bluuebunny/crossref_metadata_2025_split huggingface dataset:
Weight Loss in Combination With Physical Activity Improves Endothelial Dysfunction in Human Obesity
Authors: Sciacqua Angela , Candigliota Mafalda , Ceravolo Roberto , Scozzafava Angela , Sinopoli Flora , Corsonello Andrea , Sesti Giorgio , Perticone Francesco 
Published: March 2007

OBJECTIVE—To test whether weight loss may improve endothelial dysfunction in human obesity, we recruited 28 healthy obese subjects, aged 30–46 years, with BMI 30–43 kg/m2.
RESEARCH DESIGN AND METHODS—Endothelium-dependent and -independent vasodilation were investigated by intra-arterial infusion of increasing doses of acetylcholine (ACh; 7.5, 15, and 30 μg · ml−1 · min−1) and sodium nitroprusside (0.8, 1.6, and 3.2 μg · ml−1 · min−1). Insulin resistance was estimated by homeostasis model assessment (HOMA). Weight loss was obtained by caloric restriction and physical activity.
RESULTS—We observed a significant reduction in BMI (from 33.1 ± 4.2 to 27.5 ± 4.5 kg/m2, −16.9%, P &lt; 0.0001) and in waist circumference (from 108.2 ± 12.1 to 96.8 ± 12.9 cm, −10.5%, P &lt; 0.0001). Weight loss was also associated with a significant increase in ACh-stimulated forearm blood flow (FBF), from 7.4 ± 2.8 to 12.9 ± 3.4 ml · 100 ml−1 of tissue · min−1 kg/m2 (P &lt; 0.0001). Multivariate regression analysis demonstrated that the only independent predictor of FBF was HOMA, accounting for 44.5% of the variation, whereas the addition of BMI explained another 2.3% of the variation.
CONCLUSIONS—Our data demonstrate that energy-restricted diet associated with physical activity induce a significant and clinically relevant improvement in ACh-stimulated vasodilation in obese healthy subjects.
Racial Differences in Glycemic Control in a Well-Functioning Older Diabetic Population
Authors: de Rekeneire Nathalie , Rooks Ronica N. , Simonsick Eleanor M. , Shorr Ronald I. , Kuller Lewis H. , Schwartz Ann V. , Harris Tamara B. 
Published: March 2007

OBJECTIVE—To evaluate racial differences and factors associated with worse glycemic control in well-functioning older individuals with type 2 diabetes. Our hypothesis was that glycemic control would be worse among black than white diabetic individuals but that this association would be explained by differences in severity of diabetes, health status, health care indicators, and social, psychological, or behavorial factors. We further hypothesized that the association of race with poorer glycemic control would be limited to those with lower education or lower income.
RESEARCH DESIGN AND METHODS—Cross-sectional analysis of 468 diabetic participants among a cohort of 3,075 nondisabled blacks and whites aged 70–79 years living in the community enrolled in the Health, Aging and Body Composition Study. Glycemic control was measured by the level of HbA1c.
RESULTS—A total of 58.5% of the diabetic individuals were black. Although control was poor in all diabetic participants (HbA1c ≥7% in 73.7%), blacks had worse glycemic control than whites (age- and sex-adjusted mean HbA1c, 8.4% in blacks and 7.4% in whites; P &lt; 0.01). Race differences in glycemic control remained significant, even after adjusting for current insulin therapy, cardiovascular disease, higher total cholesterol, and not receiving a flu shot in the previous year, all of which were associated with higher HbA1c concentrations. Controlling for these factors reduced the association by 27%. Race remained an important factor in glycemic control, even when results were stratified by education or income.
CONCLUSIONS—HbA1c concentrations were higher in older black diabetic individuals. Differences in glycemic control by race were associated with disease severity, health status, and poorer quality of care, but these factors did not fully explain the higher HbA1c levels in older black diabetic individuals.
Effects of Metformin and Rosiglitazone Monotherapy on Insulin-Mediated Hepatic Glucose Uptake and Their Relation to Visceral Fat in Type 2 Diabetes
Authors: Iozzo Patricia , Hallsten Kirsti , Oikonen Vesa , Virtanen Kirsi A. , Parkkola Riitta , Kemppainen Jukka , Solin Olof , Lonnqvist Fredrik , Ferrannini Ele , Knuuti Juhani , Nuutila Pirjo 
Published: March 2007

OBJECTIVE—Impaired insulin-mediated hepatic glucose uptake (HGU) has been implicated in the hyperglycemia of type 2 diabetes. We examined the effects of metformin (2 g/day) and rosiglitazone (8 mg/day) monotherapy on HGU and its relation to subcutaneous fat, visceral fat (VF), and whole-body insulin-mediated glucose metabolism in type 2 diabetic patients.
RESEARCH DESIGN AND METHODS—Glucose uptake was measured before and after 26 weeks of treatment using positron emission tomography with [18F]2-fluoro-2-deoxyglucose during euglycemic hyperinsulinemia; fat depots were quantified by magnetic resonance imaging.
RESULTS—Fasting plasma glucose levels were significantly decreased after either rosiglitazone (−0.9 ± 0.5 mmol/l) or metformin treatment (−1.1 ± 0.5 mmol/l) in comparison with placebo; only metformin was associated with weight loss (P &lt; 0.02 vs. placebo). When controlling for the latter, the placebo-subtracted change in whole-body glucose uptake averaged −1 ± 4 μmol · min−1 · kg−1 in metformin-treated patients (NS) and +9 ± 3 μmol · min−1 · kg−1 in rosiglitazone-treated patients (P = 0.01). Both rosiglitazone and metformin treatment were associated with an increase in HGU; versus placebo, the change reached statistical significance when controlling for sex (placebo-subtracted values = +0.008 ± 0.004 μmol · min−1 · kg−1 · pmol/l−1, P &lt; 0.03, for metformin; and +0.007 ± 0.004, P &lt; 0.07, for rosiglitazone). After treatment with either drug, insulin-mediated VF glucose uptake (VFGU) was higher than with placebo. In the whole dataset, changes in HGU were negatively related to changes in HbA1c (r = 0.43, P = 0.01) and positively associated with changes in VFGU (r = 0.48, P &lt; 0.01).
CONCLUSIONS—We conclude that both metformin and rosiglitazone monotherapy increase HGU in type 2 diabetes; direct drug actions, better glycemic control, and enhanced VF insulin sensitivity are likely determinants of this phenomenon.
Adiponectin Is Present in Cord Blood but Is Unrelated to Birth Weight
Authors: Lindsay Robert S. , Walker James D. , Havel Peter J. , Hamilton Barbara A. , Calder Andrew A. , Johnstone Frank D. ,   on behalf of The Scottish Multicentre Study of Diabetes in Pregnancy
Published: March 2007

OBJECTIVE—In adults, adiponectin is reduced in association with excess adiposity, type 2 diabetes, and hyperinsulinemia. We assessed whether adiponectin was 1) present in the fetal circulation, 2) altered in the fetal circulation in the presence of maternal diabetes, and 3) had relations to fetal cord blood insulin or adiposity.
RESEARCH DESIGN AND METHODS—We assessed adiponectin in cord blood in a large cohort of singleton offspring of diabetic mothers (ODM; n = 134) and control mothers (n = 45).
RESULTS—Adiponectin was present in cord blood and, in ODM, was higher in those delivered at later gestational ages (Spearman r = 0.18, P = 0.03). Adiponectin was slightly lower in ODM than control subjects (ODM 19.7 ± 6.1 vs. control 21.8 ± 5.3 μg/ml; P = 0.04), although this difference could potentially reflect different gestational ages in the two groups (ODM 37.6 ± 1.5 and control 40.1 ± 1.1 weeks). In contrast to adults, adiponectin levels in the fetus were unrelated to the degree of adiposity, blood insulin, or leptin in either control subjects or ODM.
CONCLUSIONS—Adiponectin is present in cord blood but does not show expected physiological relations with adiposity as observed in adults.
The Direct Medical Cost of Type 2 Diabetes
Authors: Brandle Michael , Zhou Honghong , Smith Barbara R.K. , Marriott Deanna , Burke Ray , Tabaei Bahman P. , Brown Morton B. , Herman William H. 
Published: March 2007

OBJECTIVE—To describe the direct medical costs associated with type 2 diabetes, as well as its treatments, complications, and comorbidities.
RESEARCH DESIGN AND METHODS—We studied a random sample of 1,364 subjects with type 2 diabetes who were members of a Michigan health maintenance organization. Demographic characteristics, duration of diabetes, diabetes treatments, glycemic control, complications, and comorbidities were assessed by surveys and medical chart reviews. Annual resource utilization and costs were assessed using health insurance claims. The log-transformed annual direct medical costs were fitted by multiple linear regression to indicator variables for demographics, treatments, glycemic control, complications, and comorbidities.
RESULTS—The median annual direct medical costs for subjects with diet-controlled type 2 diabetes, BMI 30 kg/m2, and no microvascular, neuropathic, or cardiovascular complications were $1,700 for white men and $2,100 for white women. A 10-kg/m2 increase in BMI, treatment with oral antidiabetic or antihypertensive agents, diabetic kidney disease, cerebrovascular disease, and peripheral vascular disease were each associated with 10–30% increases in cost. Insulin treatment, angina, and MI were each associated with 60–90% increases in cost. Dialysis was associated with an 11-fold increase in cost.
CONCLUSIONS—Insulin treatment and diabetes complications have a substantial impact on the direct medical costs of type 2 diabetes. The estimates presented in this model may be used to analyze the cost-effectiveness of interventions for type 2 diabetes.
Diabetes and Driving Mishaps
Authors: Cox Daniel J. , Penberthy Jennifer Kim , Zrebiec John , Weinger Katie , Aikens James E. , Frier Brian , Stetson Barbara , DeGroot Mary , Trief Paula , Schaechinger Hartmut , Hermanns Norbert , Gonder-Frederick Linda , Clarke William 
Published: March 2007

OBJECTIVE—The intensive treatment of diabetes to achieve strict glycemic control is a common clinical goal, but it is associated with an increased incidence of hypoglycemia. Becoming hypoglycemic while driving is a hazardous condition and may lead to a greater incidence of driving mishaps. This study investigated whether diabetes is associated with increased risk of driving mishaps and correlates of such a relationship.
RESEARCH DESIGN AND METHODS—During routine visits to diabetes specialty clinics in seven U.S. and four European cities, consecutive adults with type 1 diabetes, type 2 diabetes, and nondiabetic spouse control subjects (n = 341, 332, and 363, respectively) completed an anonymous questionnaire concerning diabetes and driving.
RESULTS—Type 1 diabetic drivers reported significantly more crashes, moving violations, episodes of hypoglycemic stupor, required assistance, and mild hypoglycemia while driving as compared with type 2 diabetic drivers or spouse control subjects (P &lt; 0.01–0.001). Type 2 diabetic drivers had driving mishap rates similar to nondiabetic spouses, and the use of insulin or oral agents for treatment had no effect on the occurrence of driving mishaps. Crashes among type 1 diabetic drivers were associated with more frequent episodes of hypoglycemic stupor while driving, less frequent blood glucose monitoring before driving, and the use of insulin injection therapy as compared with pump therapy. One-half of the type 1 diabetic drivers and three-quarters of the type 2 diabetic drivers had never discussed hypoglycemia and driving with their physicians.
CONCLUSIONS—Type 1 diabetic drivers are at increased risk for driving mishaps, but type 2 diabetic drivers, even on insulin, appear not to be at a higher risk than nondiabetic individuals. Clinical and treatment factors appear to increase risk, e.g., more frequent hypoglycemia while driving, method of insulin delivery, and infrequent self-testing before driving. Physicians are encouraged to talk to their type 1 diabetic patients about hypoglycemia and driving.
Fulminant Type 1 Diabetes
Authors: Imagawa Akihisa , Hanafusa Toshiaki , Uchigata Yasuko , Kanatsuka Azuma , Kawasaki Eiji , Kobayashi Tetsuro , Shimada Akira , Shimizu Ikki , Toyoda Tetsuya , Maruyama Taro , Makino Hideichi 
Published: March 2007

OBJECTIVE— To describe the clinical and immunologic characteristics of fulminant type 1 diabetes, a novel subtype of type 1 diabetes, we conducted a nationwide survey.
RESEARCH DESIGN AND METHODS—History and laboratory data, including islet-related autoantibodies, were examined in 222 patients with fulminant and nonfulminant type 1 diabetes in our hospitals in addition to another 118 patients with fulminant type 1 diabetes located outside our hospitals in Japan.
RESULTS—In our hospitals, of the 222 patients studied, 43 (19.4%) were diagnosed with fulminant type 1 diabetes, 137 (61.7%) were classified as having autoimmune type 1 diabetes, and 42 were type 1 diabetic subjects who were not fulminant and did not have anti-islet antibodies. An additional 118 fulminant patients outside our hospitals were enrolled, making a total of 161 fulminant type 1 diabetic subjects (83 male and 78 female subjects; 14 children/adolescents and 147 adults) identified from all over Japan. (In 2000, the average incidence was three cases per month.) Flu-like symptoms and pregnancy were more frequently observed in the fulminant than in the autoimmune group (P &lt; 0.001). In the fulminant patients, 4.8% were positive for anti-GAD antibodies and none were positive for anti–islet antigen 2 antibodies.
CONCLUSIONS—Fulminant type 1 diabetes is a distinct subtype and accounts for ∼20% of the ketosis-onset type 1 diabetes cases in Japan. Flu-like symptoms are characteristic of disease onset. Metabolic derangement is more severe in this subtype than in autoimmune type 1 diabetes.
Plasma Adiponectin and Leptin Levels, Body Composition, and Glucose Utilization in Adult Women With Wide Ranges of Age and Obesity
Authors: Ryan Alice S. , Berman Dora M. , Nicklas Barbara J. , Sinha Madhur , Gingerich Ronald L. , Meneilly Grady S. , Egan Josephine M. , Elahi Dariush 
Published: March 2007

OBJECTIVE—The purpose of this study was to determine the relationships between plasma adiponectin and leptin levels, total and central obesity, and glucose utilization across the adult age span.
RESEARCH DESIGN AND METHODS—We studied 148 women aged 18–81 years with a BMI range of 17.2–44.3 kg/m2. Total percent body fat was determined by dual-energy X-ray absorptiometry and abdominal fat by computed tomography. Glucose tolerance in non-type 2 diabetic volunteers was determined with an oral glucose tolerance test. Glucose utilization (M) was measured during the last 60 min of hyperinsulinemic-euglycemic clamps (240 pmol · m−2 · min−1). Plasma adiponectin levels were measured by radioimmunoassay. The women were separated into three age-groups: young, middle, and old (&lt;40, 40–59, and ≥60 years, respectively), as well as by glucose tolerance status.
RESULTS—Adiponectin concentrations did not differ by age-groups. There were significant age effects for BMI, percent body fat, visceral fat, subcutaneous abdominal fat, Vo2max, and M. Adiponectin levels were lower in the prediabetic women (n = 18) than in the normal glucose-tolerant women (n = 108) and the women with type 2 diabetes (n = 22) (both P &lt; 0.05). Univariate correlations revealed significant negative relationships between plasma adiponectin levels and BMI, percent body fat, visceral fat, subcutaneous abdominal fat, fasting leptin, and fasting insulin and positive relationship with M (all P &lt; 0.05). In a multiple stepwise regression model to predict adiponectin, only M remained in the model at P &lt; 0.001. Multivariate analyses revealed a significant relation for M as a function of adiponectin, insulin, and Vo2max.
CONCLUSIONS—The data suggest that plasma adiponectin does not change with age but levels are negatively associated with percent body fat, visceral fat, subcutaneous abdominal fat, insulin, and leptin levels in women. Adiponectin is positively associated with M across the age span in women.
Optimal Blood Glucose Control During 18 Years Preserves Peripheral Nerve Function in Patients With 30 Years’ Duration of Type 1 Diabetes
Authors: Larsen Jakob R. , Sjoholm Hans , Hanssen Kristian F. , Sandvik Leiv , Berg Tore J. , Dahl-Jorgensen Knut 
Published: March 2007

OBJECTIVE—To assess the association between 18 years of mean HbA1c and nerve conduction parameters of the lower limb in patients with type 1 diabetes of 30 years’ duration.
RESEARCH DESIGN AND METHODS—HbA1c has been examined prospectively since 1982 in a group of 39 patients with type 1 diabetes. Mean age at baseline was 25 years (range 18–40) with 12 years’ disease duration. The mean age at diagnosis of diabetes was 12.5 years. Nerve function of lower limbs was assessed at baseline, after 8 years, and after 18 years.
RESULTS—A total of 23 men and 16 women were studied. Mean age was 43 years. Mean HbA1c was 8.2% (range 6.6–11.3) during 18-year follow-up. Nerve conduction velocity (NCV) and nerve action potential amplitude (NAPA) at the last examination were significantly associated with mean HbA1c (P &lt; 0. 05). From 1982 to 1999, there was a significant reduction in nerve function in patients with mean HbA1c ≥8.4% (highest tertile). For example, the mean NCV in the tibial nerve was reduced from 47 to 31 m/s (P &lt; 0.01). The number of nerves with NCV (P &lt; 0.01) and NAPA (P = 0.01) reduced to below the reference level in each patient was also significantly associated to mean HbA1c. No significant associations were found between nerve function parameters, sex, disease duration, blood pressure, serum cholesterol, microalbuminuria, or smoking.
CONCLUSIONS—The present study shows that mean HbA1c is a strong predictor of nerve function. Mean HbA1c &lt;8.4% over 18 years was associated with near-normal nerve function.
ACE Inhibitors Improve Diabetic Nephropathy Through Suppression of Renal MCP-1
Authors: Amann Berthold , Tinzmann Ralph , Angelkort Bernhard 
Published: March 2007

OBJECTIVE—Chemokines play an important role in the pathogenesis of diabetic nephropathy. Angiotensin II induces several fibrogenic chemokines, namely monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor-β. The progression of diabetic nephropathy can be retarded by ACE inhibitors (ACEIs) in patients with type 1 and type 2 diabetes. We examined if blockade of the renin-angiotensin system lowered urinary levels of the chemokine MCP-1 and correlated urinary MCP-1 (uMCP-1) with parameters of renal function and glucose and lipid metabolism before and after 1 year of treatment with an ACE inhibitor.RESEARCH DESIGN AND METHODS—In 22 patients with type 2 diabetes and diabetic nephropathy in stages 3–5, treatment with the ACEI lisinopril was initiated. Before treatment and after 12 months of continuous therapy, proteinuria, creatinine clearance, uMCP-1 levels, BMI, HbA1c, and serum cholesterol were assessed.RESULTS—Lisinopril treatment improved renal function. Proteinuria decreased from 410 ± 662 mg per 24 h to 270 ± 389 mg per 24 h. Creatinine clearance rose from 61 ± 26 to 77 ± 41 ml/min. Urinary MCP-1 levels decreased from 0.456 ± 0.22 ng/mg creatinine to 0.08 ± 0.096 ng/mg creatinine. The change in uMCP-1 correlated significantly (r = 0.61, P &lt; 0.001) with the change in proteinuria. No other parameter correlated with the improvement in renal function.CONCLUSIONS—Blockade of the renin-angiotensin system in type 2 diabetic patients with diabetic nephropathy reduces uMCP-1 levels and improves renal function. Because MCP-1 induces monocyte immigration and differentiation to macrophages, which augment extracellular matrix production and tubulointerstitial fibrosis, pharmacological reduction of angiotensin II may also exert its beneficial effects in diabetic nephropathy by downregulation of renal MCP-1.
Costs of Screening for Pre-diabetes Among U.S. Adults
Authors: Zhang Ping , Engelgau Michael M. , Valdez Rodolfo , Benjamin Stephanie M. , Cadwell Betsy , Venkat Narayan K.M. 
Published: March 2007

OBJECTIVE—We evaluated various strategies to identify individuals aged 45–74 years with pre-diabetes (either impaired glucose tolerance or impaired fasting glucose).
RESEARCH DESIGN AND METHODS—We conducted a cost analysis to evaluate the effectiveness (proportion of cases identified), total costs, and efficiency (cost per case identified) of five detection strategies: an oral glucose tolerance test (OGTT), a fasting plasma glucose (FPG) test, an HbA1c test, a capillary blood glucose (CBG) test, and a risk assessment questionnaire. For the first strategy, all individuals received an OGTT. For the last four strategies, only those with a positive screening test received an OGTT. Data were from the Third U.S. National Health and Nutrition Examination Survey, 2000 census, Medicare, and published literature. One-time screening costs were estimated from both a single-payer perspective and a societal perspective.
RESULTS—The proportion of pre-diabetes and undiagnosed diabetes identified ranged from 69% to 100% (12.1–17.5 million). The cost per case identified ranged from $176 to $236 from a single-payer perspective and from $247 to $332 from a societal perspective. Testing all with OGTT was the most effective strategy, but the CBG test and risk assessment questionnaire were the most efficient. If people are substantially less willing to take an OGTT than a FPG test, then the FPG testing strategy was the most effective strategy.
CONCLUSIONS—There is a tradeoff between effectiveness and efficiency in choosing a strategy. The most favorable strategy depends on if the goal of the screening program is to identify more cases or to pursue the lowest cost per case. The expected percentage of the population willing to take an OGTT is also a consideration.
Urinary Connective Tissue Growth Factor Excretion in Patients With Type 1 Diabetes and Nephropathy
Authors: Gilbert Richard E. , Akdeniz Aysel , Weitz Stephen , Usinger William R. , Molineaux Christopher , Jones Susan E. , Langham Robyn G. , Jerums George 
Published: March 2007

OBJECTIVE—Excretion of growth factors in the urine has been implicated in the pathogenesis of tubulointerstitial disease that characterizes proteinuric renal disease. In this cross-sectional study, we sought to examine the urinary excretion of the profibrotic cytokine connective tissue growth factor (CTGF) in type 1 diabetic patients with incipient and overt diabetic nephropathy.
RESEARCH DESIGN AND METHODS—We recruited 31 subjects with type 1 diabetes from a hospital diabetes outpatient clinic. Of these, 10 subjects were normoalbuminuric, 8 were microalbuminuric and not receiving ACE inhibitor treatment, and 13 were macroalbuminuric, 8 of whom were receiving ACE inhibitor treatment. Urinary CTGF NH2-terminal fragment (CTGF-N) was determined by enzyme-linked immunosorbent assay and expressed relative to urinary creatinine.
RESULTS—Urinary CTGF-N was closely correlated with the degree of albuminuria (r = 0.76, P &lt; 0.001). In comparison with normoalbuminuric subjects, urinary CTGF-N was increased 10- and 100-fold in micro- and untreated macroalbuminuric subjects, respectively (CTGF-N–to–creatinine ratio: normoalbuminuria 0.23 ×/÷ 1.3 ng/mg, microalbuminuria 2.1 ×/÷ 1.7 ng/mg, untreated macroalbuminuria 203 ×/÷ 3.8 ng/mg, and geometric mean ×/÷ tolerance factor; P &lt; 0.05 for normoalbuminuria versus microalbuminuria, P &lt; 0.001 for microalbuminuria versus macroalbuminuria). Urinary CTGF-N was lower (&lt;30-fold) in macroalbuminuric subjects treated with ACE inhibitors (6.5 ×/÷ 1.7 ng/mg; P &lt; 0.01 vs. untreated macroalbuminuria) compared with their untreated counterparts.
CONCLUSIONS—In this cross-sectional study, the magnitude of urinary CTGF-N excretion was related to the severity of diabetic nephropathy. In the context of its known profibrotic actions, these findings suggest that CTGF may contribute to the chronic tubulointerstitial fibrosis that accompanies proteinuric renal disease. Prospective and interventional studies will be needed to determine whether urinary CTGF-N may provide a reliable surrogate marker of renal injury and a meaningful indicator of response to therapy.