of variance （ANOVA） test and Duncan＇s multiple comparison test （P 〈 0.001）, but age-adjusted serum PSA concentration was significantly decreased according to increasing quartile of insulin resistance as determined by HOMA and QUICK/（P 〈 0.001）. Age, BMI, insulin resistance by HOMA or QUICK/were significantly independent variables to serum PSA level in a multivariate linear regression analysis （P 〈 0.001）. Insulin resistance was a significant independent variable to serum PSA level along with BMI. Insulin resistance and BMI were negatively correlated with serum PSA level in healthy men. Insulin resistance was positively correlated with BMI.

Coexistence of ovarian serous papillary cystadenofibroma and type A insulin resistance syndrome in a 14-year-old girl: A case report

BACKGROUND Type A insulin resistance syndrome is a rare disorder caused by mutations in the gene encoding the insulin receptor.Its coexistence with ovarian serous papillary cystadenofibroma is even rarer.CASE SUMMARY A 14-year-old girl developed type A insulin resistance syndrome and showed high fasting insulin,glucose,and hemoglobin A1c(HbA1c)levels.The girl suffered from ovarian serous papillary cystadenofibroma.The laboratory results were as follows:fasting insulin was 2624.90 pmol/L and HbA1c was 8.5%.A heterozygous missense mutation on exon 20 of the insulin receptor gene(c.3601C>T,Arg1201Trp)was observed.The histopathological diagnosis was a cystic lesion that extended to the upper right uterus,indicating a right ovarian serous papillary cystadefibroma accompanied by focal interstitial hyperplasia.The patient was treated with metformin for over 6 mo.Additionally,laparoscopic resection(bilateral)of the ovarian lesion and laparoscopic intestinal adhesiolysis were performed under general anesthesia.Diet therapy combined with exercise was then initiated.The patient had an uneventful recovery.The patient also showed improved blood glucose control,with reduced levels of fasting insulin(857.84 pmol/L)and HbA1c(7.0%).CONCLUSION Insulin resistance may play a significant role in the induction of tumors.It is important to investigate further the association between insulin resistance and tumors and the underlying mechanism.

Metabolic syndrome and non-alcoholic fatty liver disease:Asian definitions and Asian studies

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD), as conventionally recognized, is a metabolic disorder largely confined to residents of affluent industrialized Western countries. However, obesity and insulin resistance are not restricted to the West, as witnessed by their increasingly universal distribution. In particular, there has been an upsurge in metabolic syndrome in the Asia-Pacific region, although there are critical differences in the extent of adiposity between Eastern and Western populations. DATA SOURCES: An English-language literature search using PubMed (1999-2007) on obesity, metabolic syndrome and NAFLD, focusing on Asian definitions and Asian studies. RESULTS: NAFLD appears to be of long-standing insulin resistance and likely represents the hepatic manifestation of the metabolic syndrome. With insulin resistance as a common factor, the disease is associated with atherosclerosis and cardiovascular risk. All features of the metabolic syndrome and related events are assessed for practical management of NAFLD, although the criteria for the diagnosis of obesity and central obesity differ across racial groups. CONCLUSIONS: The increasing prevalence of obesity, coupled with diabetes, dyslipidemia, hypertension and ultimately metabolic syndrome, puts a very large population at risk of developing NAFLD in the coming decades. The simultaneous identification and appropriate treatment of the components of metabolic syndrome are crucial to reduce hepatic as well as cardiovascular morbidity and mortality.

Metabolic syndrome as a risk factor for gallstone disease

AIM: To establish an association between the presence of metabolic syndrome and the development of gallstone disease. METHODS: We carried out a cross-sectional study in a check-up unit in a university hospital in Mexico City. We enrolled 245 subjects, comprising 65 subjects with gallstones (36 women, 29 men) and 180 controls (79 women and 101 men without gallstones). Body mass index, waist circumference, blood pressure, plasma insulin, and serum lipids and lipoproteins levels were measured. Insulin resistance was calculated by homeostasis model assessment. Unconditional logistic regression analysis (univariate and multivariate) was used to calculate the risk of gallstone disease associated with the presence of at least three of the criteria (Adult Treatment Panel Ⅲ). Analyses were adjusted for age and sex. RESULTS: Among 245 subjects, metabolic syndrome was present in 40% of gallstone disease subjects, compared with 17.2% of the controls, adjusted by age and gender (odds ratio (OR) = 2.79; 95%CI, 1.46-5.33; P= 0.002), a dose-dependent effect was observed with each component of metabolic syndrome (OR=2.36, 95%CI, 0.72-7.71; P= 0.16 with one component and OR = 5.54, 95%CI, 1.35-22.74; P = 0.02 with four components of metabolic syndrome). Homeostasis model assessment was significantly associated with gallstone disease (adjusted OR = 2.25; 95%CI, 1.08-4.69; P= 0.03). CONCLUSION: We conclude that as for cardiovascular disease and diabetes mellitus, gallstone disease appears to be strongly associated with metabolic syndrome.

Metabolic syndrome and risk of subsequent colorectal cancer

The metabolic syndrome and visceral obesity have anincreasing prevalence and incidence in the generalpopulation. The actual prevalence of the metabolicsyndrome is 24% in US population and between24.6% and 30.9% in Europe. As demonstrated by many clinical trials (NAHANES , INTERHART) the metabolic syndrome is associated with an increased risk of both diabetes and cardiovascular disease. In addition to cardiovascular disease, individual components of the metabolic syndrome have been linked to the development of cancer, particularly to colorectal cancer. Colorectal cancer is an important public health problem; in the year 2000 there was an estimated total of 944 717 incident cases of colorectal cancer diagnosed world-wide. This association is sustained by many epidemiological studies. Recent reports suggest that individuals with metabolic syndrome have a higher risk of colon or rectal cancer. Moreover, the clusters of metabolic syndrome components increase the risk of associated cancer. The physiopathological mechanism that links metabolic syndrome and colorectal cancer is mostly related to abdominal obesity and insulin resistance. Population and experimental studies demonstrated that hyperinsulinemia, elevated C-peptide, elevated body mass index, high levels of insulin growth factor-1, low levels of insulin growth factor binding protein-3, high leptin levels and low adiponectin levels are all involved in carcinogenesis. Understanding the pathological mechanism that links metabolic syndrome and its components to carcinogenesis has a major clinical signifi cance and may have profound health benefi ts on a number of diseases including cancer, which represents a major cause of mortality and morbidity in our societies.

Visceral fat and insulin resistance as predictors of non-alcoholic steatohepatitis

AIM： To examine whether visceral fat is associated with non-alcoholic steatohepatitis （NASH）, to assess for parameters associated with visceral adiposity and to investigate for factors associated with fibrotic severity in NASH. METHODS： Thirty NASH and 30 control subjects underwent biochemical tests, anthropometric assessment, bioelectrical impedance, dual energy X-ray absorptiometry and abdominal fat study by CT scan. Liver biopsies were graded according to the Brunt criteria. RESULTS： NASH subjects had elevated blood pressure, body mass index, waist circumference and waist-to-hip ratio. A greater number of diabetes rnellitus, impaired glucose tolerance test and HOMA-IR 〉 3.5 were found in NASH patients. HOMA-IR 〉 2.8 （OR 20.98, 95% CI 3.22-136.62; P 〈 0.001） and visceral fat area 〉 158 cm^2 （OR 18.55, 95% CI 1.60-214.67; P = 0.019） were independent predictors for NASH. Advanced stage of NASH was found in 15 （50%） patients. HOMA-IR 〉 3.5 （OR 23.12, 95% CI 2.00-266.23; P = 0.012） and grading of portal inflammation （OR 7.15, 95% CI 1.63-31.20; P = 0.009） were determined as independent risk factors for advanced stage of NASH. CONCLUSION： Obesity （especially central obesity） and metabolic syndrome are common in Thai NASH. Insulin resistance and elevated visceral fat are risk factors for the presence of NASH. The advanced stage of thedisease is related to insulin resistance.

Association between Adiponectin and Metabolic Syndrome in Older Adults from Major Cities of China

Objective To investigate the association between adiponectin and metabolic syndrome （MetS） and related diseases in older adults from major cities of China. Methods A total of 2 049 adults at the age of 60-96 years from18 major cities of China were enrolled in the study. Plasma adiponectin and insulin concentrations were measured. Insulin resistance was assessed by homeostasis model assessment of insulin resistance （HOMA-IR）. The definitions proposed by International Diabetes Federation （IDF） and American Heart Association/National Heart, Lung, and Blood/nstitute （AHA/NLHBI） were used to identify MetS. Results The adiponectin concentration increased with the advance of age and was higher in women than in men. The sex specific adiponectin concentration was inversely correlated with body mass index （BMI）, waist circumference, diastolic blood pressure, triglycerides, glucose and fasting blood insulin, and positively correlated with HDL-C （P〈0.001）. The adiponectin concentration decreased with increasing MetS components. Compared with the 4th sex-specific adiponectin quartile, the odds ratio （OR） for prevalent MetS-IDF and MetS-AHA/NLHBI in subjects of the 1st quartile group was 3.25 （95% CI： 2.24, 4.71） and 3.21 （95% CI： 2.26, 4.55）, respectively. The association was independent of age, sex, life-style factors, medication, family history of chronic diseases, BMI, and HOMA-IR, The OR for MetS was much higher than those of MetS components and its related diseases. Conclusion Adiponectin is strongly associated with MetS independent of insulin resistance and obesity in older adults from major cities in China. The adiponectin concentration is a useful predictor for the risk of MetS.

Metabolic Syndrome and Perioperative Complications during Scheduled Surgeries with Spinal Anesthesia

Background: Metabolic syndrome (MS) is a constellation of factors associated with increased risk of developing cardiovascular diseases and Diabetes Mellitus. Despite of the many studies related to MS, little is known about its impact on scenarios such as surgical anesthesia. Objective: To examine the correlation between demographic and metabolic variables with the occurrence of perioperative complications in patients with MS undergoing scheduled surgeries using a spinal anesthesia technique in the surgery department at the University Clinic San Juan de Dios in Cartagena de Indias, Colombia. Methods: Observational, analytical, cross-sectional, single-center study of 150 subjects with MS and 150 control subjects. Perioperative complications, socio-demographic, hemodynamic and respiratory variables were registered. Groups were compared using t test, Fisher’s exact test or Chi-square, as appropriate. We applied a logistic multiple regression model, adjusted by backward stepwise at 0.25 and forward at 0.05, to find possible incompatible associations. p value < 0.05 was considered significant. Results: There were significant differences between groups in age, American Society of Anesthesiologists physical status classification, frequency of diseases associated to MS and perioperative complications. There were no cases of mortality among patients. There was statistically significant difference between the two groups for intraoperative hypotension and hypertension with p values of <0.0001 and 0.034. Among postoperative complications there was statistically significant difference in pain (13.3% vs 5.3% in patients without MS) and nausea and/or postoperative vomiting (8% vs 2% in patients without MS) with a p value of 0.027 and 0.015 (by Fisher) respectively. Conclusions: Metabolic abnormalities in MS are a risk factor for developing complications in the perioperative period of patients scheduled for surgeries using the subarachnoid anesthesia technique. Accordingly, it is appropriate to implement health intervention strategies by the surgical team, aiming at their prevention and management.

Metabolic syndrome and gastro-esophageal reflux:A link towards a growing interest in developed countries

The aim of this Editorial is to describe the growing possibility of a link between gastro-esophageal reflux disease (GERD) and metabolic syndrome on the light of recent epidemiological and pathophysiological evidence. The state of the art of GERD is described,based on recent definitions,pathophysiological evidence,epidemiology in developed countries,clinical subtypes together with a diagnostic approach specifically focussed on the appropriateness of endoscopy. Metabolic syndrome is accurately defined and the pivotal role of insulin resistance is emphasized. The strong relationship between GERD and metabolic syndrome has been pathophysiologically analyzed,taking into account the role of obesity,mechanical factors and metabolic changes. Data collected by our group regarding eating habits and GERD are briefly summarized at the end of a pathophysiological analysis. The literature on the subject strongly supports the possibility that lifestyle and eating habits may be involved in both GERD and metabolic syndrome in developed countries.

Evaluate the effects of metabolic syndrome in adolescents and children

The metabolic syndrome(MS)in adolescents and children can cause serious consequences that lead researchers to pay efforts to study in such area.Presently,MS definition is still not standardized.Different versions of MS definition have been used by numerous studies,which may be a problem to identify MS and then to predict and prevent clinical diseases.The pediatric literature shows that insulin resistance and obesity might be the key underlying pathophysiology of MS to cause many related diseases.High prevalence of MS is in overweight and obese children and adolescents.This article focuses on such above issues and also effects of MS on two main disease outcomes:cardiovascular disease and type 2 diabetes.

Metabolic syndrome in the development and progression of prostate cancer

Prostate cancer(PCa)is the most common noncutaneous malignancy and second leading cause of cancerspecific mortality for men in the United States.There is a wide spectrum of aggressiveness ranging from biologically significant to indolent disease,which has led to an interest in the identification of risk factors for its development and progression.Emerging evidence has suggested an association between metabolic syndrome(MetS)and PCa.MetS represents a cluster of metabolic derangements that confer an increased risk of cardiovascular disease and type 2 diabetes mellitus.Its individual components include obesity,dyslipidemias,high blood pressure,and high fasting glucose levels.Met S has become pervasive and is currently associated with a high socioeconomic cost in both industrialized and developing countries throughout the world.The relationship between MetS and PCa is complex and yet to be fully defined.A better understanding of this relationship will facilitate the development of novel therapeutic targets for the prevention of PCa and improvement of outcomes among diagnosed men in the future.In this review,we evaluate the current evidence on the role of MetS in the development and progression of PCa.We also discuss the clinical implications on the manage-ment of PCa and consider the future direction of this subject.

代谢综合征与阿尔茨海默病的相关性及机制研究进展

近期研究发现代谢综合征(MetS)患者有认知功能下降甚至向痴呆进展的趋势,而阿尔茨海默病(AD)是痴呆最重要的分型。本文回顾总结既往研究中MetS导致的认知功能障碍与AD发病的相关性,指出有较多证据支持MetS作为整体及其组分中的高血压、高血糖是AD的危险因素,而胰岛素抵抗、神经慢性炎症、脂肪因子紊乱等在发病过程中起到重要作用,因尚缺乏可有效延缓或逆转AD病理进展的治疗方案,期待以相对可治MetS为干预靶标,为早期防治AD综合策略的制订提供科学证据。

二甲双胍联合奥利司他治疗肥胖型多囊卵巢综合征伴胰岛素抵抗的临床效果

目的:研究肥胖型多囊卵巢综合征(polycystic ovary syndrome,PCOS)伴胰岛素抵抗患者采用二甲双胍联合奥利司他治疗的临床效果。方法:选择150例肥胖型PCOS伴胰岛素抵抗患者,随机分为对照组与研究组,每组各75例;对照组给予二甲双胍、炔雌醇环丙孕酮等基础治疗,研究组采用基础治疗联合奥利司他治疗;治疗3个月,比较两组人体测量学指标、糖脂代谢指标及性激素水平差异。结果:治疗3个月后,与对照组比较,研究组体重、体重指数、腰臀比、体脂率、空腹血糖、餐后2 h血糖、空腹胰岛素、糖化血红蛋白、稳态模型评估-IR(HOMA-IR)均明显降低(P<0.05);三酰甘油、总胆固醇、低密度脂蛋白胆固醇均明显降低(P<0.05),高密度脂蛋白胆固醇明显升高(P<0.05);黄体生成素(LH)、雌二醇、睾酮、泌乳素和LH/卵泡刺激素(FSH)明显降低(P<0.05),FSH比较差异无统计学意义(P>0.05)。结论:肥胖型PCOS伴胰岛素抵抗患者采用二甲双胍联合奥利司他治疗可更好地改善糖脂代谢,减轻体重及胰岛素抵抗,改善性激素紊乱。

肥胖型多囊卵巢综合征患者不孕的危险因素分析

目的探讨肥胖型多囊卵巢综合征(PCOS)患者不孕的危险因素,以提供更有效的治疗策略和预防措施。方法选取2020年3月—2023年3月在上饶市妇幼保健院就诊的126例PCOS伴不孕患者作为PCOS组,并选取同期在该院体检的健康志愿者102例作为对照组。通过调查问卷的形式收集两组一般临床资料,采用生育问题量表(FPI)评估不孕相关的压力水平,匹兹堡睡眠质量指数(PSQI)量表评估睡眠障碍,酶联免疫吸附试验(ELISA)检测血抑制素B(INHB)、抗苗勒氏管激素(AMH)水平,电化学发光法检测促卵泡激素(FSH)、黄体生成激素(LH)、孕酮、雌二醇(E_(2))、睾酮(T)、性激素结合球蛋白(SHBG),彩色多普勒超声仪计算两侧卵泡数量。采用多因素一般Logistic回归分析影响肥胖型PCOS不孕的危险因素。结果两组受试者一般资料比较,差异无统计学意义(P>0.05);两组受试者的体质量指数(BMI)、睡眠障碍、生育压力、两侧卵泡数量、INHB、AMH、FSH、LH、孕酮、E_(2)、T、SHBG水平比较,差异均有统计学意义(P<0.05)。多因素一般Logistic回归分析结果显示,BMI[OR=1.272(95%CI:1.153,1.402)]、睡眠障碍[OR=3.191(95%CI:2.045,4.978)]、生育压力[OR=1.021(95%CI:1.014,1.027)]、左侧卵巢泡数[OR=1.092(95%CI:1.006,1.186)]、右侧卵巢泡数[OR=1.160(95%CI:1.074,1.252)]、INHB[OR=1.007(95%CI:1.001,1.013)]、AMH[OR=1.138(95%CI:1.032,1.256)]、LH[OR=1.190(95%CI:1.115,1.271)]、T[OR=1.304(95%CI:1.173,1.450)]是肥胖型PCOS患者不孕的独立危险因素(P<0.05),FSH[OR=0.762(95%CI:0.670,0.867)]、孕酮[OR=0.624(95%CI:0.463,0.841)]、E_(2)[OR=0.994(95%CI:0.988,1.000)]、SHBG[OR=0.977(95%CI:0.956,0.999)]是肥胖型PCOS患者不孕的保护因素(P<0.05);模型的受试者工作特征曲线下面积为0.972(95%CI:0.951,0.993)、敏感性为96.8%(95%CI:0.913,0.991),特异性为94.3%(95%CI:0.813,0.971),拟合曲线显示回归模型拟合效果良好。结论肥胖型PCOS患者不孕的危险因素是BMI较高、睡眠障碍、生育压力大、两侧卵巢卵泡数增多、INHB、AMH、FSH、LH,而孕酮、E_(2)、SHBG为保护因素。

补肾涤痰汤治疗不同代谢状态多囊卵巢综合征模型小鼠疗效的实验研究

目的 分析补肾涤痰汤(BDD)对不同代谢状态多囊卵巢综合征(PCOS)模型小鼠的疗效。方法 分别采用高脂日粮(HFD)喂养或正常饲料喂养C57BL/6J小鼠,并同时经脱氢表雄酮(DHEA)注射建立肥胖或非肥胖的PCOS模型,肥胖与非肥胖PCOS模型各分为对照组、肥胖/非肥胖PCOS组、肥胖/非肥胖BDD组3组,共6组,肥胖/非肥胖BDD组皆使用BDD治疗,对照组使用等体积溶剂处理;检测小鼠血清空腹血糖(FBG)、胰岛素(INS)、雌二醇(E2)、睾酮(T)、促黄体生成素(LH)、促卵泡生成素(FSH)等指标,以及雌二醇受体1/2基因(Esr1/2)、小鼠卵巢骨形态发生蛋白15基因(Bmp15)、促黄体生成素受体基因(Lhcgr)、促卵泡生成素受体基因(Fshr)mRNA表达情况。结果 肥胖型PCOS模型小鼠经BDD治疗后,葡萄糖耐量实验值(GTT)、睾酮(T)、胰岛素(INS)及雌二醇受体1基因(Esr1)、Bmp15水平显著下降(P<0.05),E2水平显著上升(P<0.05);而非肥胖PCOS模型小鼠经BDD治疗后,LH、FSH、T水平显著上升(P<0.05),总胆固醇(TC)、Bmp15水平显著下降(P<0.05),呈现与BDD治疗肥胖型PCOS模型小鼠不同甚至相反的趋势。结论 从动情周期与卵巢结构水平看,BDD对肥胖与非肥胖型PCOS小鼠均有疗效,尽管激素水平出现不一样的调节趋势。