Proposal on the diagnosis and classification of polycystic ovary syndrome

In order to improve the treatment outcome and facilitate the clinical practice,a diagnostic classification of heterogeneous disease-polycystic ovary syndrome(PCOS)is proposed.PCOS is classified into 2 main types(Ⅰ,Ⅱ)and 4 subtypes(Ⅰa,Ⅰb,Ⅱa,Ⅱb):PCOSⅠrefers to cases with hyperandrogenemia derived from the ovary(Ⅰa)or from both the ovary and the adrenal cortex(Ⅰb).PCOS Ⅱ refers to cases with both hyperandrogenemia and hyperinsulinemia,while Ⅱb being severer than Ⅱa,like hyperthecosis.Better efficacy of integrative medicine treatment on this classification is mentioned.     

Role of insulin and insulin resistance in androgen excess disorders

Insulin has complex effects on cell growth, metabolism and differentiation, and these effects are mediated by a cell-surface bound receptor and eventually a cascade of intracellular signaling events. Among the several metabolic and growth-promoting effects of insulin, insulin resistance is defined as an attenuated effect of insulin on glucose metabolism, primarily the limited export of blood glucose into skeletal muscle and adipose tissue. On the other hand, not all the signaling pathways and insulin-responsive tissues are equally affected, and some effects other than the metabolic actions of insulin are overexpressed. Ovaries and the adrenal glands are two examples of tissues remaining sensitive to insulin actions where insulin may contribute to increased androgen secretion. Polycystic ovary syndrome (PCOS) is the most common form of androgen excess disorder (AED), and its pathogenesis is closely associated with insulin resistance. Patients with idiopathic hirsutism also exhibit insulin resistance, albeit lower than patients with PCOS. Although it is not as evident as in PCOS, patients with congenital adrenal hyperplasia may have insulin resistance, which may be further exacerbated with glucocorticoid overtreatment and obesity. Among patients with severe insulin resistance syndromes, irrespective of the type of disease, hyperinsulinemia promotes ovarian androgen synthesis independently of gonadotropins. It is highly debated in whom and how insulin resistance should be diagnosed and treated among patients with AEDs, including PCOS. It is not suitable to administer an insulin sensitizer relying on only some mathematical models used for estimating insulin resistance. Instead, the treatment decision should be based on the constellation of the signs, symptoms and presence of obesity; acanthosis nigricans; and some laboratory abnormalities such as impaired glucose tolerance and impaired fasting glucose.     

多囊卵巢综合征伴胰岛素抵抗患者肠道菌群分析

目的 基于16SrRNA高通量测序技术对多囊卵巢综合征(PCOS)伴胰岛素抵抗(IR)患者肠道菌群的结构特征进行分析.方法 选择2019年7月至2020年6月期间就诊于青岛大学附属烟台毓璜顶医院的新发PCOS女性,根据稳态模型胰岛素抵抗指数(HOMA-IR)分为IR-PCOS组(n=11)和NIR-PCOS组(n=10...     

胰岛素增敏剂治疗多囊卵巢综合征伴胰岛素抵抗临床疗效观察

目的　了解二甲双胍和阿卡波糖在多囊卵巢综合征 ( PCOS)伴高胰岛素( HI)血症和餐后高血糖 ( PHG)中的药理作用和临床疗效。　方法　 46例 PCOS-HI患者口服二甲双胍 1 2周 ,1 4例 PCOS-PHG患者应用阿卡波糖 1 2周 ,采用自身对照法观察各试验组治疗前、后临床症状、血生殖激素水平、血糖和胰岛素水平的变化。　结果　与治疗前比较 ,二甲双胍组中 3 4例 ( 74% )恢复排卵性月经 ,5例 ( 1 1 % )妊娠 ;血清游离睾酮( FT)水平下降 55% ,硫酸脱氢表雄酮 ( DHEAS)水平下降 51 % ,空腹胰岛素水平 ( FINS)下降 42 % ,胰岛素敏感指数 ( ISI)上升 52 % ,有显著性差异 ( P<0 .0 5)。阿卡波糖组中 1 2例 ( 86 % )恢复排卵 ,4例 ( 2 9% )妊娠 ;FT水平下降 50 % ,糖负荷后 2 h血糖降低 46 % ,空腹血糖和空腹胰岛素比值 ( FSG/FINS)升高 1倍 ,有显著性差异 ( P<0 .0 5)。　结论　二甲双胍能有效地改善 PCOS-HI患者胰岛素抵抗 ,降低血雄激素水平并恢复生育功能 ;阿卡波糖可缓解 PCOS-PHG患者的餐后高血糖     

多囊卵巢综合征青年患者血清脂联素、胰岛素抵抗关系的研究

目的探讨多囊卵巢综合征（PCOS）青年患者血清脂联素（APN）、抵抗素（RST）水平与胰岛素抵抗（1R）的关系。方法PCOS组为38例青年PCOS患者,对照组为27例健康女性,两组中根据体重指数（BMI）分为肥胖组BMI（≥25kg／m^2）和非肥胖组（BMI〈25kg／m^2）。在月经第3～5天晨（PCOS闭经者B超检查无优势卵泡当天）留空腹血。采用酶联免疫吸附法（ELISA）测定血清APN和RST浓度,葡萄糖氧化酶法测定血糖浓度,化学发光法测定胰岛素浓度,根据后两者计算胰岛素敏感指数（ISI）。结果（1）肥胖组与非肥胖组空腹血糖水平比较,差异无统计学意义（P〉0．05）;（2）肥胖组与非肥胖组中,PCOS组的空腹胰岛素水平分别显著高于对照组（P〈0．05）;（3）肥胖组中,PCOS组血清APN和ISI水平显著低于对照组,血清RST水平显著高于对照组（P〈0．05）;（4）非肥胖组中,PCOS组血清APN和ISI水平显著低于对照组,血清RST水平显著高于对照组（P〈0．05）。结论（1）与对照组相比,青年PCOS患者血清中APN水平较低,RST水平较高,其中PCOS肥胖患者尤为明显。（2）青年PCOS患者血清中APN水平的下降和RST水平的升高可能与胰岛素敏感性及IR相关。     

PCOS高雄激素血症患者降调节后行冻融胚胎移植的临床结局观察

目的探讨降调节对多囊卵巢综合征(PCOS)高雄激素血症患者冻融胚胎移植(FET)周期临床结局的影响。方法回顾性分析2012年1月至2016年4月在我院不孕不育科行FET的PCOS高雄激素血症患者139例的临床资料,根据内膜准备方案不同分为常规雌孕激素替代组(HRT组,n=76)和降调节雌孕激素替代组(降调节HRT组,n=63),观察两组患者雌激素使用时间和剂量、子宫内膜厚度及分型、血清激素水平及临床妊娠结局等。结果两组患者的胚胎移植(ET)日子宫内膜厚度、移植胚胎数、优质胚胎率、早期流产率、异位妊娠率比较均无显著性差异(P0.05);降调节HRT组补佳乐使用时间[(13.67±1.91)d]及总剂量[(81.55±10.80)mg]显著小于HRT组[分别为(15.28±2.47)d和(94.25±14.17)mg](P0.01);降调节HRT组的ET日A型内膜占比(77.78%)、临床妊娠率(69.84%)及胚胎种植率(47.29%)均显著高于HRT组(分别为57.89%、51.31%、32.47%)(P0.05)。结论对于PCOS高雄激素血症患者,降调节后雌孕激素替代法准备内膜可以减少雌激素使用时间及用量,改善子宫内膜分型,有效提高胚胎种植率和临床妊娠率。     

罗格列酮治疗多囊卵巢综合征对改善内分泌、代谢及排卵功能的疗效

目的　探讨罗格列酮 (Rosiglitazone)对多囊卵巢综合征 (PCOS)合并胰岛素抵抗患者内分泌、代谢及排卵功能的影响。　方法　 2 5例PCOS合并胰岛素抵抗患者于自然月经或撤退性出血第 5天服用罗格列酮 12周 ,观察治疗前后血清生殖激素、胰岛素、血糖、血脂水平及排卵功能的变化。　结果　治疗后 ,患者各时相胰岛素 (INS)水平显著下降 (P <0 .0 1)。高密度脂蛋白胆固醇 (HDL C)显著升高 (P <0 .0 1) ,低密度脂蛋白胆固醇 (LDL C)显著降低 (P <0 .0 5 )。患者血清黄体生成素(LH)、黄体生成素 /促卵泡生成素比值 (LH/FSH)、睾酮 (T)和雄烯二酮 (A)水平均显著下降 (P <0 .0 1) ;性激素结合蛋白 (SHBG)水平显著升高 (P <0 .0 1) ;治疗后克罗米酚促排卵成功率为 72 % ,明显高于治疗前 2 0 % (P <0 .0 1)。　结论　罗格列酮通过改善胰岛素抵抗 ,降低胰岛素水平 ,使PCOS患者异常的血激素、血脂及排卵功能得到明显改善。     

Endocrine and metabolic effects of metformin in combination with compound cyproterone acetate in women with polycystic ovarian syndrome

<正> Objective:To study the endocrinologic and metabolic effects of metformin in combi-nation with compound cyproterone acetate (CPA) on patients with polycystic ovariansyndrome (PCOS).Methods:A prospective study involved total 65 patients,45 PCOS patients as group Aand 20 non-PCOS infertility patients as control (group B).Complete baseline work-up inclu-ding body mass index (BMI),waist/hip ratio(WHR),Ferriman-Gallwey score(FGS),gona-dotrophin,testosterone(T),sex hormone-binding globulin (SHBG),dehydroepiandrosteronesulfate (DHEAS),and fasting lipid,glucose (FG),insulin (FI) and oral glucose tolerancetest (OGTT),were performed in all patients.Patients in group A were treated with CPA a-lone (group Al),metformin alone (group A2) or combination of CPA with metformin (groupA3),respectively by randomization.At the end of the 12-week therapy,subjects were re-evaluated and above parameters were measured.Results:Women in group A had significant increases in BMI,WHR,FGS,LH,T,FI,insulin resistance (IR),triglycerides(TG),and significant decrease in HDL-C com-paring with the control group (P<0.01).No significant difference among A1,A2 andA3 were found at baseline.LH,T,FT (free testosterone) were significant decreasedfrom (13.9±5.9)IU/L,(2.1±0.8)nmol/L and (2.84±2.3)nmol/L respectively to(5.8±2.2)IU/L,(1.2±0.4)nmol/L and (0.8±0.5)nmol/L respectively and SHBGwas significant increased from (99±42) nmol/L to (187±64) nmol/L in group A3,when compared with LH,T and FT from (13.8±7.6)IU/L,(2.2±1.1) nmol/L and(2.5±1.9) nmol/L respectively to (11.8±6.5)IU/L,(1.8±0.8) nmol/L and (1.7±1.0) nmol/L respectively and SHBG from (99±40) nmol/L to (120±51) nmol/L ingroup A2 (P<0.05,P<0.001).HDL-C was significant increased from (1.5±0.3)mmol/L to (1.8±0.3) mmol/L in group A3 comparing with HDL-C from (1.5±0.4)mmol/L to (1.6±0.4) mmol/L in groupAl(P<0.001).Conclusions.The PCOS patients treated with metformin in combination with compoundcyproterone acetate may be more effective in inhibiting hyperandrogen and hypersecretion ofLH than metfromin alone and more obvious in improving lipid profiles than CPA alone.     

Markers of insulin resistance in Polycystic ovary syndrome women: An update

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders, affecting 5%-10% of women of reproductive age. The importance of this syndrome lies in the magnitude of associated comorbidities: infertility, metabolic dysfunction, cardiovascular disease (CVD), plus psychological and oncological complications. Insulin resistance (IR) is a prominent feature of PCOS with a prevalence of 35%-80%. Without adequate management, IR with compensatory hyperinsulinemia contributes directly to reproductive dysfunction in women with PCOS. Furthermore, epidemiological data shows compelling evidence that PCOS is associated with an increased risk of impaired glucose tolerance, gestational diabetes mellitus and type 2 diabetes. In addition, metabolic dysfunction leads to a risk for CVD that increases with aging in women with PCOS. Indeed, the severity of IR in women with PCOS is associated with the amount of abdominal obesity, even in lean women with PCOS. Given these drastic implications, it is important to diagnose and treat insulin resistance as early as possible. Many markers have been proposed. However, quantitative assessment of IR in clinical practice remains a major challenge. The gold standard method for assessing insulin sensitivity is the hyperinsulinemic euglycemic glucose clamp. However, it is not used routinely because of the complexity of its procedure. Consequently, there has been an urgent need for surrogate markers of IR that are more applicable in large population-based epidemiological investigations. Despite this, many of them are either difficult to apply in routine clinical practice or useless for women with PCOS. Considering this difficulty, there is still a need for an accurate marker for easy, early detection and assessment of IR in women with PCOS. This review highlights markers of IR already used in women with PCOS, including new markers recently reported in literature, and it establishes a new classification for these markers.     

血清lncRNA MEG3的表达与多囊卵巢综合征患者胰岛素抵抗的关系

目的 探讨长链非编码RNA(lncRNA)人类母系表达基因3(MEG3)的表达与多囊卵巢综合征(PCOS)患者胰岛素抵抗(IR)的关系.方法 选取2018年7月至2020年8月本院收治的123例PCOS患者为研究对象进行前瞻性分析,根据胰岛素抵抗指数(HOMA-IR)水平分为IR组(n=54)和非IR组(n=69),另...     

Review article: The role of adipose tissue in uraemia-related insulin resistance

Adipose tissue is no longer considered to be an inert tissue of which function is to store fat. It actively secretes a number of biologic active compounds that are involved in the regulation of many processes like food intake, energy expenditure, metabolism homeostasis, immunity and blood pressure homeostasis. General metabolism alteration in patients with chronic kidney disease has a profound impact on biology of adipocytes. Chronic renal failure is a pathological condition, of which two major hallmarks are chronic inflammation and insulin resistance. In uraemic patients, adipose tissue became an important source of molecules that are responsible, at least in part, for the metabolic disturbances seen in these patients. Some of these molecules act as pro-inflammatory agents contributing to the maintenance and enhancement of the chronic inflammatory response. These pro-inflammatory molecules, along with other molecules secreted by the adipose tissue, have a central position in the aetiology of uraemia-associated insulin resistance. In this review, we intend to summarize some aspects of the biology of adipokines in uraemia, with emphasis on the link between these molecules and insulin resistance.     

CCNG2 and CDK4 is associated with insulin resistance in adipose tissue

BackgroundThe involvement of cyclin G2 (CCNG2) and cyclin-dependent kinase-4 (CDK4), cell cycle regulatory proteins, in adipose tissue metabolism and insulin resistance is still unknown. The objective of this study was to analyze CCNG2 and CDK4 levels in visceral (VAT) and subcutaneous adipose tissue (SAT) from nonobese and morbidly obese patients and their relationship with insulin resistance.MethodsWe studied the mRNA and protein levels of CCNG2 and CDK4 in VAT and SAT from 12 nonobese and 23 morbidly obese patients (11 with low [MO-L-IR] and 12 with high insulin resistance [MO-H-IR]).ResultsThe nonobese patients had a significantly greater CCNG2 expression in VAT (P = .004) and SAT (P<.001) than the MO-L-IR and MO-H-IR patients. The MO-H-IR patients had a significantly lower CDK4 expression in VAT than the MO-L-IR (P = .026), but similar to the nonobese patients. CDK4 and CCNG2 expression correlated significantly in VAT (r = 0.511, P<.001) and SAT (r = .535, P = .001). In different multiple regression analysis models, CCNG2 and CDK4 expression in VAT was mainly predicted by glucose (P = .047 and P = .008, respectively), and CCNG2 expression in SAT was mainly predicted by body mass index (P = .041). No significant associations were found with CDK4 expression in SAT. Moreover, VAT CCNG2 expression was the main determinant of the improvement in the homeostasis model assessment of insulin resistance index at 3 months after bariatric surgery (B = -271.7, P = .026).ConclusionOur data show for the first time that the human CCNG2 and CDK4 expression of VAT are inversely associated with glucose and insulin resistance.     

Heat shock protein 60 as a mediator of adipose tissue inflammation and insulin resistance

The stress protein heat shock protein 60 (Hsp60) induces secretion of proinflammatory mediators from murine adipocytes. This study aimed to study Hsp60 as a mediator of adipose tissue inflammation and skeletal muscle cell (SkMC) insulin sensitivity and to quantify plasma Hsp60 concentrations in lean and obese individuals. Regulation of Hsp60 release and Hsp60-induced cytokine secretion and signaling was measured in human adipocytes and SkMCs. Adipocytes exhibited higher Hsp60 release than preadipocytes and SkMCs, which was further stimulated by cytokines and Toll-like receptor (TLR)-4 activation. Hsp60 activated extracellular signal-related kinase (ERK)-1/2, Jun NH(2)-terminal kinase (JNK), p38, nuclear factor (NF)-κB, and impaired insulin-stimulated Akt phosphorylation in adipocytes. Furthermore, Hsp60 stimulated adipocytes to secrete tumor necrosis factor-α, interleukin (IL)-6, and IL-8. In SkMCs, Hsp60 activated ERK1/2, JNK, and NF-κB and inhibits insulin signaling and insulin-stimulated glucose uptake. SkMCs released IL-6, IL-8, and monocyte chemoattractant protein-1 on Hsp60 stimulation. Plasma Hsp60 was higher in obese males than in lean males and correlated positively with BMI, blood pressure, leptin, and homeostasis model assessment-insulin resistance. In summary, Hsp60 is released by human adipocytes, increased in plasma of obese humans, and induces insulin resistance. This is accompanied by activation of proinflammatory signaling in human adipocytes and SkMCs. Thus, Hsp60 might be a factor underlying adipose tissue inflammation and obesity-associated metabolic disorders.     

PCOS患者抗苗勒管激素水平与胰岛素抵抗及生殖激素水平的相关性研究

目的探讨多囊卵巢综合征(PCOS)患者血清抗苗勒管激素(AMH)水平与胰岛素抵抗(IR)及生殖激素水平的相关性。方法选取2017年1月至2020年2月在东莞东华医院生殖医学科就诊的PCOS患者62例,根据患者是否存在胰岛素抵抗,分为胰岛素抵抗组(HOMA-IR>2.1,PCOS-IR组,34例)和非胰岛素抵抗组(HOMA-IR<2.1,PCOS-NIR组,28例);选择同时期在同院行健康体检的30例正常女性为对照组。测定所有研究对象的血清生殖激素(AMH、FSH、LH、E2、T、PRL、P)水平,以及硫酸脱氢表雄酮(DHEA)、性激素结合球蛋白(SHBG)及空腹血糖(GLU)空腹胰岛素(FIN)水平等指标,统计分析组间各指标的差异;采用Spearman相关分析分析AMH水平与稳态模型胰岛素抵抗指数(HOMA-IR)的关系。结果3组间平均年龄、体重指数(BMI)及血清FSH、P、PRL、SHBG及DHEA水平均无统计学差异(P>0.05)。与对照组比较,PCOS组(包括PCOS-IR组和PCOS-NIR组)血清AMH、LH及T水平显著升高(P<0.05);与PCOS-NIR组比较,PCOS-IR组FIN[(20.31±12.71)mU/L vs.(5.69±1.98)mU/L]、GLU[(5.58±1.98)mmol/L vs.(4.89±1.98)mmol/L]和HOMA-IR[3.7(2.42,7.09)vs.1.28(0.84,1.63)]显著升高(P<0.05)。相关性分析结果显示,PCOS患者AMH水平与LH水平(r=0.403,P=0.001)及T水平(r=0.403,P=0.000)呈正相关,与FSH水平呈负相关(r=-0.253.P=0.044),而与年龄、BMI、E 2、P、PRL、FIN、GLU、SHBG、DHEA及HOMA-IR不存在显著相关(P>0.05)。结论PCOS患者血清AMH水平高于正常女性,其原因与高雄激素密切相关;PCOS患者血清AMH水平与胰岛素抵抗无相关性。     

多囊卵巢综合征合并妊娠期糖尿病患者铁代谢与胰岛素抵抗的关系

目的分析多囊卵巢综合征(polycystic ovary syndrome,PCOS)合并妊娠期糖尿病(gestational diabetes mellitus,GDM)患者铁代谢改变及与胰岛素抵抗(insulin resistance,IR)的关系。方法选择2017年1月至2018年2月在烟台毓璜顶医院常规产检,妊娠24~28周的孕妇为筛查对象。确诊为GDM的孕妇60例为GDM组,既往诊断为PCOS且合并GDM的孕妇60例为多囊卵巢合并妊娠期糖尿病(polycystic ovary syndrome with gestational diabetes mellitus,PGDM)组,同时按年龄段进行1∶1∶1匹配,选择正常孕妇60例为正常对照(NC)组。检测3组患者血糖、胰岛素、血红蛋白(Hb)、铁代谢(血清铁、铁蛋白、转铁蛋白饱和度)水平,并评估患者氧化应激损伤及炎症水平的改变,利用多元线性回归法分析铁代谢指标与炎症指标及IR的关系。结果与NC组相比,PGDM组Hb水平降低,铁蛋白(SF)、转铁蛋白饱和度(TS)升高(F=3.55、8.24、5.10,均P<0.05);丙二醛(MDA)水平升高,超氧化物歧化酶(SOD)水平降低(F=11.11、7.24,均P<0.01);肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)水平升高(F=4.02、19.06,均P<0.05);与GDM组相比,PGDM组Hb水平降低,SF、TS升高,HOMA-IR、MDA、TNF-α、IL-6水平均升高(均P<0.05)。MDA、TNF-α、IL-6与SF呈正相关(r=0.42、0.43、0.56,均P<0.05),与TS呈正相关(r=0.61、0.42、0.52,均P<0.01);SF、TS与胰岛素抵抗指数呈正相关(r=0.39、0.41,均P<0.01)。结论PGDM患者铁沉积状况导致机体氧化应激损伤程度升高,炎症反应增加,从而加重了IR程度。铁代谢紊乱可能与PGDM患者血糖升高机制有关。     

Effects of pioglitazone on adipose tissue remodeling within the setting of obesity and insulin resistance

Obesity and dysfunctional energy partitioning can lead to the development of insulin resistance and type 2 diabetes. The antidiabetic thiazolidinediones shift the energy balance toward storage, leading to an increase in whole-body adiposity. These studies examine the effects of pioglitazone (Pio) on adipose tissue physiology, accumulation, and distribution in female Zucker (fa/fa) rats. Pio treatment (up to 28 days) decreased the insulin-resistant and hyperlipidemic states and increased food consumption and whole-body adiposity. Magnetic resonance imaging (MRI) analysis and weights of fat pads demonstrated that the increase in adiposity was not only limited to the major fat depots but also to fat deposition throughout the body. Adipocyte sizing profiles, fat pad histology, and DNA content show that Pio treatment increased the number of small adipocytes because of both the appearance of new adipocytes and the shrinkage and/or disappearance of existing mature adipocytes. The remodeling was time dependent, with new small adipocytes appearing in clusters throughout the fat pad, and accompanied by a three- to fourfold increase in citrate synthase and fatty acid synthase activity. The appearance of new fat cells and the increase in fat mass were depot specific, with a rank order of responsiveness of ovarian > retroperitoneal > subcutaneous. This differential depot effect resulted in a redistribution of the fat mass in the abdominal region such that there was an increase in the visceral:subcutaneous ratio, as confirmed by MRI analysis. Although the increased adiposity is paradoxical to an improvement in insulin sensitivity, the quantitative increase of adipose mass should be viewed in context of the qualitative changes in adipose tissue, including the remodeling of adipocytes to a smaller size with higher lipid storage potential. This shift in energy balance is likely to result in lower circulating free fatty acid levels, ultimately improving insulin sensitivity and the metabolic state.     

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.     

Visceral and subcutaneous adipose tissue,which one induced thyroid dysfunction in patients with morbid obesity

BackgroundThyroid dysfunction in patients with morbid obesity usually resolves after bariatric surgery. However, the role of diverse types of adipose tissue in the process remains unknown.ObjectivesWe aim to investigate the effects of visceral and subcutaneous fat on thyroid function in a Chinese population with morbid obesity who underwent sleeve gastrectomy (SG).SettingUniversity hospital, Shanghai, ChinaMethodsRepeated measurement data of thyroid hormone and body fat were collected at 0, 3, 6, 12, 24, and 36 months after sleeve gastrectomy. Dual-energy X-ray absorptiometer and quantitative computerized tomography (CT) were used to compute visceral fat and subcutaneous fat. Repeated measures correlation (rmmcorr) package was employed for correlation analysis with generalized additive mixed model (GAMM) determining the independent factors.ResultsThyroid stimulating-hormone (TSH) showed notable decrease at 36 months after surgery, coupled with reduction of BMI (38.08 kg/cm² versus 24.28 kg/cm²), C-reactive protein (CRP), visceral adipose tissue (786.74 cm² versus 367.44 cm²), body fat rate, and waistline (118.13 cm versus 100.87 cm). Only visceral fat, diabetes, and CRP proved to be independent variables for TSH decline, without correlation with subcutaneous fat.ConclusionThe present study is first to report the effects of different types of body fat on thyroid function in a Chinese population with morbid obesity, revealing that loss of visceral fat is the key to improving endocrine and metabolic activity after bariatric surgery.