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PubMed2001

Naturally occurring mutations in the melanocortin receptor 3 gene are not associated with type 2 diabetes mellitus in French Caucasians.

Familial genetic studies of type 2 diabetes (T2DM) of different human populations, including the French Caucasians, suggested evidence for linkage of T2DM and human chromosome 20q13, a region where maps the melanocortin 3 receptor gene (MC3R). Likewise, its homologous MC4R in human obesity, MC3R gene is also a good candidate for genetic susceptibility to glucose intolerance and T2DM. We therefore undertook a molecular study to assess the role of genetic variations of this gene in a large cohort of French families with T2DM. In these patients, we identified two missense mutations in the MC3R gene: Val(81)Ile and Lys(6)Thr. These two variants, which were in complete linkage disequilibrium, were also present in nondiabetic controls. Based on association and familial linkage disequilibrium tests results, we found that these MC3R gene-coding variants were not associated with diabetes or obesity. These variants were found, however, marginally associated with insulin and glucose levels during oral glucose tolerance testing in normoglycemic subjects. Overall, the present study provides no evidence for a major role of the MC3R coding mutations underlying the genetic linkages of T2DM and the MC3R gene region on chromosome 20q13 in T2DM families from France and other geographical origins.

Adult↗
PubMed2005

Contrasting clinical and cardiovascular risk status between early and later onset type 2 diabetes.

The prevalence of type 2 diabetes (T2DM) is increasing rapidly and the age of presentation is falling. These changes are likely to be linked to the current obesity epidemic. Our objective was to compare the characteristics of younger patients with T2DM (diagnosed at age < 40 years) with those of older patients (diagnosed at age 50-70 years). We identified 149 younger patients with T2DM, from our diabetes clinic database, and compared them with 217 older T2DM patients randomly identified from the same database. Younger patients with T2DM were more obese, more hypertriglyceridaemic, with lower high-density lipoprotein (HDL) cholesterol, higher total cholesterol/HDL ratio and worse initial and ongoing glycaemic control than older patients from the same clinic. Additional cardiovascular risk factors are associated with T2DM in the young. Treatment should be aimed at early modification of lifestyle and other forms of therapy to avoid long-term complications.

Adult↗
PubMed2000

Diffuse idiopathic skeletal hyperostosis in diabetes mellitus, impaired glucose tolerance and obesity.

BACKGROUND: Diffuse idiopathic skeletal hyperostosis (DISH) is a rheumatic disease characterized by a significant association with metabolic alterations, such as an impaired lipidic profile. METHODS: One-hundred-thirty consecutive patients and 40 normal subjects were studied. The patients were affected by type 1 and type 2 diabetes mellitus, impaired glucose tolerance and obesity. The diagnosis of DISH was performed by clinical examination and X-ray study of the thoracolumbar spine. The determination of total cholesterol, triglycerides, HLD-cholesterol and LDL-cholesterol was realized by routine biochemical methods; an oral glucose tolerance test was performed in order to determine the levels of C-peptide and blood glucose. RESULTS: We demonstrate a high incidence of the disease in a cohort of patients affected by overt and non-overt diabetes mellitus (T1DM and T2DM) as well as in obese subjects and a correlation between this disorder and hypertryglyceridemia (T1DM, obese-T2DM and obese patients), hypo-HDL-cholesterolemia (obese-T2DM, non-obese-T2DM and obese patients) and hyper-LDL-cholesterolemia (obese patients). In obese-T2DM patients, as well as in obese patients, we observed 40% of DISH, in non obese-T2DM patients the presence of DISH was 30%, while in T1DM patients and impaired glucose tolerance 26.6% and 22.2, respectively. However, a correlation between DISH and the relative hyperinsulinemia in obese patients during an oral glucose tolerance test is not documented. CONCLUSIONS: Our study confirms the prevalence of DISH in diabetes mellitus and obesity, the association with an impaired lipidic profile and the low percentage of symptomatic patients.

Adult↗
PubMed2002

Body composition and pulmonary function in obese type 2 diabetic women.

Most patients with Type 2 diabetes mellitus (T2DM) are overweight and their fat-distribution pattern shows more truncal and less peripheral subcutaneous fat. Obesity also influences the respiratory system by mechanical effects on the diaphragm and chest wall depending on the distribution and size of excess adipose tissues. To determine if the impairment of pulmonary function in T2DM is associated with truncal fat distribution, we performed dynamic spirometric tests and body composition analysis, by dual X-ray absorptiometry, in 12 non-smoker mildly obese T2DM women and in an equal number of control normoglycaemic females, matched for age, body mass index and smoking habits. The forced vital capacity and forced expiratory volume in one second for T2DM women (2.67 +/- 0.30 and 2.15 +/- 0.20 1, respectively) were significantly (p < 0.05) lower than for control women (3.22 +/- 0.30 and 2.58 +/- 0.31 1, respectively). However, trunk fat mass and trunk lean body mass for T2DM women (16.68 +/- 2.31 and 20.87 +/- 1.91 kg, respectively) were comparable with those for controls (16.46 +/- 2.54 and 19.65 +/- 3.42 kg, respectively). Thus, we deduce that pulmonary function impairment in T2DM obese women is not associated with truncal fat mass deposition or with lean mass depletion.

Absorptiometry, Photon↗
PubMed2002

Postprandial dysmetabolism and large-vessel disease.

The increased cardiovascular disease morbidity and mortality in people with Type 2 diabetes mellitus (T2DM) is not explained by the prevalence of cardiovascular disease risk factors and is often attributed to poor glycaemic control. Epidemiological studies have shown fasting and especially postprandial or post-challenge hyperglycaemia to be strong predictors of cardiovascular disease morbidity and mortality in people with either T2DM or prediabetic states. Post-challenge hyperglycaemia in people with impaired glucose tolerance has been associated with increased cardiovascular disease mortality, regardless of the fasting blood glucose (FBG) concentration, but the relationship between FBG and cardiovascular disease was dependent on post-challenge glycaemia. Improving blood glucose and HbA1c concentrations by intensive insulin treatment reduced the risk of cardiovascular disease in a small group of Japanese patients with T2DM and, in another study, improved the outcome in patients with T2DM who had suffered a myocardial infarction. However, on the basis of currently available data, there is no evidence that improved glycaemic control results in a significant reduction of cardiovascular disease risk in people with T2DM. The aim in the present article is to review existing information on the relationship between glycaemia, particularly postprandial glucose concentrations, and cardiovascular disease in people with T2DM or impaired glucose tolerance, and to point at possible mechanisms by which postprandial hyperglycaemia could lead to cardiovascular disease.

Blood Glucose↗
PubMed2003

[Identification of the two subtypes of latent autoimmune diabetes in adults by glutamic acid decarboxylase 65 antibody titers].

OBJECTIVE: To compare the clinical characteristics between type 2 diabetes and latent autoimmune diabetes in adults (LADA) and to define the two distinct types of LADA with different glutamic acid decarboxylase antibody (GADA) titers. METHODS: Sera of 750 patients with an initial diagnosis of type 2 diabetes mellitus (T2DM) were screened for GADA with radioimmunoprecipitation assay. The distribution and frequency of different GADA indices were described. Two hundred and ninety five patients were further studied and divided into four groups (T2DM; GADA index < 0.05; index > or = 0.5 and index > or = 0.05 but < 0.5) to compare the age of onset, body mass index, level of major component of adult hemoglobin (HbA1c) and C peptide as well as the rates of hypertension, hyperlipidemia and chronic complications. RESULTS: A total of 64 antibody-positive patients were identified. Compared with T2DM, these patients had younger age of onset, lower C peptide level (fasting C peptide 500 pmol/L vs 414 pmol/L, P < 0.01), lower body mass index (23.2 kg/m(2) vs 21.2 kg/m(2), P < 0.01) and also lower rates of hypertension (48.7% vs 31.7%, P < 0.05) and hyperlipidemia (60.2% vs 38.5%, P < 0.01). However, only the patients with high GADA titer had reduced beta cell function as compared with T2DM and low titer patients. Their diabetic complications were less than those of T2DM. Low GADA titer (index 0.05 - < 0.5) patients were similar to T2DM patients, except that they were prone to ketoacidemia. CONCLUSION: Two clinically distinct types of LADA can be identified by GADA titers. High titer GADA (GADA > or = 0.5) patients have more resemblance to insulin dependent diabetes and can be regarded as LADA-type 1 diabetes, while low titer GADA patients (0.05 - < 0.5) have clinical and metabolic phenotype of type 2 diabetes and can be regarded as LADA-type 2 diabetes.

Adult↗
PubMed2003

Glutamic acid decarboxylase 65 autoantibody levels discriminate two subtypes of latent autoimmune diabetes in adults.

OBJECTIVE: To compare the clinical characteristics between type 2 diabetes mellitus (T2DM) and latent autoimmune diabetes in adults (LADA) with different titers of glutamic acid decarboxylase autoantibody (GADA) and to define the two distinct subtypes of LADA. METHODS: Sera of 750 patients with an initial diagnosis of T2DM from central south of China were screened for GADA using a radioligand assay. The distribution and frequency of GADA levels were described. Two hundred and ninety-five patients were divided into the T2DM group (n = 233) and the LADA group (n = 62) to compare the age of onset, body mass index, HbA(1c), C-peptide, hypertension, dyslipidemia and chronic diabetic complications. Furthermore, LADA patients with different GADA titers were subdivided to analyze the same indexes as the above. RESULTS: The prevalence of LADA (defined as GADA > or = 0.05, namely GADA positive) was 9.7% in the 750 initially diagnosed type 2 diabetic patients. Compared with T2DM, LADA patients were younger at their ages of onset, had lower C-peptide and body mass index, and also had less cases with hypertension and with dyslipidemia. However, only patients with high titer of GADA had poorer beta cell functions and less diabetic complications compared to T2DM and low GADA titer of LADA patients. Patients with low GADA titer were similar to T2DM patients, except that they were prone to develop ketosis more frequently. CONCLUSIONS: Two clinically distinct subtypes of LADA can be identified by GADA levels in patients initially-diagnosed as type 2 diabetes. Patients with high titer of GADA (GADA > or = 0.5) subsequently develop more insulin dependency, which are classified as LADA-type 1; while those with lower GADA titer (0.05 < or = GADA < 0.5) and having clinical and metabolic phenotypes of type 2 diabetes are classified as LADA-type 2.

Adult↗
PubMed2005

[Study on the relationship between polymorphisms of peroxisome proliferators-activated receptor-gamma coactivator-1alpha gene and type 2 diabetes in Shanghai Hans in China].

OBJECTIVE: To observe the association between single nucleotide polymorphism (SNP) of peroxisome proliferators-activated receptor-gamma coactivator-1alpha (PGC-1alpha ) gene and type 2 diabetes mellitus(T2DM). METHODS: Four common SNPs of PGC-1alpha gene were genotyped with polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) and then analyzed with transmission-disequilibrium test (TDT) and sib transmission-disequilibrium test (STDT) in 69 T2DM pedigrees (310 individuals). Furthermore, the authors performed a case-control study to genotype Gly482Ser in 156 patients with T2DM and 111 normal glucose tolerance people without family history. RESULTS: (1)There were no positive results in four variances in TDT-STDT analysis(P> 0.05). (2)The Gly482Ser exhibited a significant difference between the two groups. GA genotype carriers were at increased risk for T2DM (OR=1.85), and there was statistically significant difference in the allele frequency between the case and control groups(P=0.046). (3) The subjects with GG genotype at position Gly482Ser had a higher HDL-C and lower LDL-C and TG levels when compared against those with GA+AA genotype in the control group without family history(P=0.043,lzP=0.046, P=0.037 respectively). CONCLUSION: This study suggested that the PGC-1alpha gene might be implicated in the pathogenesis of T2DM. But the studied SNPs in PGC-1alpha gene may not be major susceptibility ones of T2DM mellitus in Han people of Shanghai.

Asian People↗
PubMed2005

Type 2 diabetes mellitus: from genes to disease.

The development of type 2 diabetes (T2DM) is determined by two factors: genetics and environment. The genetic background of T2DM is undoubtedly heterogeneous. Most patients with T2DM exhibit two different defects: the impairment of insulin secretion and decreased insulin sensitivity. This means that there are at least two pathophysiological pathways and at least two groups of genes that may be involved in the pathogenesis of T2DM. As far as genetic background [corrected] of T2DM is concerned, the disease may be divided into two large groups: monogenic and polygenic forms. In this review, we present genes known to cause rare monogenic forms of diabetes with predominant insulin deficiency (MODY - maturity-onset diabetes of the young, MIDD - maternally inherited diabetes with deafness) and uncommon syndromes of severe insulin resistance. We also describe some of the main approaches used to identify genes involved in the more common forms of T2D and the reasons for the lack of spectacular success in this field. Although major genes for T2DM still await to be discovered, we have probably established a "road map" that we should follow.

Deafness↗
PubMed2006

[Type 2 diabetes mellitus in children in black Africa: description of first five cases in Togo].

The purpose of this report is to describe epidemiological, clinical and therapeutic features of the first five cases of childhood type 2 diabetes mellitus (T2DM) documented in Togo. The five children were admitted to either the Barruet Clinic (n=4) or Tokoin de Lomé University Hospital Centre (n=1) between 1999 and 2004. All presented one or more of the following risk factors for T2DM: obesity, familial history of T2DM, acanthosis nigricans, polycystic ovary syndrome, dyslipidemia, and high blood pressure. Age at diagnosis was 15 years in two cases and 13, 11 and 12 years in the other three cases (mean, 13.2 + 1.79 years). There were three females and two males. All five patients were obese and had risk factors for obesity (high fat intake, sedentary lifestyle and lack of physical exercise). All had a familial history of T2DM and two had Acanthosis nigricans. All five patients were treated initially with insulin that was gradually discontinued in favor of exercise and diet in four. These are the first reported cases of childhood T2DM in Togo. An education campaign is necessary to inform the population on about the risk factors for T2DM.

Adolescent↗
PubMed2005

Factor V G1691A (Leiden) and prothrombin G20210A single-nucleotide polymorphisms in type 2 diabetes mellitus.

The association of the single nucleotide polymorphisms (SNPs) G1691A in coagulation factor V (FV)-Leiden and G20210A in prothrombin (PRT) genes with type 2 diabetes mellitus (T2DM) were analyzed in 112 T2DM patients (58 males, 54 females; mean age 55.24 +/- 13.5 years) and 249 healthy control subjects (118 males, 131 females; mean age 53.03 +/- 13.8 years). No association was found for FV-Leiden with T2DM, as the frequency of the G/G (82.1% vs. 85.5%), G/A (17.0% vs. 14.1%), and A/A (0.9% vs. 0.4%) genotypes was not different between patients and controls, respectively (P = 0.644). Similarly, lack of association of PRT G20210A with T2DM was seen among the population studied, and the frequency of the G/G (92.9% vs. 97.2%), G/A (6.3% vs. 2.8%), and A/A (0.9% vs. 0.0%) genotypes was similar among patients and controls, respectively (P = 0.094). Neither FV-Leiden nor PRT G20210A was associated with, and no evidence for interactions between these mutations was seen in, T2DM.

DNA↗
PubMed2001

Missense polymorphism in the human carboxypeptidase E gene alters enzymatic activity.

Carboxypeptidase E (CPE) is involved in the biosynthesis of peptide hormones and neurotransmitters, including insulin. One of the features of type 2 diabetes mellitus (T2DM) is an elevation in the proinsulin level and/or proinsulin/insulin molar ratio, suggesting that mutations in proinsulin processing enzymes may contribute to the development of T2DM. We scanned CPE for mutations in a collection of Ashkenazi T2DM families and identified five novel single nucleotide polymorphisms (SNPs). An SNP in the 283(rd) codon, c.847C>T, changes arginine to tryptophan (R283W). The residue Arg283 is conserved among CPE orthologs as well as most enzymatically active metallocarboxypeptidases. Of the 272 Ashkenazi T2DM pedigrees screened, we found four families segregating R283W. Within these four families, patients who inherited one copy of this variant had much earlier age of onset for T2DM. The R283W CPE protein cleaves peptide substrates with substantially lower efficiencies and is less stable at elevated temperature. In addition, the R283W CPE variant has a narrower pH optimum and is much less active at pH 6.0-6.5, indicating that the R283W CPE variant would be substantially less active than wild type CPE in the trans-Golgi network and immature secretory vesicles where the enzyme functions in vivo. To summarize, we uncovered a rare non-conservative missense mutation in CPE and demonstrated that the mutant protein has altered enzymatic properties. We predict that this mutant could cause hyperproinsulinism and diabetes in the homozygous state.

5' Untranslated Regions↗
PubMed2005

Genetic polymorphisms in the transforming growth factor beta-induced gene associated with BMI.

In an effort to identify genetic polymorphisms in potential candidate genes for type 2 diabetes mellitus (T2DM), we have sequenced the transforming growth factor beta-induced gene (TGFBI), and examined the association with T2DM and diabetic phenotypes in a Korean T2DM study (775 T2DM patients and 316 normal controls). Twenty-eight polymorphisms were identified in TGFBI. Although no significant associations were detected with the risk of T2DM, one SNP in intron 16 (c.2011+137C>T) and one SNP in the 3' untranslated region (UTR) (c.2589T>G), showed significant association with the levels of insulin and body mass index (BMI) among nondiabetic controls. The lower insulin and BMI were observed in individuals who carry one or two copies of minor alleles than others. For example, the highest BMI (24.21 kg/m(2)) in individuals with homozygote major alleles (T) of c.2589T>G (n=99), the intermediate BMI (23.68 kg/m(2)) in individuals with heterozygote alleles (n=156), and the lowest BMI (22.69 kg/m(2)) in individuals with homozygote minor alleles (G) (n=57, P=0.005) were observed. The present study provides, for the first time, information about genetic polymorphisms in TGFBI and positive associations of those polymorphisms with levels of insulin and BMI in the Korean population.

3' Untranslated Regions↗
PubMed2004

Relationship between calpain-10 gene polymorphism and insulin resistance phenotypes in Chinese.

In order to determine whether the variations in the calpain-10 gene constitutes risk of type 2 diabetes (T2DM) in Chinese, the frequency of UCSNP-43, 44 in 268 adults newly diagnosed with T2DM (according to the 1999 ADA criteria) and 153 non-diabetic control subjects was investigated. For all subjects, the height, weight, waist-to-hip ratio (W/H) and blood pressure, as well as following parameters were measured: (1) 75-g oral glucose tolerance test with insulin, C-peptide, HbA1c and blood lipid profiles; (2) Genomic DNA extracted from peripheral blood lymphocytes was genotyped for UCSNP-43 (calpain-10-g. 4852 G/A) and UCSNP-44 (calpain-10-g. 4841 T/C) by sequencing a polymerase chain reaction (PCR)-amplified fragment. PCR product was selected by single strand conformation polymorphism (SSCP) and then sequenced. The results showed that there was significant difference between T2DM group and normal control group in allele frequencies, haplotype frequencies, or haplotype combinations of UCSNP-43 and -44 either. But in newly diagnosed T2DM group, it was found that the individuals with the genotype UCSNP-44 T/C + C/C had significantly increased fasting and post-challenge insulin levels (Fins and P2hIns), consistent with reduced insulin sensitivity. In the BMI> 25 subgroup, the differences were even more significant. It was demonstrated that the Calpain-10 gene polymorphism UCSNP-44 was associated with insulin sensitivity and Fins and P2hIns in newly diagnosed T2DM, although Calpain-10 doesn't appear as a major diabetes susceptible gene in this population.

Adult↗
PubMed2005

Effect of the peroxisome proliferator-activated receptor-gamma C161T polymorphism on lipid profile in Brazilian patients with Type 2 diabetes mellitus.

AIM: The aim of the present study was to examine the effects of the C161T polymorphism of the peroxisome proliferator-activated receptor gamma (PPARgamma) gene in Brazilian subjects with Type 2 diabetes mellitus (T2DM) and controls residing in Sao Paulo City, Brazil. METHODS: Genomic DNA was obtained from 207 patients with T2DM and 170 unrelated normoglycemic individuals (CG). Anthropometric data included: body mass index, waist, hip, waist-to-hip ratio; biochemical parameters: fasting plasma glucose, total cholesterol, HDL- and LDL-cholesterol, triglycerides, glycated hemoglobin and insulin. Systolic and diastolic blood pressure was also measured. Screening for mutations in the entire coding region of the PPARgamma gene was carried out by PCR, single strand conformational polymorphism analysis (SSCP) and sequencing. C161T polymorphism was analyzed by PCR-RFLP. RESULTS: The C161T polymorphism was the only variant found in exon 6 of the PPARgamma gene. The frequency of the 161T allele in T2DM (0.10) was similar to that found in CG (0.07, p=0.210). Serum triglycerides (p=0.040), VLDL-cholesterol (p=0.040) and Atherogenic Index of Plasma (AIP; p=0.003) were significantly lower in 161T allele carriers than non-carriers in women of the T2DM group. CONCLUSIONS: Our results show that the C161T polymorphism in the PPARgamma gene is not associated with variables related to T2DM or insulin resistance in the Brazilian population. However, a reduction of serum triglycerides and AIP was observed in women with 161T allele of the C161T polymorphism of the PPARgamma gene.

Adult↗
PubMed2005

Type 2 diabetes mellitus in children and adolescents.

Over the last decade, there has been an alarming increase of Type 2 diabetes mellitus (T2DM) in youths, concomitant with the rise of obesity in this age group. T2DM is a progressive disease with a gradual increase in insulin resistance associated later with a decline in insulin secretion with fasting hyperglycemia. Prevalence of T2DM in children is mostly linked to some risk factors: obesity and sedentary lifestyle, puberty, membership of ethnic minorities, features of insulin resistance, family history of T2DM, female gender and perinatal factors. Prevention is essential and can be considered a public health approach directed to the general population. Treatment of T2DM in youth is complex and based on different strategies: diet, exercise and pharmacotherapy. An appropriated intervention program must be started early, in order to prevent or retard the progression of the disease and associated comorbidities.

Acanthosis Nigricans↗
PubMed2003

Type 2 diabetes mellitus is rare but not absent in children under 15 years of age in Austria.

UNLABELLED: Until recently, most children with diabetes mellitus had type 1 diabetes (T1DM). The prevalence of type 2 diabetes (T2DM) is on the rise in North America, especially in risk populations such as the American Indians. Few epidemiological data on the incidence of the disease exist in Europe. In a prospective population-based epidemiological study, all newly diagnosed cases of diabetes mellitus in patients under 15 years of age were registered nation-wide in Austria between 1999 and 2001. Differential diagnosis (according to the American Diabetes Association diagnostic criteria) was based on clinical case definition. During the 3 years of the study period, 529 cases of DM <15 years were documented, of which 510 were clinically assigned to T1DM (271 boys, 239 girls) resulting in an incidence rate of 12.4/100,000. In the same network, eight cases were diagnosed as T2DM (one boy, seven girls) and two cases with an atypical form of T2DM (two girls). The age of onset of T2DM was 12-15 years and all patients were overweight (body mass index >90th percentile). The calculated incidence for T2DM <15 years in Austria was 0.25/100,000. CONCLUSION: at present, type 2 diabetes mellitus is rare but exists in children aged under 15 years in Austria. Follow-up of this registration will help to describe the secular trend.

Adolescent↗
PubMed2006

A mechanism-based disease progression model for comparison of long-term effects of pioglitazone, metformin and gliclazide on disease processes underlying Type 2 Diabetes Mellitus.

Effective long-term treatment of Type 2 Diabetes Mellitus (T2DM) implies modification of the disease processes that cause this progressive disorder. This paper proposes a mechanism-based approach to disease progression modeling of T2DM that aims to provide the ability to describe and quantify the effects of treatment on the time-course of the progressive loss of beta-cell function and insulin-sensitivity underlying T2DM. It develops a population pharmacodynamic model that incorporates mechanism-based representations of the homeostatic feedback relationships between fasting levels of plasma glucose (FPG) and fasting serum insulin (FSI), and the physiological feed-forward relationship between FPG and glycosylated hemoglobin A1c (HbA1c). This model was developed on data from two parallel one-year studies comparing the effects of pioglitazone relative to metformin or sulfonylurea treatment in 2,408 treatment-naïve T2DM patients. It was found that the model provided accurate descriptions of the time-courses of FPG and HbA1c for different treatment arms. It allowed the identification of the long-term effects of different treatments on loss of beta-cell function and insulin-sensitivity, independently from their immediate anti-hyperglycemic effects modeled at their specific sites of action. Hence it avoided the confounding of these effects that is inherent in point estimates of beta-cell function and insulin-sensitivity such as the widely used HOMA-%B and HOMA-%S. It was also found that metformin therapy did not result in a reduction in FSI levels in conjunction with reduced FPG levels, as expected for an insulin-sensitizer, whereas pioglitazone therapy did. It is concluded that, although its current implementation leaves room for further improvement, the mechanism-based approach presented here constitutes a promising conceptual advance in the study of T2DM disease progression and disease modification.

Adult↗