<b><span style="font-family:Verdana;">Aims:</span></b><span style="font-family:Verdana;"> Obesity is the major contributor of the metabolic syndrome (MetS), but a uniq...<b><span style="font-family:Verdana;">Aims:</span></b><span style="font-family:Verdana;"> Obesity is the major contributor of the metabolic syndrome (MetS), but a unique phenotype of obesity known as metabolically healthy obese (MHO) shows healthier metabolic profile</span><span style="font-family:Verdana;">;</span><span style="font-family:Verdana;"> however understanding of their biochemical correlates is poorly understood. Obesity is defined by Body mass index (BMI), but controversy exists regarding ethnic-specific BMI cut-offs. The present study used the Asian Indian BMI cut</span><span style="font-family:Verdana;">-</span><span style="font-family:;" "=""><span style="font-family:Verdana;">offs to assess relationships of MHO phenotypes with oxidative stress (OS) and inflammation. </span><b><span style="font-family:Verdana;">Methods: </span></b><span style="font-family:Verdana;">In this case-control study, 299 metabolically-healthy (MH) respondents were divided into four groups as per Asian criteria for obesity: MH non-obese </span><span style="font-family:Verdana;">(MHNO), MH overweight</span></span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">(MHOW), MHO and MH severely obese (MHSO</span><span style="font-family:;" "=""><span style="font-family:Verdana;">). Their oxidative stress and pro-inflammatory markers were measured. </span><b><span style="font-family:Verdana;">Results: </span></b><span style="font-family:Verdana;">Levels of hydroxyl radicals (</span></span><span style="font-family:Verdana;">·</span><span style="font-family:Verdana;">OH), fluorescent oxidation products (FLOP), MDA, PCO and inflammatory markers CRP, TNF-</span><span style="font-family:Verdana;"><i></i></span><i><i><span style="font-family:Verdana;">α</span></i><i><span style="font-family:Verdana;"></span></i></i><span style="font-family:Verdana;">, IL-6</span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">were highest in MHSO phenotype followed by the MHO,</span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">MHOW</span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">and MHNO groups (p > 0.0001), whereas antioxidant markers, CuZn-SOD, catalase, glutathione peroxidase and total antioxidant activity followed the reverse trend. The MHNO and MHOW groups showed significant difference with regard to (</span><span style="font-family:Verdana;">·</span><span style="font-family:Verdana;">OH) radicals and FLOP. Moreover, </span><span style="font-family:Verdana;">·</span><span style="font-family:;" "=""><span style="font-family:Verdana;">OH radicals, FLOP and inflammatory markers were significantly correlated to BMI in MHSO and MHO but not in MHNO and MHOW group. </span><b><span style="font-family:Verdana;">Conclusion: </span></b><span style="font-family:Verdana;">The MHO and MHSO phenotype display differences in terms of OS and inflammatory markers at lower BMI cut</span></span><span style="font-family:Verdana;">-</span><span style="font-family:Verdana;">offs, indicating that they may be on the way to becoming </span><span style="font-family:Verdana;">“</span><span style="font-family:Verdana;">unhealthy</span><span style="font-family:Verdana;">”</span><span style="font-family:;" "=""><span style="font-family:Verdana;"> ob</span><span style="font-family:Verdana;">ese. The lower BMI cut-offs proposed by Indian Consensus Group would help</span><span style="font-family:Verdana;"> in understanding of manifestation of metabolic syndrome.</span></span>展开更多
Metabolically healthy obese(MHO)individuals are reported to have a lower risk of developing cardiovascular diseases in comparison with individuals with metabolic syndrome.However,the association between MHO and type 2...Metabolically healthy obese(MHO)individuals are reported to have a lower risk of developing cardiovascular diseases in comparison with individuals with metabolic syndrome.However,the association between MHO and type 2 diabetes(T2DM)is still controversial.Some studies indicated that MHO is a favorable phenotype for T2DM,but more studies showed that MHO individuals have an increased risk of developing T2DM compared with metabolically healthy normalweight individuals,especially among those who would acquire metabolically unhealthy obesity.This has been supported by finding insulin resistance and lowgrade inflammatory responses in MHO individuals with a tendency for impaired beta-cell dysfunction.Studies also showed that liver fat accumulation increased the risk of incidence of T2DM in MHO.Here,we reviewed current literature on the relationship between MHO and T2DM,discussed the determinants for the development of diabetes in MHO,and summarized the measures for the prevention of T2DM in MHO.展开更多
Objective:To investigate the prevalence of metabolically healthy obesity(MHO)and its relationship with incidence of metabolic syndrome(MetS),type 2diabetes mellitus(T2DM)and hypertension in individuals in the city of ...Objective:To investigate the prevalence of metabolically healthy obesity(MHO)and its relationship with incidence of metabolic syndrome(MetS),type 2diabetes mellitus(T2DM)and hypertension in individuals in the city of Yulin.Methods:We studied 1,666 participants,aged over18years at baseline,with free of components of the MetS except waist criteria.Participants were divided into three groups based on body mass index(Ibm):lean/normal weight(Ibm<23kg/m2),overweight(Ibm,23-24.9kg/m2),obesity(Ibm≥25 kg/m2).The cumulative incidence of MetS,T2DM and hypertension over 5.21years among groups was assessed.Results:The prevalence of MHO was 19.5%in the baseline population.During an average 5.21year follow-up,the cumulative incidence of MetS,T2DM and hypertension in1,666participants were 16.4%,19.1%and 3.9%,respectively.The obesity group had a significantly higher cumulative incidence of MetS(16.4%vs.3.2%,P<0.001),hypertension(19.1%vs.3.7%,P<0.001),and T2DM(3.9%vs.1.6%,P<0.001)compared to the lean/normal weight group.Each kg/m2 of Ibm carried increased risk for T2DM(19%),hypertension(11%)and MetS(13%).Conclusion:Metabolically healthy obesity individuals confer increased risk for hypertension,T2DM and the MetS than their non-obese counterparts.展开更多
Obesity plays relevant pathophysiological role in the development of health problems, arising as result of complex interaction of genetic, nutritional, and metabolic factors. Due to the role of adipose tissue in lipid...Obesity plays relevant pathophysiological role in the development of health problems, arising as result of complex interaction of genetic, nutritional, and metabolic factors. Due to the role of adipose tissue in lipid and glucose metabolism, and low grade inflammation, it is necessary to classify obesity on the basis of body fat composition and distribution, rather than the simply increase of body weight, and the Body Mass Index. The new term of adiposopathy(‘‘sick fat'') clearly defines the pathogenic role of adipose tissue. Four phenotypes of obese individuals have been described:(1) normal weight obese(NWO);(2) metabolically obese normal weight;(3) metabolically healthy obese; and(4) metabolically unhealthy obese or "at risk" obese. Moreover, sarcopenic obesity has been related to all the phenotypes. The category of normal weight lean, represented by metabolically healthy normal weight has been classified to distinguish from NWO. It is crucial to recommend a bariatric surgery taking into account adiposopathy and sick fat that occurs with the expansion of fat mass, changing the inflammatory and metabolic profile of the patient. Body fat percentage and genetic polymorphism have to be evaluated to personalize the best bariatric surgery intervention.展开更多
The growing obesity epidemic is becoming a major public health concern,and the associated costs represent a considerable burden on societies.Among the most common complications of severe obesity are the development of...The growing obesity epidemic is becoming a major public health concern,and the associated costs represent a considerable burden on societies.Among the most common complications of severe obesity are the development of hypertension,dyslipidemia,type 2 diabetes,cardiovascular disease,and various types of cancer.Interestingly,some obese individuals have a favorable metabolic profile and appear to be somehow protected from the detrimental effects of excessive adipose tissue accumulation.These individuals remain normoglycemic,insulin sensitive,and hypotensive with proper blood lipid levels,despite their high body mass index and/or waist circumference.Multiple independent observations have led to the concept of the metabolically healthy obese(MHO) phenotype,yet no consensus has been reached to date regarding a universal definition or the main mechanism behind this phenomenon.Recent technological advances and the use of high-throughput analysis techniques have revolutionized different areas of biomedical research.A multi-omics approach,which is used to investigate changes at different molecular levels in an organism or tissue,may provide valuable insights into the interplay between the molecules or pathways and the roles of different factors involved in the mechanisms underlying metabolic health deterioration.The aim of this review is to present the current status regarding the use of omics technologies to investigate the MHO phenotype,as well as the results of targeted analyses conducted in MHO individuals.展开更多
Metabolically healthy obesity refers to obese individuals who do not develop metabolic disorders.These people store fat in subcutaneous adipose tissue(SAT)rather than in visceral adipose tissue(VAT).However,the molecu...Metabolically healthy obesity refers to obese individuals who do not develop metabolic disorders.These people store fat in subcutaneous adipose tissue(SAT)rather than in visceral adipose tissue(VAT).However,the molecules participating in this specific scenario remain elusive.Rab18,a lipid droplet(LD)-associated protein,mediates the contact between the endoplasmic reticulum(ER)and LDs to facilitate LD growth and maturation.In the present study,we show that the protein level of Rab18 is specifically upregulated in the SAT of obese people and mice.Rab18 adipocyte-specific knockout(Rab18 AKO)mice had a decreased volume ratio of SAT to VAT compared with wildtype mice.When subjected to high-fat diet(HFD),Rab18 AKO mice had increased ER stress and inflammation,reduced adiponectin,and decreased triacylglycerol(TAG)accumulation in SAT.In contrast,TAG accumulation in VAT,brown adipose tissue(BAT)or liver of Rab18AKO mice had a moderate increase without ER stress stimulation.Rab18 AKO mice developed insulin resistance and systematic inflammation.Rab18 AKO mice maintained body temperature in response to acute and chronic cold induction with a thermogenic SAT,similar to the counterpart mice.Furthermore,Rab18-deficient 3T3-L1 adipocytes were more prone to palmitate-induced ER stress,indicating the involvement of Rab18 in alleviating lipid toxicity.Rab18 AKO mice provide a good animal model to investigate metabolic disorders such as impaired SAT.In conclusion,our studies reveal that Rab18 is a key and specific regulator that maintains the proper functions of SAT by alleviating lipid-induced ER stress.展开更多
目的初步探讨代谢正常肥胖(MHO)人群中脂联素(APN)分子构成的变化及临床意义,分析MHO人群代谢正常的原因,并探讨其与MHO的相关性。方法根据纳入标准选取成年人161例,分为MHO组(n=52)、肥胖伴代谢综合征(MS)组(n=52)、正常对照组(n=57)...目的初步探讨代谢正常肥胖(MHO)人群中脂联素(APN)分子构成的变化及临床意义,分析MHO人群代谢正常的原因,并探讨其与MHO的相关性。方法根据纳入标准选取成年人161例,分为MHO组(n=52)、肥胖伴代谢综合征(MS)组(n=52)、正常对照组(n=57)。采用酶联免疫吸附法(ELISA)测定患者血清总APN、高分子量脂联素(HMW-adp)浓度,并分析其分子构成在MHO人群中的变化及相关临床意义。结果 (1)与正常对照组相比,肥胖伴MS组及MHO组血清总APN、HMW-adp均明显降低(P<0.01);(2)MHO组总APN、HMW-adp较肥胖伴MS组明显升高(P<0.01);(3)MHO组HMW-adp/总APN(H/A)较肥胖伴MS组及正常对照组均升高(P<0.05);(4)多元逐步回归分析显示体质指数(BMI)、腰围、餐后2 h血糖(2 hP BG)是总APN的重要危险因素,腰围、2 hP BG是HMW-adp的负性预测因子,而高密度脂蛋白胆固醇(HDL-C)是其唯一的阳性预测因子,而H/A的主要影响因素却是BMI、腰围、HDL-C。结论 APN分子构成在MHO人群中呈高水平状态,该人群代谢之所以正常可能与这两种因子的保护作用有关,尤其HMW-adp。由此可以认为血清总APN、HMW-adp的检测可作为定量检测MHO人群及其转归以及判断预后的指标。展开更多
文摘<b><span style="font-family:Verdana;">Aims:</span></b><span style="font-family:Verdana;"> Obesity is the major contributor of the metabolic syndrome (MetS), but a unique phenotype of obesity known as metabolically healthy obese (MHO) shows healthier metabolic profile</span><span style="font-family:Verdana;">;</span><span style="font-family:Verdana;"> however understanding of their biochemical correlates is poorly understood. Obesity is defined by Body mass index (BMI), but controversy exists regarding ethnic-specific BMI cut-offs. The present study used the Asian Indian BMI cut</span><span style="font-family:Verdana;">-</span><span style="font-family:;" "=""><span style="font-family:Verdana;">offs to assess relationships of MHO phenotypes with oxidative stress (OS) and inflammation. </span><b><span style="font-family:Verdana;">Methods: </span></b><span style="font-family:Verdana;">In this case-control study, 299 metabolically-healthy (MH) respondents were divided into four groups as per Asian criteria for obesity: MH non-obese </span><span style="font-family:Verdana;">(MHNO), MH overweight</span></span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">(MHOW), MHO and MH severely obese (MHSO</span><span style="font-family:;" "=""><span style="font-family:Verdana;">). Their oxidative stress and pro-inflammatory markers were measured. </span><b><span style="font-family:Verdana;">Results: </span></b><span style="font-family:Verdana;">Levels of hydroxyl radicals (</span></span><span style="font-family:Verdana;">·</span><span style="font-family:Verdana;">OH), fluorescent oxidation products (FLOP), MDA, PCO and inflammatory markers CRP, TNF-</span><span style="font-family:Verdana;"><i></i></span><i><i><span style="font-family:Verdana;">α</span></i><i><span style="font-family:Verdana;"></span></i></i><span style="font-family:Verdana;">, IL-6</span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">were highest in MHSO phenotype followed by the MHO,</span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">MHOW</span><span style="font-family:;" "=""> </span><span style="font-family:Verdana;">and MHNO groups (p > 0.0001), whereas antioxidant markers, CuZn-SOD, catalase, glutathione peroxidase and total antioxidant activity followed the reverse trend. The MHNO and MHOW groups showed significant difference with regard to (</span><span style="font-family:Verdana;">·</span><span style="font-family:Verdana;">OH) radicals and FLOP. Moreover, </span><span style="font-family:Verdana;">·</span><span style="font-family:;" "=""><span style="font-family:Verdana;">OH radicals, FLOP and inflammatory markers were significantly correlated to BMI in MHSO and MHO but not in MHNO and MHOW group. </span><b><span style="font-family:Verdana;">Conclusion: </span></b><span style="font-family:Verdana;">The MHO and MHSO phenotype display differences in terms of OS and inflammatory markers at lower BMI cut</span></span><span style="font-family:Verdana;">-</span><span style="font-family:Verdana;">offs, indicating that they may be on the way to becoming </span><span style="font-family:Verdana;">“</span><span style="font-family:Verdana;">unhealthy</span><span style="font-family:Verdana;">”</span><span style="font-family:;" "=""><span style="font-family:Verdana;"> ob</span><span style="font-family:Verdana;">ese. The lower BMI cut-offs proposed by Indian Consensus Group would help</span><span style="font-family:Verdana;"> in understanding of manifestation of metabolic syndrome.</span></span>
文摘Metabolically healthy obese(MHO)individuals are reported to have a lower risk of developing cardiovascular diseases in comparison with individuals with metabolic syndrome.However,the association between MHO and type 2 diabetes(T2DM)is still controversial.Some studies indicated that MHO is a favorable phenotype for T2DM,but more studies showed that MHO individuals have an increased risk of developing T2DM compared with metabolically healthy normalweight individuals,especially among those who would acquire metabolically unhealthy obesity.This has been supported by finding insulin resistance and lowgrade inflammatory responses in MHO individuals with a tendency for impaired beta-cell dysfunction.Studies also showed that liver fat accumulation increased the risk of incidence of T2DM in MHO.Here,we reviewed current literature on the relationship between MHO and T2DM,discussed the determinants for the development of diabetes in MHO,and summarized the measures for the prevention of T2DM in MHO.
基金supported by the National Natural Science Foundation of China(No.30660203)the National Science and Technology Major Project(No.2013ZX10002009)the Key laboratory of High-Incidence Tumor Prevention (Guangxi Medical University),Ministry of Education(No.GK2015-ZZ06)
文摘Objective:To investigate the prevalence of metabolically healthy obesity(MHO)and its relationship with incidence of metabolic syndrome(MetS),type 2diabetes mellitus(T2DM)and hypertension in individuals in the city of Yulin.Methods:We studied 1,666 participants,aged over18years at baseline,with free of components of the MetS except waist criteria.Participants were divided into three groups based on body mass index(Ibm):lean/normal weight(Ibm<23kg/m2),overweight(Ibm,23-24.9kg/m2),obesity(Ibm≥25 kg/m2).The cumulative incidence of MetS,T2DM and hypertension over 5.21years among groups was assessed.Results:The prevalence of MHO was 19.5%in the baseline population.During an average 5.21year follow-up,the cumulative incidence of MetS,T2DM and hypertension in1,666participants were 16.4%,19.1%and 3.9%,respectively.The obesity group had a significantly higher cumulative incidence of MetS(16.4%vs.3.2%,P<0.001),hypertension(19.1%vs.3.7%,P<0.001),and T2DM(3.9%vs.1.6%,P<0.001)compared to the lean/normal weight group.Each kg/m2 of Ibm carried increased risk for T2DM(19%),hypertension(11%)and MetS(13%).Conclusion:Metabolically healthy obesity individuals confer increased risk for hypertension,T2DM and the MetS than their non-obese counterparts.
文摘Obesity plays relevant pathophysiological role in the development of health problems, arising as result of complex interaction of genetic, nutritional, and metabolic factors. Due to the role of adipose tissue in lipid and glucose metabolism, and low grade inflammation, it is necessary to classify obesity on the basis of body fat composition and distribution, rather than the simply increase of body weight, and the Body Mass Index. The new term of adiposopathy(‘‘sick fat'') clearly defines the pathogenic role of adipose tissue. Four phenotypes of obese individuals have been described:(1) normal weight obese(NWO);(2) metabolically obese normal weight;(3) metabolically healthy obese; and(4) metabolically unhealthy obese or "at risk" obese. Moreover, sarcopenic obesity has been related to all the phenotypes. The category of normal weight lean, represented by metabolically healthy normal weight has been classified to distinguish from NWO. It is crucial to recommend a bariatric surgery taking into account adiposopathy and sick fat that occurs with the expansion of fat mass, changing the inflammatory and metabolic profile of the patient. Body fat percentage and genetic polymorphism have to be evaluated to personalize the best bariatric surgery intervention.
文摘The growing obesity epidemic is becoming a major public health concern,and the associated costs represent a considerable burden on societies.Among the most common complications of severe obesity are the development of hypertension,dyslipidemia,type 2 diabetes,cardiovascular disease,and various types of cancer.Interestingly,some obese individuals have a favorable metabolic profile and appear to be somehow protected from the detrimental effects of excessive adipose tissue accumulation.These individuals remain normoglycemic,insulin sensitive,and hypotensive with proper blood lipid levels,despite their high body mass index and/or waist circumference.Multiple independent observations have led to the concept of the metabolically healthy obese(MHO) phenotype,yet no consensus has been reached to date regarding a universal definition or the main mechanism behind this phenomenon.Recent technological advances and the use of high-throughput analysis techniques have revolutionized different areas of biomedical research.A multi-omics approach,which is used to investigate changes at different molecular levels in an organism or tissue,may provide valuable insights into the interplay between the molecules or pathways and the roles of different factors involved in the mechanisms underlying metabolic health deterioration.The aim of this review is to present the current status regarding the use of omics technologies to investigate the MHO phenotype,as well as the results of targeted analyses conducted in MHO individuals.
基金supported by the National Key Research and Development Program of China(2018YFA0506901,2019YFA0801701,2022YFA0806502)the National Natural Science Foundation of China(92254308,92157107)the Lingang Laboratory(LG-QS-202204-06)。
文摘Metabolically healthy obesity refers to obese individuals who do not develop metabolic disorders.These people store fat in subcutaneous adipose tissue(SAT)rather than in visceral adipose tissue(VAT).However,the molecules participating in this specific scenario remain elusive.Rab18,a lipid droplet(LD)-associated protein,mediates the contact between the endoplasmic reticulum(ER)and LDs to facilitate LD growth and maturation.In the present study,we show that the protein level of Rab18 is specifically upregulated in the SAT of obese people and mice.Rab18 adipocyte-specific knockout(Rab18 AKO)mice had a decreased volume ratio of SAT to VAT compared with wildtype mice.When subjected to high-fat diet(HFD),Rab18 AKO mice had increased ER stress and inflammation,reduced adiponectin,and decreased triacylglycerol(TAG)accumulation in SAT.In contrast,TAG accumulation in VAT,brown adipose tissue(BAT)or liver of Rab18AKO mice had a moderate increase without ER stress stimulation.Rab18 AKO mice developed insulin resistance and systematic inflammation.Rab18 AKO mice maintained body temperature in response to acute and chronic cold induction with a thermogenic SAT,similar to the counterpart mice.Furthermore,Rab18-deficient 3T3-L1 adipocytes were more prone to palmitate-induced ER stress,indicating the involvement of Rab18 in alleviating lipid toxicity.Rab18 AKO mice provide a good animal model to investigate metabolic disorders such as impaired SAT.In conclusion,our studies reveal that Rab18 is a key and specific regulator that maintains the proper functions of SAT by alleviating lipid-induced ER stress.
文摘选取2006年4月~2010年1月期间在湖南省人民医院体检的人员中资料齐全、于1~3年后随访的1 367例,比较正常对照组、代谢正常肥胖（Metabolically Healthy Obese,MHO）及肥胖伴代谢综合征（MS）三组的血清谷丙转氨酶（alanine aminotransferase,ALT）活性.将血清ALT活性正常的MHO（n=40）行四分位数分组（A、B、C、D组）,比较4组MHO个体发生非酒精性脂肪性肝病（NAFLD）的发病情况,分析不同组别发生NAFLD的风险.结果：（1）MHO个体ALT水平低于肥胖伴MS者（30.71±19.59 vs 39.47±27.56,P〈0.05）,高于正常对照者（30.71±19.59 vs 21.39±14.98,P〈0.05）.（2）血清ALT活性正常的MHO个体发生NAFLD的风险较正常对照组明显增加（55%vs 5.71%,OR=20.167,95%CI：8.594~47.323;P〈0.05）.（3）D组发生NAFLD风险明显增高（80%vs30%,OR=9.333,95%CI：1.193~72.991;P〈0.05）.证明正常范围内较高活性的ALT可预测MHO个体中NAFLD的发生.
文摘目的初步探讨代谢正常肥胖(MHO)人群中脂联素(APN)分子构成的变化及临床意义,分析MHO人群代谢正常的原因,并探讨其与MHO的相关性。方法根据纳入标准选取成年人161例,分为MHO组(n=52)、肥胖伴代谢综合征(MS)组(n=52)、正常对照组(n=57)。采用酶联免疫吸附法(ELISA)测定患者血清总APN、高分子量脂联素(HMW-adp)浓度,并分析其分子构成在MHO人群中的变化及相关临床意义。结果 (1)与正常对照组相比,肥胖伴MS组及MHO组血清总APN、HMW-adp均明显降低(P<0.01);(2)MHO组总APN、HMW-adp较肥胖伴MS组明显升高(P<0.01);(3)MHO组HMW-adp/总APN(H/A)较肥胖伴MS组及正常对照组均升高(P<0.05);(4)多元逐步回归分析显示体质指数(BMI)、腰围、餐后2 h血糖(2 hP BG)是总APN的重要危险因素,腰围、2 hP BG是HMW-adp的负性预测因子,而高密度脂蛋白胆固醇(HDL-C)是其唯一的阳性预测因子,而H/A的主要影响因素却是BMI、腰围、HDL-C。结论 APN分子构成在MHO人群中呈高水平状态,该人群代谢之所以正常可能与这两种因子的保护作用有关,尤其HMW-adp。由此可以认为血清总APN、HMW-adp的检测可作为定量检测MHO人群及其转归以及判断预后的指标。
