Monogenic diabetes in children:An underdiagnosed and poorly managed clinical dilemma

Monogenic diabetes,constituting 1%-2%of global diabetes cases,arises from single gene defects with distinctive inheritance patterns.Despite over 50 associated genetic disorders,accurate diagnoses and management of monogenic diabetes remain inadequate,underscoring insufficient clinician awareness.The disease spectrum encompasses maturity-onset diabetes of the young(MODY),characterized by distinct genetic mutations affecting insulin secretion,and neonatal diabetes mellitus(NDM)-a heterogeneous group of severe hyperglycemic disorders in infants.Mitochondrial diabetes,autoimmune monogenic diabetes,genetic insulin resistance and lipodystrophy syndromes further diversify the monogenic diabetes landscape.A tailored approach based on phenotypic and biochemical factors to identify candidates for genetic screening is recommended for suspected cases of MODY.NDM diagnosis warrants immediate molecular genetic testing for infants under six months.Identifying these genetic defects presents a unique opportunity for precision medicine.Ongoing research aimed to develop cost-effective genetic testing methods and gene-based therapy can facilitate appropriate identification and optimize clinical outcomes.Identification and study of new genes offer a valuable opportunity to gain deeper insights into pancreatic cell biology and the pathogenic mechanisms underlying common forms of diabetes.The clinical review published in the recent issue of World Journal of Diabetes is such an attempt to fill-in our knowledge gap about this enigmatic disease.

Analysis of an adult diabetes mellitus caused by a rare mutation of the gene:A case report

BACKGROUND This study presents the clinical and genetic mutation characteristics of an unusual case of adult-onset diabetes mellitus occurring in adolescence,featuring a unique mutation in the peroxisome proliferator-activated receptor gamma(PPARG)gene.Data Access Statement:Research data supporting this publication are available from the NN repository at www.NNN.org/download/.CASE SUMMARY The methodology employed entailed meticulous collection of comprehensive clinical data from the probands and their respective family members.Additionally,high-throughput sequencing was conducted to analyze the PPARG genes of the patient,her siblings,and their offspring.The results of this investigation revealed that the patient initially exhibited elevated blood glucose levels during pregnancy,accompanied by insulin resistance and hypertriglyceridemia.Furthermore,these strains displayed increased susceptibility to diabetic kidney disease without any discernible aggregation patterns.The results from the gene detection process demonstrated a heterozygous mutation of guanine(G)at position 284 in the coding region of exon 2 of PPARG,which replaced the base adenine(A)(exon2c.284A>Gp.Tyr95Cys).This missense mutation resulted in the substitution of tyrosine with cysteine at the 95th position of the translated protein.Notably,both of her siblings harbored a nucleotide heterozygous variation at the same site,and both were diagnosed with diabetes.CONCLUSION The PPARG gene mutation,particularly the p.Tyr95Cys mutation,may represent a newly identified subtype of maturity-onset diabetes of the young.This subtype is characterized by insulin resistance and lipid metabolism disorders.

Management of monogenic diabetes in pregnancy:A narrative review

Pregnancy in women with monogenic diabetes is potentially complex,with significant implications for both maternal and fetal health.Among these,maturity-onset diabetes of the young(MODY)stands out as a prevalent monogenic diabetes subtype frequently encountered in clinical practice.Each subtype of MODY requires a distinct approach tailored to the pregnancy,diverging from management strategies in non-pregnant individuals.Glucokinase MODY(GCK-MODY)typically does not require treatment outside of pregnancy,but special considerations arise when a woman with GCK-MODY becomes pregnant.The glycemic targets in GCK-MODY pregnancies are not exclusively dictated by the maternal/paternal MODY genotype but are also influenced by the genotype of the developing fetus.During pregnancy,the choice between sulfonylurea or insulin for treating hepatocyte nuclear factor 1-alpha(HNF1A)-MODY and HNF4A-MODY depends on the mother’s specific circumstances and the available expertise.Management of other rarer MODY subtypes is individu-alized,with decisions made on a case-by-case basis.Therefore,a collaborative approach involving expert diabetes and obstetric teams is crucial for the compre-hensive management of MODY pregnancies.

Maturity-onset diabetes of the young type 9 or latent autoimmune diabetes in adults:A case report and review of literature

BACKGROUND Maturity-onset diabetes of the young(MODY)is a monogenic genetic disease often clinically misdiagnosed as type 1 or type 2 diabetes.MODY type 9(MODY9)is a rare subtype caused by mutations in the PAX4 gene.Currently,there are limited reports on PAX4-MODY,and its clinical characteristics and treatments are still unclear.In this report,we described a Chinese patient with high autoimmune antibodies,hyperglycemia and a site mutation in the PAX4 gene.CASE SUMMARY A 42-year-old obese woman suffered diabetes ketoacidosis after consuming substantial amounts of beverages.She had never had diabetes before,and no one in her family had it.However,her autoantibody tested positive,and she managed her blood glucose within the normal range for 6 mo through lifestyle interventions.Later,her blood glucose gradually increased.Next-generation sequencing and Sanger sequencing were performed on her family.The results revealed that she and her mother had a heterozygous mutation in the PAX4 gene(c.314G>A,p.R105H),but her daughter did not.The patient is currently taking liraglutide(1.8 mg/d),and her blood glucose levels are under control.Previous cases were retrieved from PubMed to investigate the relationship between PAX4 gene mutations and diabetes.CONCLUSION We reported the first case of a PAX4 gene heterozygous mutation site(c.314G>A,p.R105H),which does not appear pathogenic to MODY9 but may facilitate the progression of latent autoimmune diabetes in adults.

Novel gene mutation in maturity-onset diabetes of the young:A case report

BACKGROUND Maturity-onset diabetes of the young(MODY)is the most common monogenic type of diabetes.Recently,14 gene mutations have been found to be associated with MODY.In addition,the KLF11 gene mutation is the pathogenic gene of MODY7.To date,the clinical and functional characteristics of the novel KLF11mutation c.G31A have not yet been reported.CASE SUMMARY We report of a 30-year-old male patient with a one-year history of nonketosisprone diabetes and a 3-generation family history of diabetes.The patient was found to carry a KLF11 gene mutation.Therefore,the clinical data of family members were collected and investigated.A total of four members of the family were found to have heterozygous mutations in the KLF11 gene c.G31A,which resulted in a change in the corresponding amino acid p.D11N.Three patients had diabetes mellitus,and one patient had impaired glucose tolerance.CONCLUSION The heterozygous mutation of the KLF11 gene c.G31A(p.D11N)is a new mutation site of MODY7.Subsequently,the main treatment included dietary interventions and oral drugs.

Maturity-onset diabetes of the young type 10 caused by an Ala2Thr mutation of INS:A case report

Maturity-onset diabetes of the young 10 caused by the c.4G>A (p.Ala2Thr)mutation is extremely rare, with only two reported studies to date. Herein, wereport another case that differs from previous cases in phenotype.CASE SUMMARYThe proband developed diabetes at the age of 27 years, despite having a normalbody mass index (BMI). She exhibited partial impairment of islet function, testedpositive for islet antibodies, and required high doses of insulin. Her sister alsocarried the c.4G>A (p.Ala2Thr) mutation, and their mother was stronglysuspected to carry the mutated gene. Her sister developed diabetes around 40years of age and required high doses of insulin, while the mother was diagnosedin her 20s and was managed with oral hypoglycemic agents;neither of them wereobese.CONCLUSION p.Ala2Thr mutation carriers often experience relatively later onset and normalBMI. Treatment regimens vary between individuals.

Genetic perspectives on childhood monogenic diabetes:Diagnosis,management,and future directions

Monogenic diabetes is caused by one or even more genetic variations, which maybe uncommon yet have a significant influence and cause diabetes at an early age.Monogenic diabetes affects 1 to 5% of children, and early detection and geneticallyfocused treatment of neonatal diabetes and maturity-onset diabetes of theyoung can significantly improve long-term health and well-being. The etiology ofmonogenic diabetes in childhood is primarily attributed to genetic variationsaffecting the regulatory genes responsible for beta-cell activity. In rare instances,mutations leading to severe insulin resistance can also result in the developmentof diabetes. Individuals diagnosed with specific types of monogenic diabetes,which are commonly found, can transition from insulin therapy to sulfonylureas,provided they maintain consistent regulation of their blood glucose levels.Scientists have successfully devised materials and methodologies to distinguishindividuals with type 1 or 2 diabetes from those more prone to monogenicdiabetes. Genetic screening with appropriate findings and interpretations isessential to establish a prognosis and to guide the choice of therapies andmanagement of these interrelated ailments. This review aims to design a comprehensiveliterature summarizing genetic insights into monogenetic diabetes inchildren and adolescents as well as summarizing their diagnosis and management.

Physical activity,sedentary behaviors,physical fitness,and their relation to health outcomes in youth with type 1 and type 2 diabetes:A review of the epidemiologic literature

Diabetes is a leading chronic disease of childhood and adolescence. In addition to the well-known auto-immune, insulin-dependent diabetes mellitus （type 1 diabetes （T 1D））, the past two decades have witnessed the emergence of type 2 diabetes （T2D） in children and adolescents, which previously was only seen in middle-aged or older adults. One of the key components of diabetes management is physical activity （PA）. The beneficial effects of increased PA and decreased sedentary behavior are extremely important in youth with diabetes because of the markedly increased long-term risk of cardiovascular disease in this population compared to persons without diabetes. This review aims to comprehensively summarize the epidemiologic, observational research published and listed in PubMed between 1970 and 2012 on PA and sedentary behaviors, as well as physical fitness in children and adolescents with T1D and T2D. Additionally, we describe briefly the state of knowledge on perceived barriers of PA in persons with diabetes, with a focus on hypoglycemia. Finally, we provide an overview of the epidemiological literature pertaining to health benefits of increased PA in youth with TID and T2D and briefly discuss the topic of exercise-related hypoglycemia, Copyright ~ 2012, Shanghai University of Sport. Production and hosting by Elsevier B.V. All rights reserved.

Novel HNF1A gene mutation in maturity-onset diabetes of the young:A case report

BACKGROUND Maturity-onset diabetes of the young 3(MODY3),caused by mutations in the HNF1A gene,is the most common subtype of MODY.The diagnosis of MODY3 is critical because a low dose of sulfonylurea agents can achieve glucose control.CASE SUMMARY We describe a patient with MODY3 involving a novel splicing mutation,in whom low-dose gliclazide was sufficient to control clinically significant hyperglycemia.Sanger sequencing identified a splicing HNF1A mutation in 12q24 NM_000545.5 Intron5 c.1108-1G>A.Glycemic control has been maintained without insulin therapy for 28 mo after the diagnosis of diabetes.CONCLUSION This case report highlights a novel HNF1A gene mutation in MODY3 that is responsive to sulfonylurea therapy.

HNF1A mutation in a Thai patient with maturity-onset diabetes of the young: A case report

BACKGROUND Maturity-onset diabetes of the young(MODY)is the most common form of monogenic diabetes.The disease is transmitted in autosomal dominant mode and diabetes is usually diagnosed before age 25 year.MODY 3 is caused by mutation of hepatocyte nuclear factor(HNF)1A genes and is the most common MODY subtype.Diagnosis of MODY 3 is crucial since glycemic control can be accomplished by very low dose of sulfonylurea.In this report we described a Thai MODY 3 patient who had excellence plasma glucose control by treating with glicazide 20 mg per day and insulin therapy can be discontinued.CASE SUMMARY A 31-year-old woman was diagnosed diabetes mellitus at 14 years old.The disease was transmitted from her grandmother and mother compatible with autosomal dominant inheritance.Sanger sequencing of proband’s DNA identified mutation of HNF1A at codon 203 which changed amino acid from arginine to cysteine(R203C).This mutation was carried only by family members who have diabetes.The patient has been treated effectively with a combination of oral hypoglycemic agents and must include a very low dose of glicazide(20 mg/d).Insulin therapy was successfully discontinued.CONCLUSION We demonstrated a first case of pharmacogenetics in Thai MODY 3 patient.Our findings underscore the essential role of molecular genetics in diagnosis and guidance of appropriate treatment of diabetes mellitus in particular patient.

Assessment of pathogenicity and functional characterization of APPL1 gene mutations in diabetic patients

BACKGROUND Adaptor protein,phosphotyrosine interacting with PH domain and leucine zipper 1(APPL1)plays a crucial role in regulating insulin signaling and glucose metabolism.Mutations in the APPL1 gene have been associated with the development of maturity-onset diabetes of the young type 14(MODY14).Currently,only two mutations[c.1655T>A(p.Leu552*)and c.281G>A p.(Asp94Asn)]have been identified in association with this disease.Given the limited understanding of MODY14,it is imperative to identify additional cases and carry out comprehensive research on MODY14 and APPL1 mutations.AIM To assess the pathogenicity of APPL1 gene mutations in diabetic patients and to characterize the functional role of the APPL1 domain.METHODS Patients exhibiting clinical signs and a medical history suggestive of MODY were screened for the study.Whole exome sequencing was performed on the patients as well as their family members.The pathogenicity of the identified APPL1 variants was predicted on the basis of bioinformatics analysis.In addition,the pathogenicity of the novel APPL1 variant was preliminarily evaluated through in vitro functional experiments.Finally,the impact of these variants on APPL1 protein expression and the insulin pathway were assessed,and the potential mechanism underlying the interaction between the APPL1 protein and the insulin receptor was further explored.RESULTS A total of five novel mutations were identified,including four missense mutations(Asp632Tyr,Arg633His,Arg532Gln,and Ile642Met)and one intronic mutation(1153-16A>T).Pathogenicity prediction analysis revealed that the Arg532Gln was pathogenic across all predictions.The Asp632Tyr and Arg633His variants also had pathogenicity based on MutationTaster.In addition,multiple alignment of amino acid sequences showed that the Arg532Gln,Asp632Tyr,and Arg633His variants were conserved across different species.Moreover,in in vitro functional experiments,both the c.1894G>T(at Asp632Tyr)and c.1595G>A(at Arg532Gln)mutations were found to downregulate the expression of APPL1 on both protein and mRNA levels,indicating their pathogenic nature.Therefore,based on the patient’s clinical and family history,combined with the results from bioinformatics analysis and functional experiment,the c.1894G>T(at Asp632Tyr)and c.1595G>A(at Arg532Gln)mutations were classified as pathogenic mutations.Importantly,all these mutations were located within the phosphotyrosinebinding domain of APPL1,which plays a critical role in the insulin sensitization effect.CONCLUSION This study provided new insights into the pathogenicity of APPL1 gene mutations in diabetes and revealed a potential target for the diagnosis and treatment of the disease.

Corticosteroid-induced bradycardia in multiple sclerosis and maturity-onset diabetes of the young due to hepatocyte nuclear factor 4-alpha mutation:A case report

BACKGROUND Intravenous steroid pulse therapy is the treatment of choice for acute exacerbation of multiple sclerosis(MS).Although steroid administration is generally welltolerated,cases of cardiac arrhythmia have been reported.Herein,we describe a young woman who developed marked sinus bradycardia and T-wave abnormalities after corticosteroid administration.We also present plausible explanations for the abnormalities observed in this patient.CASE SUMMARY An 18-year-old woman experienced vertiginous dizziness and binocular diplopia 1 wk prior to admission.Neurological examination revealed left internuclear ophthalmoplegia with left peripheral-type facial palsy.The initial laboratory results were consistent with those of type 2 diabetes.Brain magnetic resonance imaging revealed multifocal,non-enhancing,symptomatic lesions and multiple enhancing lesions.She was diagnosed with MS and maturity-onset diabetes of the young.Intravenous methylprednisolone was administered.On day 5 after methylprednisolone infusion,marked bradycardia with T-wave abnormalities were observed.Genetic evaluation to elucidate the underlying conditions revealed a hepatocyte nuclear factor 4-alpha(HNF4A)gene mutation.Steroid treatment was discontinued under suspicion of corticosteroid-induced bradycardia.Her electrocardiogram changes returned to normal without complications two days after steroid discontinuation.CONCLUSION Corticosteroid-induced bradycardia may have a significant clinical impact,especially in patients with comorbidities,such as HNF4A mutations.

Type 2 Diabetes Mellitus in Children and Adolescents: Early Prevention and Non-Drug Therapy

The global rate of type 2 diabetes mellitus (T2DM) in youth has increased dramatically in the last 30 years. This increase mirrors the global epidemic of childhood obesity. Studies show that, compared to adults who develop T2DM, youth with T2DM ultimately suffer from more harmful symptoms. The prevalence of T2DM and obesity in youth signals a significant public health issue that financially burdens governments, families, and individuals. Since evidence suggests that T2DM in youth is different from both type 1 and type 2 diabetes in adults, researchers and clinicians face many difficulties in developing new treatments. Most treatment efforts have relied on drugs;however, recent studies suggest that non-drug therapy also effectively reduces obesity and diabetic symptoms. Healthier eating, increased physical exercise, and positive mental health, are often underappreciated factors towards managing obesity. Yet these lifestyle changes empower both young and older patients to independently fight diseases and attain better health. To manage the global health risk of obesity, further research addressing the prevention and nondrug early intervention of T2DM and obesity in youth is urgently needed. The present review focuses on the latest updates in the field.

中青年2型糖尿病患者人体成分与营养素餐次分布的相关性分析

目的 分析中青年2型糖尿病患者人体成分与膳食能量、营养素餐次分布的相关性。方法 选择102名中青年2型糖尿病患者进行膳食调查及人体成分测定。结果 患者平均体质指数处于超重范围,其上肢脂肪含量与每日加餐次数、晚餐碳水化合物餐次比呈正相关关系,与早餐优质蛋白比呈负相关关系;躯干脂肪含量与早餐碳水化合物餐次比呈正相关关系,与全日碳水化合物供能比呈负相关关系;下肢脂肪含量与每日餐次呈正相关关系,与早餐优质蛋白比呈负相关关系;躯干及上肢、下肢肌肉含量均与晚餐优质蛋白比、全日能量呈正相关关系,下肢、躯干肌肉含量与全日脂肪供能比及全日碳水化合物供能比呈负相关关系(P<0.05)。结论 为使中青年2型糖尿病患者人体成分更合理,在营养干预中,要保证能量适当、营养素科学配比,注重每日适宜的餐次及能量、营养素在各餐次中的合理分布。

Prevalence of maturity-onset diabetes of the young in phenotypic type 2 diabetes in young adults:a nationwide,multi-center,cross-sectional survey in China

Background:Maturity-onset diabetes of the young(MODY)is the most common monogenic diabetes.The aim of this study was to assess the prevalence of MODY in phenotypic type 2 diabetes(T2DM)among Chinese young adults.Methods:From April 2015 to October 2017,this cross-sectional study involved 2429 consecutive patients from 46 hospitals in China,newly diagnosed between 15 years and 45 years,with T2DM phenotype and negative for standardized glutamic acid decarboxylase antibody at the core laboratory.Sequencing using a custom monogenic diabetes gene panel was performed,and variants of 14 MODY genes were interpreted as per current guidelines.Results:The survey determined 18 patients having genetic variants causing MODY(6 HNF1A,5 GCK,3 HNF4A,2 INS,1 PDX1,and 1 PAX4).The prevalence of MODY was 0.74%(95%confidence interval[CI]:0.40-1.08%).The clinical characteristics of MODY patients were not specific,72.2%(13/18)of them were diagnosed after 35 years,47.1%(8/17)had metabolic syndrome,and only 38.9%(7/18)had a family history of diabetes.No significant difference in manifestations except for hemoglobin A1c levels was found between MODY and non-MODY patients.Conclusion:The prevalence of MODY in young adults with phenotypic T2DM was 0.74%,among which HNF1A-,GCK-,and HNF4A-MODY were the most common subtypes.Clinical features played a limited role in the recognition of MODY.

单基因突变糖尿病与2型糖尿病糖脂代谢指标的比较

目的观察中国人单基因突变糖尿病与2型糖尿病间糖、脂代谢指标的差异。方法选择22例(女15例,男7例)携带线粒体tRNA^(Leu(UUR))3243A→G基因突变的糖尿病患者(MDM组)以及13例(女7例,男6例)携带HNF-1α(MODY3组)或HNF-1β基因突变(MODY5组)的糖尿病患者,分别与151例(女80例,男71例)2型糖尿病患者(T2DM组)比较病程、体脂参数和空腹血糖(FPG)、胰岛素(FINS)、C肽(FCP)以及稳态模型评估胰岛素抵抗指数(HOMA-IR)和稳态模型评估胰岛B细胞功能(HOMA-B)。另外比较11例糖耐量正常线粒体基因突变携带者[tRNA(+)组]与82例无此突变的正常糖耐量者[tRNA(-)组]的糖脂代谢指标。结果MDM组的体重指数、腰臀比、HOMA-IR、HOMA-B及FINS均明显低于T2DM组(P值均<0.01),高密度脂蛋白-胆固醇(HDL-C)显著升高(P<0.05)。MODY3组与T2DM组间仅HDL-C的差异有统计学意义(P<0.05)。tRNA(+)与tRNA(-)组间糖、脂代谢指标的差异均无统计学意义(P值均>0.05)。结论与2型糖尿病相比,单基因突变糖尿病发病较早、体形偏瘦、胰岛细胞分泌功能明显降低。

一体化系统管理模式在初发青年2型糖尿病患者中的应用效果探讨

目的探讨一体化系统管理模式对初发青年2型糖尿病患者疾病知识及治疗的影响。方法将120例青年2型糖尿病初发患者随机分为观察组和对照组各60例。观察组应用一体化系统管理模式;对照组采用常规护理模式,比较两组患者的依从性、住院天数、医疗费用、患者满意度、血糖和糖尿病知识评分。结果:糖尿病患者依从性、满意度和糖尿病知识水平达标率以及治疗有效率,观察组明显高于对照组(P<0.05);糖尿病患者血糖血脂、住院时间、住院费用观察组明显低于对照组(P<0.05)。结论应用一体化系统管理模式可以有效地降低初发2型青年糖尿病患者的血糖、住院天数和医疗费用,提高患者糖尿病足病预防知识水平和治疗依从性,减少糖尿病并发症的发生。

基于移动医疗的自我管理支持对中青年糖尿病患者自护能力及焦虑抑郁状态的影响

目的探讨基于移动医疗的自我管理支持对中青年糖尿病患者自护能力、焦虑抑郁状态、血糖、糖化血红蛋白值的影响。方法100例糖尿病患者按照便利抽样法将患者分为观察组和对照组,每组50例。对照组患者住院期间给予常规护理措施,观察组患者组在常规护理基础上,出院后给予为期6个月的基于移动医疗的自我管理支持。分别在干预前、干预后6个月评估2组患者自护能力、焦虑抑郁状态、血糖、糖化血红蛋白值。结果干预前,2组患者自护能力、焦虑抑郁评分、血糖、糖化血红蛋白值等差异均无统计学意义(P>0.05),干预后观察组患者自护能力、焦虑抑郁评分、血糖、糖化血红蛋白等情况明显优于对照组患者,差异有统计学意义(P<0.05)。结论基于移动医疗的自我管理支持可以提高中青年糖尿病患者自护能力水平,改善焦虑抑郁状态,促进血糖和糖化血红蛋白指标达标。

糖尿病患病危险因素在初诊青、老年糖尿病人中差异及分析

目的 :通过青年及老年初诊 2型糖尿病人糖尿病患病危险因素现状的调查 ,探讨青年 2型糖尿病人早发糖尿病的可能原因。方法 :499例初诊 2型糖尿病人按年龄分为≤ 3 9岁组及≥ 60岁组。调查内容 :职业、糖尿病家族史、饮食习惯、体力活动、体格检查、生化检查。结果 :≤ 3 9岁组病程及最早体重指数持续时间最短 ,男性、糖尿病家族阳性史、饮食油腻、办公室职员、管理人员、商人构成比高于老年组 (P <0 .0 0 1)。两组空腹及餐后 2h血糖及胰岛素、血浆胆固醇、高密度脂蛋白 C差异无显著意义 (P >0 .0 5 )。结论 :青年 2型糖尿病人比老年糖尿病人有更强遗传倾向 ,存在糖尿病患病相关环境因素更显著。因为如此 ,可能是他们较老年人早发糖尿病的原因。

依托心肺运动试验校准运动处方对青年2型糖尿病患者实施运动管理三人行的效果探讨

目的 探讨依托心肺运动试验校准运动处方对青年2型糖尿病患者实施运动管理三人行的血糖控制水平及运动自我效能的干预效果。方法 2019年3月-2020年6月对住院青年2型糖尿病患者130例,采用随机数字表法将其均分为2组(每组65例),2组患者均给予心肺运动试验校准后,对照组(64例,脱落1例)运动师出具运动处方后实施常规管理模式,观察组(62例,脱落3例)在实施常规管理的基础上,实施运动康复技师、教育护士及患者三人行管理模式。干预6个月后,观察并比较2组患者糖尿病相关代谢指标水平及体质指数(BMI)、腰围、自我管理能力、运动自我效能水平、焦虑状态的变化。结果 干预6个月后,观察组患者的血糖、血脂指标较干预前及对照组显著降低(P<0.01);观察组患者的BMI、腰围指标较干预前及对照组降低(P<0.05);观察组自我管理能力、运动自我效能水平较对照组及干预前明显提高;焦虑状态显著降低(P<0.01)。结论 依托心肺运动试验校准运动处方对青年2型糖尿病患者实施运动管理三人行模式,有利于患者平稳控制血糖,促进青年患者运动自我效能及自我管理行为的建立与提高,坚持健康饮食和规律科学运动,规避运动中不良心血管事件的发生,培养患者形成健康的生活方式习惯,缓解青年患者对疾病的焦虑与恐惧,正确面对生活和工作,延缓糖尿病急慢并发症的发生。