bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypertriglyceridemia Enhances Monocyte Binding to Endothelial Cells in NIDDM
Authors: Hoogerbrugge Nicoline , Verkerk Anton , Jacobs Marloes L , Postema Pieter TE , Jongkind Johan F 
Published: March 2007

OBJECTIVE
The mechanisms by which diabetes leads to rapidly progressive atherosclerosis are not fully understood. Adherence of monocytes to the arterial wall is an early event in the development of atherosclerotic lesions.

RESEARCH DESIGN AND METHODS
The binding of freshly isolated monocytes from patients with NIDDM, IDDM, and healthy control subjects to a monolayer of endothelial cells obtained from human umbilical vein was investigated.

RESULTS
Endothelial adherence of monocytes from normolipidemic patients with IDDM (15.8 ± 4.5%) or NIDDM (16.9 ± 4.6%) was comparable to that of monocytes from a control population (15.3 ± 3.5%). In patients with NIDDM with a serum triglyceride concentration &gt; 2.5 mmol/l, the percentage of cells that adhere to endothelial cells in vitro was significantly increased (23.3 ± 3.1%). Glycemic control did not correlate with monocyte adherence. The presence of symptomatic atherosclerotic disease, age, or sex was not associated with a change in monocyte binding in vitro.

CONCLUSIONS
The results suggest that in NIDDM hypertriglyceridemia should be treated to reduce the high risk for atherosclerosis.
The Effect of Acarbose on Insulin Sensitivity in Subjects With Impaired Glucose Tolerance
Authors: Chiasson Jean-Louis , Josse Robert G , Leiter Lawrence A , Mihic Marko , Nathan David M , Palmason Carol , Cohen Robert M , Wolever Thomas MS 
Published: March 2007

OBJECTIVE
To study the effect of acarbose, an α-glucosidase inhibitor, on postprandial plasma glucose and insulin and insulin sensitivity in subjects with impaired glucose tolerance (IGT).

RESEARCH DESIGN AND METHODS
Subjects with IGT were randomly treated in a double-blind fashion with placebo (n = 10) or acarbose (n = 8) at 100 mg t.i.d. for 4 months. All subjects were submitted before randomization and at the end of the study to a standardized breakfast and a 12-h daytime plasma glucose and plasma insulin profile, and insulin sensitivity was measured as steady-state plasma glucose (SSPG) using the insulin suppression test.

RESULTS
While placebo had no effect on postprandial plasma glucose and plasma insulin incremental area under the curve (AUC) (3.03 ± 0.5 vs. 3.76 ± 0.6 mmol·h−1 · l−1, P = NS; 1,488 ± 229 vs. 1,609 ± 253 pmol · h−1 · l−1, P = NS), acarbose resulted in a significant reduction for both glucose (1.44 ± 0.3 vs. 4.45 ± 0.9 mmol · h−1 · l−1, P = 0.002) and insulin (626.7 ± 104.3 vs. 1,338.3 ± 220.5 pmol · h−1 · l−1, P = 0.003). The reduction in 12-h plasma glucose and insulin AUC on acarbose (11.2 ± 2.1 mmol · h−1 · l−1 and 7.5 ± 0.7 nmol · h−1 · l−1) was significantly greater than that on placebo (4.0 ± 1.6 mmol · h−1 · l−1 and 0.8 ± 0.4 nmol · h−1 · l−1) (P = 0.014 and 0.041). While SSPG was not affected by placebo (13.9 ± 0.4 vs. 13.8 ± 0.3 mmol/l; P = NS), it was significantly improved by acarbose (10.9 ± 1.4 vs. 13.1 ± 1.5 mmol/l, P &lt; 0.004) and was also significantly different from placebo at 4 months (P &lt; 0.02).

CONCLUSIONS
It is concluded that in subjects with IGT, acarbose treatment decreases postprandial plasma glucose and insulin and improves insulin sensitivity. Acarbose may therefore be potentially useful to prevent the progression of IGT to NIDDM.
The Antidiabetogenic Effect of GLP-1 Is Maintained During a 7-Day Treatment Period and Improves Diabetic Dyslipoproteinemia in NIDDM Patients
Authors: Juntti-Berggren Lisa , Pigon Jan , Karpe Fredrik , Hamsten Anders , Gutniak Mark , Vignati Louis , Efendic Suad 
Published: March 2007

OBJECTIVE
To investigate the long-term antidiabetogenic effect of glucagon-like peptide 1 (GLP-1) and its influence on diabetic dyslipoproteinemia, patients with NIDDM were treated with GLP-1 subcutaneously for 1 week.

RESEARCH DESIGN AND METHODS
Twelve patients participated in the study. The 1st week of the study, all of them were on intensive insulin treatment and from day 8, four were randomized to a control group continuing with insulin, and eight to a treatment group where GLP-1 was given at meals together with regular insulin from day 8 to 12. On days 13 and 14, they were only given GLP-1 at meals. NPH insulin at bedtime was given throughout the study.

RESULTS
In the GLP-1-treated patients, the doses of regular insulin, given to keep a satisfactory blood glucose control, were reduced compared with treatment with insulin only. GLP-1 virtually inhibited the early increase in blood glucose after the meals, whereas an increase of ∼ 2 mmol was seen during an optimized insulin treatment. In agreement with the short half-life of the peptide, 2-h postprandial plasma insulin levels were significantly decreased both at day 12 and 14, suggesting that there was not enough GLP-1 left to stimulate endogenous insulin release and compensate for the decrease in the dose of exogenous insulin. Therefore, the effect of GLP-1 was lost before the next meal, resulting in increased preprandial blood glucose values at lunch and dinner. The concentration of VLDL triglycerides decreased already during the 1st week. This decrease persisted during the 2nd week when GLP-1 was included in the treatment. No changes were observed in the levels of LDL and HDL cholesterol. The LDL particle diameter increased from a mean of 22.3 to 22.6 nm (P &lt; 0.01) in response to insulin treatment. A further increment to 22.9 nm (P &lt; 0.05) was seen after GLP-1 treatment. The LDL particle size did not change in the control group. Lipoprotein lipase activity was decreased by 27% and hepatic lipase was reduced by 13% in the GLP-1-treated group.

CONCLUSIONS
We confirm the antidiabetogenic effect of GLP-1 in NIDDM patients. This effect was maintained during 7 days, which implies that the patients did not develop tolerance during this treatment period. Intensive insulin treatment, leading to normotriglyceridemia, increased the mean LDL particle diameter, which is likely to lower the risk of future coronary heart disease in patients with NIDDM. Furthermore, an additive effect of GLP-1 is indicated. Hence, this study gives additional evidence that GLP-1 may be useful as an agent for treating NIDDM.
Brainstem Auditory Evoked Potentials and Visually Evoked Potentials in Young Patients With IDDM
Authors: Seidl Rainer , Birnbacher Robert , Hauser Erwin , Bernert Günther , Freilinger Michael , Schober Edith 
Published: March 2007

OBJECTIVE
To investigate whether young IDDM patients develop central nervous dysfunction and to establish a possible relationship with various disease parameters.

RESEARCH DESIGN AND METHODS
Thirty-two patients, aged 13.5 ± 2 years, with disease duration of 6 ± 2.6 years and age of onset of 7.7 ± 3.2 years (group 1), and 21 patients with short-term disease, age 9.7 ± 3.5 years, duration of disease &lt; 2 years and age of onset of 9.4 ± 3.3 years (group 2) were compared with age- and sex-matched control subjects. Exclusion criteria were clinical signs of neuropathy, retinopathy, nephropathy, or hearing impairment. Neurophysiological studies included auditory and visually evoked potentials (EPs).

RESULTS
Patients in group 1 revealed increased P100 latencies of visually EPs (103.4 ± 4.5 vs. 96.8 ± 3.7 ms) and interpeak latencies I-V of auditory EPs (4.16 ± 0.10 vs. 3.99 ± 0.09 ms) and had abnormal latencies (values outside 2.5 SD) in 37%. However, short-term patients (group 2) had results within normal limits compared with control subjects. In group 1, longer disease duration and younger age at onset correlated with an increase of P100 latency (P &lt; 0.001) and IPL I-V (P &lt; 0.001). Patients with a history of severe hypoglycemic episodes had increased latencies compared with patients without hypoglycemia (P &lt; 0.05). Furthermore, metabolic control during the last 2 years was related to P100 latencies (P &lt; 0.05).

CONCLUSIONS
EPs noninvasively detect subclinical central nervous system involvement in children and adolescents with IDDM. Most important risk factors are duration of disease and frequency of severe hypoglycemia.
Rationale and Design of a Large Study to Evaluate the Renal and Cardiovascular Effects of an ACE Inhibitor and Vitamin E in High-Risk Patients With Diabetes: The MICRO-HOPE Study
Authors: Gerstein Hertzel C , Bosch Jackie , Pogue Janice , Taylor D Wayne , Zinman Bernard , Yusuf Salim ,   The HOPE Study investigators
Published: March 2007

OBJECTIVE
To describe the rationale and design of a large international study (microalbuminuria, cardiovascular, and renal outcomes [MICRO] in the HOPE [Heart Outcomes Prevention Evaluation] study) of an ACE inhibitor and vitamin E for the prevention of diabetic nephropathy (DN) and cardiovascular disease (CVD) in patients with diabetes and microalbuminuria (MA).

RESEARCH DESIGN AND METHODS
A total of 3,657 diabetic subjects, including 1,129 with MA, are randomly allocated to receive the ACE inhibitor ramipril (or placebo) and vitamin E (or placebo) for 4 years in a two-by-two factorial design. Diabetic subjects are a subset of the 9,541 subjects enrolled in the HOPE study.

RESULTS
The development of DN in microalbuminuric diabetic subjects and the development of MA in normoalbuminuric subjects, as well as cardiovascular death, myocardial infarction, and storke, are the main outcomes. The correlation of changes in albuminuria with changes in carotid atherosclerosis documented in a subset of subjects will also be analyzed.

CONCLUSIONS
The effect of both an ACE inhibitor and vitamin E on the progression of renal and CVD in patients with diabetes is being assessed in the MICRO-HOPE study.
Urinary Albumin Excretion as a Predictor of Diabetic Retinopathy, Neuropathy, and Cardiovascular Disease in NIDDM
Authors: Savage Susan , Estacio Raymond O , Jeffers Barrett , Schrier Robert W 
Published: March 2007

OBJECTIVE
The relationship between urinary albumin excretion (UAE) and diabetic complications in NIDDM has not been studied in a large American population. The demonstrated relationship between increased UAE and the development of retinopathy, nephropathy, and neuropathy in IDDM makes this an important issue to also be studied in NIDDM patients.

RESEARCH DESIGN AND METHODS
A large population study of 947 NIDDM patients living predominantly in a metropolitan area was undertaken. Three categories of UAE, namely, normal albuminuria (&lt; 20 μg/min), microalbuminuria (20–200 μg/min), and overt albuminuria (&gt;200 μg/min) were compared with 1) retinopathy as assessed by stereoscopic fundus photographs; 2) cardiovascular disease as assessed by a history of cardiac disease or stroke; ischemic changes on exercise treadmill testing; Q wave myocardial infarction; Estes, Sokolow, or Cornell criteria for left ventricular hypertrophy; positive Rose questionnaire for angina; and an abnormal Doppler exam for peripheral vascular disease; and 3) neuropathy as assessed by neurological symptom and disability scores, autonomic function testing, and quantitative sensory exams involving thermal and vibratory sensation. Selected patient characteristics were then evaluated to determine their effects on the presence of diabetic complications using univariate analyses. Multiple logistic regression analyses were then performed to determine the independent effect of UAE on these diabetic complications.

RESULTS
χ2 analyses revealed that UAE was significantly associated with the presence of retinopathy (P &lt; 0.001), neuropathy (P &lt; 0.001), and cardiovascular disease (P &lt; 0.001). In the multiple logistic regression analyses, UAE had strong independent associations with retinopathy, neuropathy, and cardiovascular disease.

CONCLUSIONS
Thus, increasing UAE in this large NIDDM population in the U.S. was associated with an increased prevalence of diabetic retinopathy, neuropathy, and cardiovascular disease. This suggests that UAE may be more than an indicator of renal disease in NIDDM patients and, in fact, may reflect a state of generalized vascular damage occurring throughout the body. Prospective studies in NIDDM patients are needed to determine the predictive effect of UAE and the effect of decreasing UAE on future diabetic micro- and macrovascular complications.
β-fibrinogen gene −455 G/A Polymorphism and Fibrinogen Levels: Risk factors for coronary artery disease in subjects with NIDDM
Authors: Carter Angela M , Mansfield Michael W , Stickland Max H , Grant Peter J 
Published: March 2007

OBJECTIVE
To investigate the association of a G/A polymorphism at position −455 of the β-fibrinogen gene and fibrinogen levels in the development of coronary artery disease (CAD) in subjects with NIDDM.

RESEARCH DESIGN AND METHODS
In 187 Caucasian subjects with NIDDM, presence of CAD was taken as a clinical history of angina, myocardial infarction, coronary angioplasty, or coronary artery bypass grafting, confirmed from medical case notes.

RESULTS
Fibrinogen levels were significantly higher in subjects with CAD (n = 38, 3.41 [3.12–3.73] g/l) than those without (n = 149, 2.99 [2.87–3.11] g/l, P = 0.004 [geometric mean, 95% CI]). Comparing the genotype frequencies by X2 testing, there was a significant difference between subjects with CAD (GG = 0.84, GA + AA = 0.16) and those without (GG = 0.64, GA + AA = 0.36, P = 0.02). In a logistic regression model, including age, BMI, cholesterol, sex, smoking, triglycerides, and plasminogen activator inhibitor antigen as covariates, genotype and fibrinogen levels were significantly associated with CAD. The odds ratio for having CAD in individuals homozygous for the G allele compared with those possessing the A allele was 1.77 (1.08−2.90), P = 0.03; and for an increase of 1 g/l in fibrinogen levels was 1.60 (1.00–2.60), P = 0.05.

CONCLUSIONS
These data suggest a relationship between the −455 G/A β-fibrinogen gene polymorphism and the development of CAD in subjects with NIDDM. This relationship was not associated with variations in fibrinogen levels, suggesting that this polymorphism may be in linkage with a polymorphism within the coding region of the β-fibrinogen gene, which results in an alteration in the stability of the fibrin clot.
Age-Specific Incidence and Duration of Known Diabetes: The Cremona Study
Authors: Garancini Maria Paola , Gobbi Cecilia , Errera Antonino , Sergi Alessandro , Gallus Giuseppe 
Published: March 2007

OBJECTIVE
To estimate the overall and age-specific incidence of known diabetes and its total duration through prevalence data and to assess the consistency of the results by mortality analysis of the same cohort.

RESEARCH DESIGN AND METHODS
Two different sources were used. The first was a representative sample of 2,274 prevalent known-diabetic subjects. These data provided overall and age-specific incidence estimates by fitting a logistic model to the partial incidence rates for different diagnosis cohorts and to the disease duration. The age at diagnosis structure was built from the age-specific estimates. Prevalence data also provided total duration estimates by converting the prevalent duration-to-date structure into an incident total duration structure. The second source was 145 deceased subjects who were taken from the 6-year follow-up sample of 1,132 prevalent subjects. The age at diagnosis and estimates of total disease duration were provided for these subjects, who paralleled the characteristics of the incident cohort.

RESULTS
The two independent estimates of total disease duration were similar (prevalent subjects, 15.7 years; deceased subjects, 14.1 years): the average duration was 14.9 years. The ratio between prevalence and total duration yielded an independent yearly incidence estimate of 2.2 per 1,000 person-years (men, 2.0; women, 2.4), which was close to the value given by the model of 2.1 per 1,000 person-years (men, 1.9; women, 2.3). Also, the independently determined age structures overlapped, and their average was used to calculate the age-specific incidence. Incidence was negligible for individuals &lt;30 years of age, and it was about 6.0 per 1,000 person-years for individuals &gt;50 years of age.

CONCLUSIONS
This study provided reliable estimates of NIDDM age-specific incidence rates and total disease duration, data that are seldom investigated in this type of disease.
The Dietary Intake of Children With IDDM
Authors: Randecker Greg A , Smiciklas-Wright Helen , McKenzie Jeannie M , Shannon Barbara M , Mitchell Diane C , Becker Dorothy J , Kieselhorst Kessey 
Published: March 2007

OBJECTIVE
To assess the dietary intake of children with IDDM and to determine whether the intake meets the current nutritional recommendations for children with IDDM.

RESEARCH DESIGN AND METHODS
A total of 66 children with IDDM who were &lt; 10 years of age were recruited from two suburban Pennsylvania hospitals. To collect dietary intake data, subjects were asked, via telephone interview, to complete three random-day 24-h dietary recalls. Data were analyzed for the content of nutrients and other food components by a computerized database program. Intakes were expressed as a 3-day average intake for each subject.

RESULTS
Overall mean intake of protein and cholesterol approximated the current recommendations. The mean intake of saturated fat exceeded recommendations, while fiber intake was &lt; the recommended level. Many of the children consumed levels of saturated fat well above recommendations. Energy, vitamin, and mineral intakes were adequate for the overall sample. However, from 10 to 40% of the sample had an inadequate intake of vitamin D, vitamin E, and zinc. The percentage of those with inadequate intakes of these nutrients decreased with age.

CONCLUSIONS
These data suggest that, on average, among this sample of children with IDDM aged &lt; 10 years, adherence to the current nutritional recommendations for children with IDDM was adequate, but some individual children had intakes that were not consistent with the recommendations for optimal management of IDDM.
Cellular Ions in NIDDM: Relation of Calcium to Hyperglycemia and Cardiac Mass
Authors: Barbagallo Mario , Gupta Raj K , Resnick Lawrence M 
Published: March 2007

OBJECTIVE
To investigate the role of hyperglycemia in mediating the clinical association of NIDDM with hypertension and left ventricular dysfunction and hypertrophy.

RESEARCH DESIGN AND METHODS
Since hyperglycemia elevates cytosolic free calcium (Cai) both in myocardial and vascular smooth muscle cells, we utilized nuclear magnetic resonance (NMR) spectroscopy to measure erythrocyte Cai levels and compared them with serum ionized calcium (Caio), glucose, and insulin values before and following an oral glucose tolerance test (OGTT) and with previously obtained cardiac structural indexes in normotensive and hypertensive NIDDM (n = 32) and normal control subjects (n = 35).

RESULTS
Compared with control subjects, normotensive NIDDM subjects had higher Cai (31.5 ± 2.3 vs. 24.3 ± 1.9 nmol/l, P = 0.05), lower intracellular free magnesium (Mgi) (200 ± 10 vs. 225 ± 7 μumol/l, P = 0.05), and greater posterior wall thickness (0.98 ± 0.04 vs. 0.86 ± 0.03 cm, P = 0.05). Hypertensive NIDDM subjects exhibited a further increase in Cai (43.1 ± 4.4 nmol/l, P = 0.05 vs. control subjects) and left ventricular mass (LVM) (201.5 ± 12.2 vs. 155.8 ± 7.7 g, P = 0.05 vs. control subjects). For all subjects, significant relationships were observed between Cai and fasting blood glucose (r = 0.510, P &lt; 0.01), HbA1c (r = 0.389, P &lt; 0.05), and the glycemic response to OGTT (the area under the curve [AUC] for glucose; r = 0.519, P &lt; 0.01) and to systolic (r = 0.504, P &lt; 0.01) and diastolic (r = 0.624, P &lt; 0.01) blood pressure. Left ventricular mass index (LVMI) was related to fasting glucose levels (r = 0.406, P &lt; 0.01) and the AUC for glucose (r = 0.380, P &lt; 0.01), but not to fasting insulin or insulin responses to an OGTT. The LVMI was best related to Cai (r = 0.516, P &lt; 0.01), while being inversely related to Caio (r = −0.486, P &lt; 0.01). Multivariate regression indicated the contribution of glucose to LVMI was independent of age, BMI, insulin, and blood pressure but demonstrated a significant interaction with Cai.

CONCLUSIONS
Altogether, these data suggest that glucose-related excess Cai is a fundamental lesion in diabetes that contributes to the elevated blood pressure and cardiac mass in this disease.
NIDDM, Impaired Glucose Tolerance, and Pulmonary Function in Older Adults: The Rancho Bernardo Study
Authors: Barrett-Connor Elizabeth , Frette Catherine 
Published: March 2007

OBJECTIVE
To determine whether NIDDM or plasma glucose level in subjects without diabetes is associated with reduced pulmonary function in 525 men and 714 women, 51–95 years of age.

RESEARCH DESIGN AND METHODS
The analysis was based on data from a community-based study, the Rancho Bernardo Study. Between 1984 and 1987, 82% of community-dwelling residents had an oral glucose tolerance test. Between 1988 and 1991, 80% had lung function assessed by spirometry (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]).

RESULTS
In analyses adjusted for age, height, and cigarette smoking, pulmonary function was not associated with known or newly diagnosed NIDDM in men or women. However, FEV1 and FVC were each independently reduced in men with diabetes of 10 or more years' duration. Fasting plasma glucose (FPG) levels were correlated with FEV1 and FVC in men without diabetes. No associations were found in women.

CONCLUSIONS
The overall absence of an association of NIDDM with pulmonary function in these older adults may reflect survival bias and the small number of subjects with severe diabetes or diabetes of prolonged duration. The apparent relation of FPG levels to FEV1 and FVC suggests that any effect of glycemia precedes diabetes and contradicts any putative causal role for duration and severity of glycemia, however. More epidemiological studies are needed to provide further information about the relationship between NIDDM and lung function.
Retinopathy Predicts Coronary Heart Disease Events in NIDDM Patients
Authors: Miettinen Heikki , Haffner Steven M , Lehto Seppo , Rönnemaa Tapani , Pyörälà Kalevi , Laakso Markku 
Published: March 2007

OBJECTIVE
Proliferative retinopathy has been shown to be associated with increased all-cause mortality in diabetic patients. We assessed the relationship between the different degrees of retinopathic changes at baseline and serious coronary heart disease (CHD) events (CHD death or nonfatal myocardial infarction) in a prospective population-based study of NIDDM patients.

RESEARCH DESIGN AND METHODS
Our study is based on the 7-year follow-up cohort of 1,059 NIDDM patients in east and west Finland. Classification of retinopathic changes was based on clinical examination of fundi, and the findings were classified to three categories according to the status of the worse eye: no retinopathic changes, background retinopathy, and proliferative retinopathy.

RESULTS
During the 7-year follow-up, 255 (24%) patients developed serious CHD event. In patients with proliferative retinopathy at baseline, the risk of CHD events during the follow-up was statistically significantly higher compared with patients without retinopathic changes (odds ratio [OR] 2.31, 95% CI 1.21–4.40). The association between proliferative retinopathy and CHD events remained significant when other cardiovascular risk factors were controlled for.

CONCLUSIONS
Proliferative retinopathy in NIDDM patients was associated with CHD events. Our findings suggest that retinopathy and CHD may have similar pathophysiological backgrounds.
Phenformin-Associated Lactic Acidosis Due to Imported Phenformin
Authors: Lu Hua Chung , Parikh Purvi P , Lorber Daniel L 
Published: March 2007

OBJECTIVE
To emphasize the continued incidence of phenformin-associated lactic acidosis.

CASE REPORT
We report a case of phenformin-associated lactic acidosis in a Chinese man who received phenformin while in China. Diagnosis was made; the patient was treated appropriately and survived.

COMMENTS
Phenformin-associated lactic acidosis may still occur in the U.S.