bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lipid, Lipoproteins, C-Reactive Protein, and Hemostatic Factors at Baseline in the Diabetes Prevention Program
Authors:   the Diabetes Prevention Program Research Group
Published: March 2007

OBJECTIVE—Individuals with impaired glucose tolerance (IGT) appear to be at increased risk for cardiovascular disease (CVD) due at least in part to an increased prevalence of risk factors. We evaluated lipid, lipoprotein, C-reactive protein (CRP), fibrinogen, and tissue plasminogen activator (tPA) levels at study entry in the largest multiethnic cohort of participants with IGT described, namely in the Diabetes Prevention Program (DPP).
RESEARCH DESIGN AND METHODS—Measurements were performed at the baseline visit of 3,819 randomized participants of the DPP. Among 3,622 participants who were not taking lipid-lowering medicines, cardiovascular risk factors were analyzed in relation to demographic, anthropometric, and metabolic measures. Major determinants of risk factors were assessed in multivariate analysis.
RESULTS—Over 40% of participants had elevated triglyceride, LDL cholesterol, and CRP levels and reduced HDL cholesterol levels. Men had higher triglyceride and tPA and lower HDL cholesterol concentrations and smaller LDL particle size than women, whereas women had higher CRP and fibrinogen levels. African Americans had less dyslipidemia but higher fibrinogen levels, and Asian Americans had lower CRP and fibrinogen levels than Caucasians and Hispanics. The surrogate measure of insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR]) had the strongest association with HDL cholesterol, triglyceride, and tPA levels and LDL particle size. BMI had the greatest influence on CRP and fibrinogen levels. Using median splits of indexes of insulin resistance and insulin secretion (insulin-to-glucose ratio), participants with greater insulin resistance had a more adverse CVD risk-factor profile, whereas insulin secretion had little influence on risk factors.
CONCLUSIONS—The pattern of CVD risk factors in participants with IGT in the DPP exhibits substantial heterogeneity and is significantly influenced by race, sex, and age, as well as by obesity, glucose, and insulin measures. The degree of insulin resistance, as reflected by HOMA-IR, showed the greatest association with the cardiovascular risk factors.
Serum Ferritin Is Associated With Visceral Fat Area and Subcutaneous Fat Area
Authors: Iwasaki Tomoyuki , Nakajima Atsushi , Yoneda Masato , Yamada Yoshihiko , Mukasa Koji , Fujita Koji , Fujisawa Nobutaka , Wada Koichiro , Terauchi Yasuo 
Published: March 2007

OBJECTIVE—Until now, few clinical studies have reported on the association between the indexes of body fat distribution and serum ferritin, an indicator of body iron stores and a putative risk factor for insulin resistance. We investigated the association between serum ferritin concentrations and the indexes of distribution of adipose tissues in the body, such as the visceral fat area (VFA), the subcutaneous fat area (SFA), and the hepatic fat content in Japanese subjects.
RESEARCH DESIGN AND METHODS—A total of 248 Japanese subjects (127 men and 121 postmenopausal women aged 57.8 ± 13.9 years, BMI 25.7 ± 4.6 kg/m2; 140 subjects with type 2 diabetes and 108 nondiabetic subjects) were evaluated. Subjects with a history of alcohol intake were excluded from the study. We measured body height, body weight, and serum ferritin, as well as fasting plasma glucose and plasma insulin concentrations. We estimated insulin resistance by homeostasis model assessment. The fat distribution was evaluated by measuring the VFA and SFA by abdominal computed tomography at the umbilical level. To assess the hepatic fat content, the ratio of the computed tomography attenuation value of the liver to that of the spleen was calculated.
RESULTS—Serum ferritin was significantly correlated with the various indexes of adiposity examined, such as the hepatic fat content (r = −0.280, P &lt; 0.0001), VFA (r = 0.254, P &lt; 0.0001), SFA (r = 0.231, P = 0.0005), and homeostasis model assessment (r = 0.286, P = 0.0008).
CONCLUSIONS—This is the first report to directly demonstrate an association between serum ferritin and VFA and SFA. The results of this study suggest that the serum ferritin concentration may be a useful indicator of systemic fat content and degree of insulin resistance.
Longitudinal Assessment of Quality of Life in Patients With Type 2 Diabetes and Self-Reported Erectile Dysfunction
Authors: De Berardis Giorgia , Pellegrini Fabio , Franciosi Monica , Belfiglio Maurizio , Di Nardo Barbara , Greenfield Sheldon , Kaplan Sherrie H. , Rossi Maria C.E. , Sacco Michele , Tognoni Gianni , Valentini Miriam , Nicolucci Antonio ,   on behalf of the QuED (Quality of Care and Outcomes in Type 2 Diabetes) Study Group
Published: March 2007

OBJECTIVE—In the context of the QuED (Quality of Care and Outcomes in Type 2 Diabetes) project, we evaluated the longitudinal changes over 3 years in quality of life (QoL) in patients with type 2 diabetes according to the presence or the development of erectile dysfunction (ED).
RESEARCH DESIGN AND METHODS—Patients were requested to fill in a questionnaire investigating the presence of ED and QoL (SF-36 Health Survey, depression symptoms [Center for Epidemiologic Studies–Depression], and quality of sexual life) every 6 months for 3 years. The analyses were based on multilevel models, adjusted for patient clinical and sociodemographic characteristics.
RESULTS—The study involved 1,456 patients, of whom 34% reported frequent erectile problems at baseline; 192 developed ED during the follow-up. No changes in QoL measures were detected in patients without ED; in those with ED at baseline, a worsening in all SF-36 scales was observed, reaching statistical significance for physical functioning (P = 0.03). Among patients who developed ED during the study, a deterioration in all SF-36 dimensions and a worsening in depressive symptoms preceded the development of ED. The onset of ED was associated with a further marked worsening in physical functioning (P = 0.0008), general health perception (P = 0.02), and social functioning (P = 0.04) on SF-36 subscales, as well as in the summary physical and mental components scores (P = 0.04 and P = 0.07, respectively). The development of ED was also associated with a highly significant increase in depressive symptoms (P = 0.001) and a marked decrease in quality of sexual life (P &lt; 0.0001).
CONCLUSIONS—This longitudinal study documents for the first time the impact of ED onset on several aspects of QoL in patients with type 2 diabetes. The study also shows that QoL tended to further decrease during 3 years in patients with ED at baseline but not in those without this condition.
Increasing the Decrement in Insulin Secretion Improves Glucagon Responses to Hypoglycemia in Advanced Type 2 Diabetes
Authors: Israelian Zarmen , Gosmanov Niyaz R. , Szoke Ervin , Schorr Manju , Bokhari Syed , Cryer Philip E. , Gerich John E. , Meyer Christian 
Published: March 2007

OBJECTIVE—In advanced β-cell failure, counterregulatory glucagon responses may be impaired due to a reduced decrement in insulin secretion during the development of hypoglycemia. The present studies were therefore undertaken to test the hypothesis that these may be improved by increasing this decrement in insulin secretion.
RESEARCH DESIGN AND METHODS—Twelve subjects with type 2 diabetes who have been insulin requiring were studied as a model of advanced β-cell failure. Glucagon responses were examined during a 90-min hypoglycemic clamp (∼2.8 mmol/l) on two separate occasions. On one occasion, tolbutamide was infused for 2 h before the clamp so that the decrement in insulin secretion during the induction of hypoglycemia would be increased. On the other occasion, normal saline was infused as a control.
RESULTS—Before the hypoglycemic clamp, infusion of tolbutamide increased insulin secretion ∼1.9-fold (P &lt; 0.001). However, during hypoglycemia, insulin secretion decreased to similar rates on both occasions (P = 0.31) so that its decrement was approximately twofold greater following the tolbutamide infusion (1.63 ± 0.20 vs. 0.81 ± 0.17 pmol · kg−1 · min−1, P &lt; 0.001). This was associated with more than twofold-greater glucagon responses (42 ± 11 vs. 19 ± 8 ng/l, P &lt; 0.002) during the hypoglycemic clamp but unaltered glucagon responses to intravenous arginine immediately thereafter (449 ± 50 vs. 453 ± 50 ng/l, P = 0.78).
CONCLUSIONS—Increasing the decrement in insulin secretion during the development of hypoglycemia improves counterregulatory glucagon responses in advanced β-cell failure. These findings further support the concept that the impaired counterregulatory glucagon responses in advanced β-cell failure may at least partially be due to a reduced decrement in insulin secretion.
A Randomized Controlled Trial of the Effect of Real-Time Telemedicine Support on Glycemic Control in Young Adults With Type 1 Diabetes (ISRCTN 46889446)
Authors: Farmer Andrew J. , Gibson Oliver J. , Dudley Christina , Bryden Kathryn , Hayton Paul M. , Tarassenko Lionel , Neil Andrew 
Published: March 2007

OBJECTIVE—To determine whether a system of telemedicine support can improve glycemic control in type 1 diabetes.
RESEARCH DESIGN AND METHODS—A 9-month randomized trial compared glucose self-monitoring real-time result transmission and feedback of results for the previous 24 h in the control group with real-time graphical phone-based feedback for the previous 2 weeks together with nurse-initiated support using a web-based graphical analysis of glucose self-monitoring results in the intervention group. All patients aged 18–30 years with HbA1c (A1C) levels of 8–11% were eligible for inclusion.
RESULTS—A total of 93 patients (55 men) with mean diabetes duration (means ± SD) 12.1 ± 6.7 years were recruited from a young adult clinic. In total, the intervention and control groups transmitted 29,765 and 21,400 results, respectively. The corresponding median blood glucose levels were 8.9 mmol/l (interquartile range 5.4–13.5) and 10.3 mmol/l (6.5–14.4) (P &lt; 0.0001). There was a reduction in A1C in the intervention group after 9 months from 9.2 ± 1.1 to 8.6 ± 1.4% (difference 0.6% [95% CI 0.3–1.0]) and a reduction in A1C in the control group from 9.3 ± 1.5 to 8.9 ± 1.4% (difference 0.4% [0.03–0.7]). This difference in change in A1C between groups was not statistically significant (0.2% [−0.2 to 0.7, P = 0.3).
CONCLUSIONS—Real-time telemedicine transmission and feedback of information about blood glucose results with nurse support is feasible and acceptable to patients, but to significantly improve glycemic control, access to real-time decision support for medication dosing and changes in diet and exercise may be required.
Effect of Pitavastatin on Urinary Liver-Type Fatty Acid–Binding Protein Levels in Patients With Early Diabetic Nephropathy
Authors: Nakamura Tsukasa , Sugaya Takeshi , Kawagoe Yasuhiro , Ueda Yoshihiko , Osada Shiwori , Koide Hikaru 
Published: March 2007

OBJECTIVE—Liver-type fatty acid–binding protein (l-FABP) is expressed in renal proximal tubules and is reported to be a useful marker for progression of chronic glomerulonephritis. The aim of this study was to determine whether urinary l-FABP levels are altered at various stages of diabetic nephropathy and whether pitavastatin affects urinary l-FABP levels in early diabetic nephropathy.
RESEARCH DESIGN AND METHODS—Fifty-eight patients with type 2 diabetes (34 men and 24 women, median age 52 years) and 20 healthy, age-matched subjects (group E) were recruited for the study. The diabetic patients included 12 patients without nephropathy (group A), 20 patients with microalbuminuria (group B), 14 patients with macroalbuminuria and normal renal function (group C), and 12 patients with chronic renal failure but not undergoing hemodialysis (blood creatinine &gt;1.2 mg/dl; mean 2.5 mg/dl, group D). Twenty group B patients were randomly assigned to receive 1 mg/day pitavastatin (10 patients, group B1) or placebo (10 patients, group B2). Treatment was continued for 12 months. Urinary l-FABP levels were measured by enzyme-linked immunosorbent assay. Urinary 8-hydroxydeoxyguanosine and serum free fatty acids (FFAs) were also measured in group B.
RESULTS—Urinary l-FABP levels in groups A-D were 6.2 ± 4.6 μg/g creatinine, 19.6 ± 13.5 μg/g creatinine, 26.8 ± 20.4 μg/g creatinine, and 52.4 ± 46.8 μg/g creatinine, respectively. Urinary l-FABP levels in groups B-D were significantly higher than those in healthy subjects (group E, 5.8 ± 4.0 μg/g creatinine) (group B, P &lt; 0.05; group C, P &lt; 0.01; group D, P &lt; 0.01). In group B1, urinary albumin excretion (UAE) and urinary l-FABP levels were decreased after pitavastatin treatment (UAE before, 110 ± 74 μg/min; 6 months, 88 ± 60 μg/min, P &lt; 0.05; 12 months, 58 ± 32 μg/min, P &lt; 0.01; l-FABP before, 18.6 ± 12.5 μg/g creatinine; 6 months, 12.2 ± 8.8 μg/g creatinine, P &lt; 0.05; 12 months, 8.8 ± 6.4 μg/g creatinine, P &lt; 0.01). In group B2, UAE and l-FABP levels showed little change during the experimental period. In group B1, urinary 8-hydroxydeoxyguanosine was decreased 12 months after pitavastatin treatment (before 32.5 ± 19.5 ng/mg creatinine, after 18.8 ± 14.5 ng/mg creatinine, P &lt; 0.01), but in group B2, these showed little difference during the experimental period. In both groups B1 and B2, serum FFAs showed little difference during the experimental period.
CONCLUSIONS—Urinary l-FABP levels appear to be associated with the progression of diabetic nephropathy, and pitavastatin may be effective in ameliorating tubulointerstitial damage in early diabetic nephropathy.
High Incidence of Diabetes in Men With Sleep Complaints or Short Sleep Duration
Authors: Mallon Lena , Broman Jan-Erik , Hetta Jerker 
Published: March 2007

OBJECTIVE—The aim of this study was to investigate the possible relationship among sleep complaints, sleep duration, and the development of diabetes prospectively over a 12-year period in a middle-aged Swedish population.
RESEARCH DESIGN AND METHODS—A random sample of 2,663 subjects aged 45–65 years living in mid-Sweden were sent a postal questionnaire including questions about sleep complaints, sleep duration, sociodemographic characteristics, behavioral risk factors, medical conditions, and depression (response rate 70.2%). Twelve years later, a new questionnaire with almost identical questions was sent to all the survivors (n = 1,604) in 1995, and the questionnaire was answered by 1,244 subjects (77.6%).
RESULTS—Men reporting new diabetes at follow-up more often reported short sleep duration (≤5 h per night) (16.0 vs. 5.9%, P &lt; 0.01), difficulties initiating sleep (16.0 vs. 3.1%, P &lt; 0.001), and difficulties maintaining sleep (28.0 vs. 6.3%, P &lt; 0.001) at baseline than men who did not develop diabetes. Women reporting new diabetes at follow-up reported long sleep duration (≥9 h per night) more often at baseline than women not developing diabetes (7.9 vs. 2.4%, P &lt; 0.05). In multiple logistic regression models, the relative risk (95% CI) for development of diabetes was higher in men with short sleep duration (2.8 [1.1–7.3]) or difficulties maintaining sleep (4.8 [1.9–12.5]) after adjustment for age and other relevant risk factors. Short or long sleep duration or sleep complaints did not influence the risk of new diabetes in women.
CONCLUSIONS—Difficulties maintaining sleep or short sleep duration (≤5 h) are associated with an increased incidence of diabetes in men.
Type 2 Diabetes as a “Coronary Heart Disease Equivalent”
Authors: Juutilainen Auni , Lehto Seppo , Rönnemaa Tapani , Pyörälä Kalevi , Laakso Markku 
Published: March 2007

OBJECTIVE—The purpose of this study was to investigate the hypothesis that coronary heart disease (CHD) mortality in diabetic subjects without prior evidence of CHD is equal to that in nondiabetic subjects with prior myocardial infarction or any prior evidence of CHD.
RESEARCH DESIGN AND METHODS—During an 18-year follow-up total, cardiovascular disease (CVD) and CHD deaths were registered in a Finnish population-based study of 1,373 nondiabetic and 1,059 diabetic subjects.
RESULTS—Adjusted multivariate Cox hazard models indicated that diabetic subjects without prior myocardial infarction, compared with nondiabetic subjects with prior myocardial infarction, had a hazard ratio (HR) of 0.9 (95% CI 0.6–1.5) for the risk of CHD death. The corresponding HR was 0.9 (0.5–1.4) in men and 1.9 (0.6 –6.1) in women. Diabetic subjects without any prior evidence of CHD (myocardial infarction or ischemic electrocardiogram [ECG] changes or angina pectoris), compared with nondiabetic subjects with prior evidence of CHD, had an HR of 1.9 (1.4–2.6) for CHD death (men 1.5 [1.0–2.2]; women 3.5 [1.8–6.8]). The results for CVD and total mortality were quite similar to those for CHD mortality.
CONCLUSIONS—Diabetes without prior myocardial infarction and prior myocardial infarction without diabetes indicate similar risk for CHD death in men and women. However, diabetes without any prior evidence of CHD (myocardial infarction or angina pectoris or ischemic ECG changes) indicates a higher risk than prior evidence of CHD in nondiabetic subjects, especially in women.
Determinants of Diabetes-Attributable Non–Blood Glucose–Lowering Medication Costs in Type 2 Diabetes
Authors: Davis Wendy A. , Knuiman Matthew W. , Hendrie Delia , Davis Timothy M.E. 
Published: March 2007

OBJECTIVE— To prospectively examine the magnitude and predictors of diabetes-attributable non–blood glucose–lowering (non-BGL) medication costs in type 2 diabetes.
RESEARCH DESIGN AND METHODS— Detailed data from 593 community-dwelling patients were available over 4.3 ± 0.4 years. Diabetes-attributable costs (in year 2000 Australian dollars [A$]) were calculated by applying a range of attributable proportions for each complication for which medication was prescribed.
RESULTS— Non-BGL medications accounted for 75% of all prescription medication costs over the study period, and one-third were attributable to diabetes. The median annual cost (in A$) of non-BGL medications per patient increased from A$220 to A$429 over 4 years (P &lt; 0.001), whereas the diabetes-attributable contribution increased from A$31 (range 15–40) to A$159 (range 95–219) per patient (P &lt; 0.001). Diabetes-attributable hospital costs remained stable during the study. Diabetes-attributable non-BGL costs were skewed and, therefore, square root transformed before regression analysis. Independent baseline determinants of √cost/year were coronary heart disease, systolic blood pressure, total serum cholesterol, ln(serum triglycerides), ln(albumin-to-creatinine ratio), serum creatinine, education, and, negatively, male sex and fasting plasma glucose (P ≤ 0.043; R2 = 29%). Projected to the Australian population, diabetes-attributable non-BGL medication costs for patients with type 2 diabetes totaled A$79 million/year.
CONCLUSIONS— The median annual cost of diabetes-attributable non-BGL medications increased fivefold over 4 years. This increase was predicted by vascular risk factors and complications at baseline. Better-educated patients had higher costs, probably reflecting improved health care access. Men and patients with higher fasting plasma glucose levels had lower costs, suggesting barriers to health care and/or poor self-care. The contemporaneous containment of hospital costs may be due to the beneficial effect of increased medication use.
Effects of Oral Fat Load on Insulin Output and Glucose Tolerance in Healthy Control Subjects and Obese Patients Without Diabetes
Authors: Wuesten Oliver , Balz Cristoph H. , Bretzel Reinhard G. , Kloer Hans-Ulrich , Hardt Philip D. 
Published: March 2007

OBJECTIVE—Elevated plasma nonesterified fatty acid (NEFA) concentrations cause peripheral and hepatic insulin resistance and may play an important role in regulating glucose-induced insulin secretion. The aim of our study was to investigate the influence of physiologically elevated NEFA levels on glucose-stimulated insulin secretion in order to find evidence that NEFAs are a potential factor predisposing for type 2 diabetes and related metabolic disorders, which are known risk factors for cardiovascular disease.
RESEARCH DESIGN AND METHODS—We combined an orally administered fat emulsion with an intravenous glucose tolerance test and measured the time course of NEFA, insulin, and glucose. In order to find pathological conditions we applied the experiment to healthy and obese subjects.
RESULTS—The main findings are a significant increase in glucose-stimulated insulin secretion after oral fat load in both groups compared with the condition without preceding fat ingestion and a prolonged insulin secretion after fat load in obese patients compared with control subjects.
CONCLUSIONS—The results provide evidence that fat ingestion modulates β-cell function and that NEFA is a plausible mediator that acts as a link between fat and glucose metabolism by modulating glucose-stimulated insulin secretion. Under the condition of elevated plasma levels of NEFA, this mechanism may be responsible for hyperinsulinemia in obese patients and a potential target of type 2 diabetes prevention strategies.
Metabolic Syndrome, Obesity, and Mortality
Authors: Katzmarzyk Peter T. , Church Timothy S. , Janssen Ian , Ross Robert , Blair Steven N. 
Published: March 2007

OBJECTIVE—To determine in normal weight, overweight, and obese men the risk of all-cause and cardiovascular disease (CVD) mortality associated with the metabolic syndrome (MetS) and the influence of cardiorespiratory fitness (CRF).
RESEARCH DESIGN AND METHODS—This observational cohort study included 19,173 men who underwent a clinical examination, including a maximal exercise test. MetS was defined according to National Cholesterol Education Program guidelines.
RESULTS—At baseline 19.5% of the men had MetS. The ORs of the metabolic syndrome at baseline were 4.7 (95% CI 4.2–5.3) in overweight and 30.6 (26.7–35.0) in obese men compared with normal weight men. A total of 477 deaths (160 CVD) occurred in 10.2 years of follow-up. The risks of all-cause mortality were 1.11 (0.75–1.17) in normal weight, 1.09 (0.82–1.47) in overweight, and 1.55 (1.14–2.11) in obese men with MetS compared with normal weight healthy men. The corresponding risks for CVD mortality were 2.06 (0.92–4.63) in normal weight, 1.80 (1.10–2.97) in overweight, and 2.83 (1.70–4.72) in obese men with the MetS compared with normal weight healthy men. After the inclusion of CRF in the model, the risks associated with obesity and MetS were no longer significant.
CONCLUSIONS—Obesity and MetS are associated with an increased risk of all-cause and CVD mortality; however; these risks were largely explained by CRF.