SEARCH · Search PubMed

Results for “T2DM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed2005

Efficacy of once- or twice-daily extended release metformin compared with thrice-daily immediate release metformin in type 2 diabetes mellitus.

BACKGROUND: The extended-release formulation of metformin (MXR) prolongs drug absorption in the upper gastrointestinal tract and permits once-daily dosing in patients with type 2 diabetes mellitus (T2DM). This newer formulation may enhance patient compliance with oral therapy compared to conventional immediate-release metformin (MIR) in T2DM. OBJECTIVES: To analyse whether a switch from thrice daily MIR to once or twice daily MXR wouldachieve comparable degrees of glycemic control in patients with type 2 diabetes mellitus (T2DM). METHODS: We conducted an open study of the efficacy and tolerability of MXR in 40 patients with T2DM who had achieved moderate or good glycemic control with MIR alone or in combination with other antihyperglycemic agents. After a lead in period of 3 months patients were switched over to a specific brand of MIR at baseline (Visit 0). Patients were subsequently followed for 4 more visits. These visits were done monthly, after taking MIR in a dose of 1-2 g/day (Visit 1); MXR as a single dose at dinner but 0.5 g less than baseline dose of MIR (Visit 2); MXR, 1-2 g/day as a single dose at bedtime, with strength same as that of baseline dose of MIR (Visit 3); and MXR, 1-2 g/day in two divided doses keeping dose same as baseline MIR (Visit 4). Glycemic control was assessed by a four-point glucose profile (fasting and three postprandial levels) at each visit. RESULTS: At visit 2, when patients had been on 500 mg lesser dose of MXR for 1 month, glucose profile worsened. However, glycemic control, at visit 3, returned to earlier levels when dose of MXR was increased back to original dose. Overall the MXR formulation was well tolerated with minor gastrointestinal adverse effects, reported by only 3 patients. CONCLUSION: Patients with T2DM who had been receiving thrice-daily MIR achieved comparable glycemic control when therapy was switched to once- or twice-daily MXR at the same total daily dose.

Adult↗

PubMed2005

[Risk factor management in respect of type 2 diabetic complications: ABC management].

Type 2 diabetes (T2DM) is one of the most costly and burdensome chronic diseases in Taiwan and is a condition increasing in epidemic proportions all over the world. The symptoms of T2DM, including hyperglycemia, hypertension, and hyperlipidemia are among the highest risk factors for the development of complications with the disease. Blood sugar control alone is not enough for T2DM management. Proper HbA1C, blood pressure, and cholesterol level have been proven by many researchers to decrease T2DM morbidity and mortality. Therefore, the public and health care providers should know this latest ABC management to decrease the complications in T2DM.

Blood Pressure↗

PubMed2005

[Association of SNP276 in adiponectin gene with type 2 diabetes mellitus and insulin sensitivity].

OBJECTIVE: To investigate the distribution of SNP276 in adiponectin gene in Chinese Hans and its impact on type 2 diabetes mellitus and insulin sensitivity. METHODS: The study population consisted of 417 Chinese Hans residents in Anhui province, including 141 subjects with normal glucose tolerance (NGT) and 276 with type 2 diabetes (T2DM). The islet beta-cell insulin secretion and tissue insulin sensitivity were assessed by formulae of homeostasis model assessment (HOMA-IR & HOMA beta). Firstly, polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) was used to determine whether variation exists in APM1. Then, exact variation was detected by automated DNA direct sequencing. RESULTS: The genotypes of APM1 SNP276 were 0.489 GG, 0.418 GT and 0.092 TT and the major allele was G (frequency=0.699) in subjects with NGT. The distributions of genotypes and alleles of SNP276 both displayed significant difference between NGT and T2DM groups (P=0.031 and 0.013). The SNP276 non-TT (TG+GG) genotype was associated with increased risk of T2DM (OR=2.447, 95%CI: 1.067-5.612, P=0.035). In T2DM group, the subjects with SNP276 GG or GT genotype had higher body mass index, body fat content, fasting plasma glucose and HOMA-IR than did those with TT genotype (P < 0.05 or P < 0.01). Besides, GG genotype had higher systolic blood pressure (P=0.021). In NGT group, SNP276 non-TT carrier had increased body mass index, body fat content, waist hip ratio, fasting plasma insulin, oral glucose tolerance test 2 h plasma insulin and HOMA-IR when compared with TT genotype (P < 0.05 or 0.01). CONCLUSION: SNP276 in APM1 was associated with T2DM and insulin sensitivity.

Adiponectin↗

PubMed2006

[Characteristics of the daily blood glucose profiles of impaired glucose tolerance and type 2 diabetes mellitus subjects by continuous glucose monitoring system].

OBJECTIVE: To investigate the characteristics of daily glucose profiles of the impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM) subjects by continuous glucose monitoring system (CGMS) so as to instruct the development of rational programs of treatment. METHODS: The CGMS data of 6 normal glucose tolerance (NGT), 10 IGT, and 20 newly diagnosed T2DM subjects were analyzed. RESULTS: (1) The values of average blood glucose, standard deviation of blood glucose, total time of plasma glucose > or = 7.8 mmol/L (T(PG) > or = 7.8 mmol/L) of the T2DM subjects were all significantly higher than those of IGT subjects (all P < 0.05), and these values of the IGI subjects were all significantly higher than those of the NGT subjects (all P < 0.05). The CGMS blood glucose profile excursion were also more and more fluctuant with the deterioration of glucose tolerance. (2) In the IGT group, the time of PG reaching peak was 109 minutes +/- 32 minutes and the daily time of PG > or = 7.8 mmol/L was 3.0 hours +/- 0.8 hours. In the newly diagnosed T2DM group, the time of PG reaching peak was 92 minutes +/- 22 minutes, and the daily time of PG > or = 11.1 mmol/L was 12.6 hours +/- 1.3 hours. The blood glucose increased more quickly and more sharply, and continued for more time after breakfast. CONCLUSIONS: (1) CGMS data accurately display the characteristics of daily 24 h blood glucose profiles of the IGT and newly diagnosed T2DM subjects, and CGMS examination helps instruct the development of rational treatment program. (2) In daily life, the time of PG > or = 7.8 mmol/L in IGT subjects was nearly 3 hours. (3) With the deterioration of glucose tolerance, the postprandial glucose peak is elevated higher and more rapidly, and the daily blood glucose profile excursion becomes more and more fluctuant.

Blood Glucose↗

PubMedDate not supplied

Programmed disorders of beta-cell development and function as one cause for type 2 diabetes? The GK rat paradigm.

Now that the reduction in beta-mass has been clearly established in humans with type 2 diabetes mellitus (T2DM) 1-4, the debate focuses on the possible mechanisms responsible for decreased beta-cell number and impaired beta-cell function and their multifactorial etiology. Appropriate inbred rodent models are essential tools for identification of genes and environmental factors that increase the risk of abnormal beta-cell function and of T2DM. The information available in the Goto-Kakizaki (GK) rat, one of the best characterized animal models of spontaneous T2DM, are reviewed in such a perspective. We propose that the defective beta-cell mass and function in the GK model reflect the complex interactions of three pathogenic players: (1) several independent loci containing genes causing impaired insulin secretion; (2) gestational metabolic impairment inducing a programming of endocrine pancreas (decreased beta-cell neogenesis) which is transmitted to the next generation; and (3) secondary (acquired) loss of beta-cell differentiation due to chronic exposure to hyperglycemia (glucotoxicity). An important message is that the 'heritable' determinants of T2DM are not simply dependant on genetic factors, but probably involve transgenerational epigenetic responses.

Adult↗

PubMedDate not supplied

Phenotypic and genetic clustering of diabetes and metabolic syndrome in Chinese families with type 2 diabetes mellitus.

BACKGROUND: The aim of this study was to investigate the familiality and clustering of type 2 diabetes (T2DM) and metabolic syndrome (MES) predominantly in families with young-onset diabetes from the Hong Kong Family Diabetes Study. METHODS: One hundred and seventy-nine families (913 subjects) were ascertained through a diabetic proband. Anthropometry, glucose homeostasis, blood pressure and lipid levels were examined. Familial aggregation and inter-relationships of these traits were examined by recurrence risk ratio, heritability, genetic and environmental correlations. RESULTS: One hundred and forty families (78%) had at least one subject with early-onset T2DM (age-at-diagnosis </=40 years). MES was highly prevalent in probands (53%) and siblings (25%). Recurrence risk ratios in siblings were high for T2DM (4.3), hypertension (2.9) and central obesity (2.0). Body mass index, waist circumference, blood pressure, plasma insulin, triglyceride, HDL-cholesterol levels, insulin resistance and beta-cell function had high estimates of heritability (0.45-0.63). Bivariate quantitative analyses revealed differential contribution of genetic and environmental factors to the phenotypic correlation between metabolic trait pairs. Obesity indices showed the strongest phenotypic correlation with other traits, and were significantly influenced by genetic factors (genetic correlation = 0.29-0.60). CONCLUSION: There was significant familial aggregation of T2DM and related phenotypes including obesity, hypertension and dyslipidaemia. The clustering of metabolic traits is likely due to genetic effects, interacting with shared and unique lifestyle/environmental factors. The high familiality suggests that screening for MES is important, especially in families with young-onset diabetes, and that the families in HKFDS are valuable subjects for genetic studies of these metabolic diseases.

Adult↗

PubMed2007

Association of peripheral total and differential leukocyte counts with metabolic syndrome and risk of ischemic cardiovascular diseases in patients with type 2 diabetes mellitus.

BACKGROUND: There is increasing evidence that leukocytes play a central role in obesity, glucose intolerance, type 2 diabetes mellitus (T2DM), and cardiovascular diseases, but the role of differential leukocytes in metabolic syndrome (MetS) and atherosclerosis is largely unknown. The aim of this study was to examine the relationship between the component features of MetS and peripheral leukocyte counts and to explore whether leukocyte counts are associated with clustering of MetS and macrovascular diseases in patients with T2DM. METHODS: 1872 subjects with T2DM who enrolled in a diabetes disease management program were studied. The definition of MetS was modified from that outlined by the criteria of NCEP-ATP III. Areas under the receiver-operating characteristic curve and odds ratios at various intervals of the WBC counts were computed. RESULTS: The peripheral total leukocyte, monocyte, and neutrophil cell counts are increased parallel to the clustering of components of MetS. When white cell counts were analyzed per quartile and as continuous variables after adjustment for age, sex, and other known risk factors with multiple regression analysis, peripheral total leukocyte, monocyte, neutrophils, and lymphocyte counts were independently and significantly associated with specific features of clustering of MetS and prevalence of ischemic cardiovascular diseases. Leukocyte counts, especially neutrophil/lymphocyte ratio, in addition with MetS is associated with the risk of ischemic cardiovascular diseases. CONCLUSION: Our results indicate that differential leukocyte counts are associated with MetS and that peripheral leukocytes may play a role in the pathogenesis of macrovascular complications in patients with T2DM.

Aged↗

PubMed2001

Administration of glutathione in patients with type 2 diabetes mellitus increases the platelet constitutive nitric oxide synthase activity and reduces PAI-1.

Several studies suggest that nitric oxide (NO) production is impaired in diabetes mellitus. Reduced levels of NO could contribute to cardiovascular mortality. Furthermore, NO synthesis is impaired in glutathione (GSH)-depleted human umbilical vein endothelial cells and GSH is reduced in patients with type 2 diabetes mellitus (T2DM). We tested the hypothesis that treatment with GSH may improve platelet constitutive NO sinthase (cNOS) activity in patients with T2DM. Fifteen patients with T2DM underwent a treatment with GSH 600 mg/day i.m. for 10 days. With respect to the basal values on the 10th day of treatment, the red blood cell GSH concentration and platelets cNOS increased (1.4+/-0.1 vs 1.9+/-0.1 micromol/10(10) RBC, p<0.001 and 0.7+/-0.1 vs 2.9+/-0.2 fmol x min(-1) x 10(-9) PLTs, p<0.001, respectively) and the plasma PAI-1 levels diminished (81.4+/-3.7 vs 68.7+/-4.0 ng/ml, p<0.002). A negative correlation between the cNOS and the PAI-1 was found on the basal values. After a wash-out of 30 days the values of red blood cell GSH concentration, platelet cNOS activity and PAI-1 Ag returned to the basal levels. These data suggest that the administration of GSH, in patients with T2DM, is able to improve platelet cNOS activity together with a reduction of PAI-1.

Aged↗

PubMed2003

Evaluation of the microsomal glutathione S-transferase 3 (MGST3) locus on 1q23 as a Type 2 diabetes susceptibility gene in Pima Indians.

Elevation of plasma glucose concentration may induce generation of oxygen-free radicals, which can play an important role in the progression of diabetes and/or development of its complications. Various glutathione transferases utilize the availability of reduced glutathione for the cellular defense against oxygen-free radicals. One such enzyme is microsomal glutathione S-transferase 3 encoded by MGST3, which maps to chromosome 1q23, a region linked to Type 2 diabetes mellitus (T2DM) in Pima Indians, Caucasian, and Chinese populations. We investigated the MGST3 gene as a potential susceptibility gene for T2DM by screening this locus for single nucleotide polymorphisms (SNPs) in diabetic and non-diabetic Pima Indians. We also measured the skeletal muscle MGST3 mRNA level by Real-Time (RT) PCR and its relationship with insulin action in non-diabetic individuals. We identified 25 diallelic variants, most of which, based on their genotypic concordance, could be divided into three distinct linkage disequilibrium (LD) groups. We genotyped unique representative SNPs in selected diabetic and non-diabetic Pima Indians and found no evidence for association with T2DM. Furthermore, inter-individual variation of skeletal muscle MGST3 mRNA was not correlated with differences in insulin action in non-diabetic subjects. We conclude that alterations of MGST3 are unlikely to contribute to T2DM or differences in insulin sensitivity in the Pima Indians.

Adult↗

PubMed2003

The effect of physical activities of various intensities on the energy expenditure of type 2 diabetic men.

Interventions that focus on changing lifestyles through the combined use of dietary management, weight reduction, and increased physical activity are essential for managing type 2 diabetes mellitus (T2DM). The objective of the present study was to examine mildly obese T2DM patients [ n=10; mean age (+/-SD), 51.29+/-6.80 years; body mass index (BMI), 30.26+/-6.19 kg/m(2); and glycosylated haemoglobin (HbA(1c)), 8.16+/-1.16%)] and to compare them with normoglycaemic persons ( n=10; age, 53.00+/-9.48 years; BMI, 27.63+/-3.33 kg/m(2), and HbA(1c), 5.85+/-0.56%) in terms of energy expenditure while performing physical activities of various intensities (i. e. light, moderate, and heavy). The resting metabolic rate for T2DM patients was significantly higher than that for healthy controls (2200+/-354 kcal/day vs. 1628+/-176 kcal/day, respectively; p<0.0001). The values of energy expenditure at all three levels of physical activity were comparable between the two groups. Physical activity seems to have various beneficial effects on mildly obese T2DM patients because it increases the plasma glucose consumption, resulting in similar energy expenditure in comparison with normoglycaemic individuals.

Adult↗

PubMed2026

Sodium-glucose cotransporter-2 inhibitors and gastrointestinal neoplasm risk in type 2 diabetes: a systematic review and meta-analysis of randomized controlled trials.

The potential carcinogenic effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors in patients with type 2 diabetes mellitus (T2DM) remain controversial, particularly regarding site-specific gastrointestinal (GI) neoplasms. This systematic review and meta-analysis aimed to determine the relationship between SGLT2 inhibitors and the risk of GI neoplasms in patients with T2DM. We searched PubMed, EMBASE, Cochrane CENTRAL, Scopus, and Web of Science through March 17, 2025, for RCTs in T2DM comparing SGLT2 inhibitors with placebo or active comparators. Two reviewers independently screened studies, extracted data, and assessed the risk of bias. The primary outcome was GI neoplasms reported in publications, supplementary materials, or trial registries, usually as adverse events rather than centrally adjudicated cancer endpoints. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated in Stata 17.0. In 48 RCTs (n = 48,765), SGLT2 inhibitor therapy was not associated with overall GI neoplasm risk (OR = 1.10, 95% CI: 0.84-1.44; p = 0.46; I² = 0%). Site-specific analyses showed no statistically significant association for esophageal (OR = 1.12, 95% CI 0.37-3.45), gastric (1.20, 0.65-2.23), hepatic (0.62, 0.31-1.22), pancreatic (0.91, 0.51-1.64), colonic (1.28, 0.78-2.08), colorectal (0.76, 0.27-2.17), and rectal neoplasms (0.98, 0.49-1.97), with all p-values > 0.05. Subgroup analyses by agents (e.g., canagliflozin, dapagliflozin, empagliflozin), baseline age, body mass index (BMI), HbA1c, treatment duration, and dose were also non-significant (all p > 0.05). Approximately half of the trials had follow-up of one year or less, limiting our ability to evaluate long-term risk. Available RCT evidence does not show a clear increase in GI neoplasm risk with SGLT2 inhibitors in T2DM. However, limited follow-up, low event counts, and non-cancer-specific outcome ascertainment, the findings should be interpreted as reassuring but not definitive evidence of long-term oncologic safety.Systematic review registration: PROSPERO No. CRD42024619019.

Humans↗

PubMed2006

Asymmetric dimethylarginine is associated with macrovascular disease and total homocysteine in patients with type 2 diabetes.

BACKGROUND: The endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) and total homocysteine (tHcy) are elevated in patients at increased cardiovascular risk. Patients with type 2 diabetes (T2DM) have higher incidence of macrovascular disease than the general population. Recent reports suggest a relationship between tHcy and ADMA. To evaluate the connection between ADMA and tHcy and macrovascular disease, we determined both risk factors in T2DM patients with and without macrovascular disease. SUBJECTS AND METHODS: Plasma concentrations of ADMA and tHcy were cross-sectionally determined in 136 T2DM patients. Fifty-five patients had macrovascular disease defined by history of stroke, myocardial infarction, coronary heart disease or peripheral arterial occlusive disease. Logistic regression analysis was performed to examine the relationship between macrovascular disease and these risk factors. Potential confounders were identified by significant Spearman rank correlation coefficients. RESULTS: In unadjusted models ADMA (per 0.1 micromol/l) and tHcy (per 5 micromol/l) were both significantly related to macrovascular disease (OR=1.63, 95% CI: 1.21-2.19 and OR=1.49, 95% CI: 1.04-2.14). In multivariate models, ADMA was significantly associated with macrovascular disease independent of l-arginine, albumin excretion rate, tHcy and glomerular filtration rate (GFR; OR=1.53, 95% CI: 1.04-2.26). The connection between tHcy and macrovascular disease was not independent of diastolic blood pressure, age, ADMA or GFR. Linear regression analyses revealed that ADMA, GFR and low-density lipoprotein cholesterol were independent predictors for tHcy. CONCLUSION: ADMA is associated with macrovascular disease independent of tHcy and traditional cardiovascular risk factors in patients with T2DM.

Aged↗

PubMed2004

Metabolic risk during antipsychotic treatment.

BACKGROUND: Compared with the general population, individuals with schizophrenia demonstrate an increased prevalence of obesity, type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD). Increased adiposity is associated with decreases in insulin sensitivity, leading to an increased risk of hyperglycemia and hyperlipidemia. Antipsychotic medications can increase adiposity, and a range of evidence from case reports, observational studies, retrospective database analyses, and controlled experimental studies (including randomized clinical trials) suggests that treatment with antipsychotic medications may be associated with an increased risk for insulin resistance, hyperglycemia, dyslipidemia, and T2DM. OBJECTIVE: This article reviews current evidence for the hypothesis that treatment with antipsychotic medications may be associated with increased risks for weight gain, insulin resistance, hyperglycemia, dyslipidemia, and T2DM, and examines the relationship of adiposity to medical risk. METHODS: Relevant publications were identified through a search of MEDLINE from 1975 to the present using the primary search parameters "diabetes or hyperglycemia or glucose or insulin or lipids" and "antipsychotic." Meeting abstracts and earlier nonindexed articles concerning antipsychotic-associated weight gain and metabolic disturbance were also reviewed. Key studies in this emerging literature were summarized, including case reports, observational studies, retrospective database analyses, and controlled experimental studies. RESULTS: Individual antipsychotic medications are associated with different degrees of treatment-induced increases in body weight and adiposity, ranging from modest effects (<2 kg) with amisulpride, ziprasidone, and aripiprazole to clinically significant increases with olanzapine (4-10 kg). In addition to strong evidence concerning the effect of adiposity on insulin sensitivity in nonpsychiatric populations, increased adiposity in patients with schizophrenia has been associated with decreases in insulin sensitivity; this and other effects may contribute to increases in plasma glucose concentrations and lipid levels. CONCLUSION: Metabolic changes in psychiatric patients who receive antipsychotic agents can contribute to the development of the metabolic syndrome and increase the risk for T2DM and CVD.

Antipsychotic Agents↗

PubMed2005

Effects of acute starvation on insulin resistance in obese patients with and without type 2 diabetes mellitus.

BACKGROUND & AIMS: Starvation decreases insulin sensitivity and glucose tolerance in both lean and obese (OB) non-diabetic subjects. Influence of drastic calorie reduction on insulin resistance in patient with type 2 diabetes (T2DM) is not known. METHODS: We enrolled 10 T2DM (diabetes duration 11.1+/-7.9 years) and 10 OB age and weight-matched subjects and performed isoglycaemic hyperinsulinaemic clamp (two 120 min phases of 60 and 120 mIU min-1 m-2 i.v. insulin) with indirect calorimetry at baseline and after 60 h of fasting. RESULTS: After starvation insulin-mediated glucose disposal decreased significantly in both hyperinsulinaemic phases in T2DM (phase 1: from 46+/-28 to 33+/-17, P<0.04; phase 2 from 122+/-47 to 80+/-30 microg kg-1 min-1, P<0.01) as well as in OB (phase 1: from 94+/-52 to 52+/-24, P<0.04; phase 2: from 131+/-46 to 106+/-43 microg kg-1 min, P<0.01). Both oxidative and non-oxidative components of glucose disposal tended to be reduced after fasting. A change of insulin sensitivity was found to be highly dependent upon pre-starvation conditions: more insulin resistant subjects tended to maintain (or modestly improve) insulin resistance whilst subjects with better insulin sensitivity tended to worse it. CONCLUSION: Insulin sensitivity worsens similarly in both T2DM and OB subjects during 60-h fast. The change is probably predictable according to pre-starvation insulin sensitivity.

Area Under Curve↗

PubMed2006

Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance.

Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. We aimed to investigate the plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), who had no obesity or hypertension. Twenty-two patients with T2DM, 18 subjects with IGT and 40 healthy controls were enrolled. Visfatin levels were measured along with the BMI, blood pressure, lipids, glucose, insulin, adiponectin and hsCRP levels, and HOMA-IR indexes. Age, sex and BMI were similar in all groups. Visfatin levels were higher in the diabetic group than the controls (p=0.01). There was no significant difference in the visfatin levels between the T2DM and IGT groups as well as IGT group and healthy controls. Plasma visfatin concentrations did not differ between men and women. Visfatin levels did not correlate with BMI, blood pressure, plasma adiponectin, insulin, hsCRP, glucose and lipid levels or HOMA-IR indexes in the three groups. These results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with T2DM but not with IGT, this increase gets more prominent as the glucose intolerance worsens.

Adult↗

PubMed2006

Differential effects of n-3 polyunsaturated fatty acids on metabolic control and vascular reactivity in the type 2 diabetic ob/ob mouse.

Diets rich in monounsaturated fatty acids (MUFA) are recommended for individuals with type 2 diabetes mellitus (T2DM). The American Heart Association recommends increasing intakes of n-3 polyunsaturated fatty acids (PUFA) to reduce the risk of vascular disease in high-risk individuals; however, the long-term effects of these bioactive fatty acids on glucose metabolism in insulin resistance are controversial. The present studies were conducted to evaluate the effects of diets rich in both MUFA and alpha linolenic acid (C18:3n-3, ALA), eicosapentaenoic acid (C20:5n-3, EPA), or docosahexaenoic acid (C22:6n-3, DHA), on glycemic control and other parameters related to vascular health in a mouse model of T2DM and insulin resistance. Male ob/ob mice (n = 15 per treatment) were fed 1 of 4 lipid-modified formula diets (LFDs) for 4 weeks: (1) MUFA control, (2) ALA blend, (3) EPA blend, and (4) DHA blend. A portion of a MUFA-rich lipid blend in the control LFD was replaced with 11% to 14% energy as n-3 PUFA. After 4 weeks, plasma glucose response to a standard meal (1.5 g carbohydrate/kg body weight) and insulin challenge (2 U/kg body weight, IP) was assessed, and samples were collected for analysis of glucose, insulin, and lipids. Vascular reactivity of isolated aortic rings was assessed in an identical follow-up study. The results showed that insulin-resistant mice fed an LFD with EPA and/or DHA blends had significantly (P < .05) lower triglycerides and free fatty acids, but insulin sensitivity and fasting plasma glucose were not improved. However, mice fed with the ALA blend had significantly improved insulin sensitivity when compared to those fed with other LFD (P < .05). Animals fed an LFD with n-3 PUFA from marine or plant sources showed significantly improved vascular responses as compared with the MUFA-rich LFD (E(max), P < .05) and ob/ob reference mice consuming chow (E(max) and pEC(50), P < .05). In summary, long-term consumption of LFD with n-3 PUFAs improved blood lipids and vascular function in an animal model of insulin resistance and T2DM; however, only MUFA-rich LFD with ALA also improved both insulin sensitivity and glycemic responses. Further studies of MUFA-rich LFD with ALA with individuals who have T2DM are warranted.

Animals↗

PubMedDate not supplied

Value of peripheral vascular endothelial function in the detection of relative myocardial ischemia in asymptomatic type 2 diabetic patients who underwent myocardial perfusion imaging.

BACKGROUND: Endothelial dysfunction precedes overt atherosclerosis and is present in patients with type 2 diabetes mellitus (T2DM). Myocardial perfusion imaging (MPI) is an effective method of detection of coronary artery disease (CAD); however, the relationship between endothelial function and MPI in asymptomatic patients with T2DM has not been examined. METHODS AND RESULTS: This study used a subset of the population from the Detection of Ischemia in Asymptomatic Diabetics (DIAD) study. Endothelium-dependent vasodilation (EDV) and endothelium-independent vasodilation (EIV) were measured by use of brachial artery ultrasonography in 75 asymptomatic patients with T2DM (56 men; mean age, 58.6 +/- 6.4 years; mean duration of diabetes, 8.4 +/- 7.5 years) who underwent adenosine MPI. Of the patients, 15 (20%) had evidence of relative ischemia (MPI(+)) whereas 60 (80%) had a normal study (MPI(-)). Both EDV (3.5% +/- 3.7% vs 4.5% +/- 6.6%, P = not significant) and EIV (15.1% +/- 7.5% vs 16.8% +/- 8.4%, P = not significant) were similar in the 2 groups. On the basis of a receiver-operator analysis, an EDV response of 8% was selected as a cut point, with a negative predictive value of 93% (13/14 subjects with EDV >or=8% were MPI(-)). CONCLUSIONS: Endothelial function in asymptomatic patients with T2DM is not associated with the presence of relative myocardial ischemia by MPI; however, an EDV of 8% or greater has a high negative predictive value for the exclusion of CAD.

Adult↗

PubMed2026

Construction of precision clinical-proteomics risk model based on machine learning for predicting heart failure in type II diabetes mellitus.

BACKGROUND AND AIMS: Heart failure (HF) is a severe complication in type 2 diabetes mellitus (T2DM), but current risk stratification scores have limited predictive accuracy. We aimed to develop novel prediction tools integrating clinical variables with proteomics to improve risk stratification of hospitalization for HF in T2DM. METHODS AND RESULTS: In this study, we included 2111 UK Biobank participants with T2DM but no prior HF, and profiled 2920 proteins to predict 10-year incident HF hospitalization. Participants were randomly divided into training (70%), tuning (10%), and validation (20%) sets.Three prediction models were developed: a Clinical model based on demographic characteristics, comorbidities, medication use, and laboratory indices; a Protein model based on 40 proteins selected by the Light Gradient Boosting Machine (LGBM); and the Clinical OMics and Protein ASSessment for Heart Failure (COMPASS-HF) model, which integrated both clinical variables and the LGBM-selected proteins. Models were evaluated for area under the curve (AUC), sensitivity, and specificity. During follow-up, 168 participants (7.96%) developed incident HF. The COMPASS-HF model showed better discrimination than the Clinical model, with an AUC of 0.897 (95% CI: 0.850-0.945) versus 0.790 (95% CI: 0.723-0.856). It also demonstrated higher sensitivity (0.882; 95% CI: 0.725-0.967) and consistent performance in subgroups. COMPASS-HF effectively stratified risk of hospitalization for HF, with cumulative incidence rates of 31.9% in the high-risk group and 1.2% in the low-risk group. CONCLUSIONS: By combining clinical and proteomic variables, we developed a high-performance HF prediction model for T2DM, enabling precise risk stratification and informing early intervention strategies.

Humans↗