bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accumulation of NH2-Terminal Fragment of Connective Tissue Growth Factor in the Vitreous of Patients With Proliferative Diabetic Retinopathy
Authors: Hinton David R. , Spee Christine , He Shikun , Weitz Stephen , Usinger William , LaBree Laurie , Oliver Noelynn , Lim Jennifer I. 
Published: March 2007

OBJECTIVE—To evaluate the expression of connective tissue growth factor (CTGF) and its fragments in the vitreous of patients with proliferative diabetic retinopathy (PDR) and to localize CTGF expression in associated preretinal membranes.
RESEARCH DESIGN AND METHODS—Vitreous was obtained from 24 patients with active PDR, 4 patients with quiescent PDR, and 23 patients with other retinal diseases and no diabetes, including 5 patients with vitreous hemorrhage. Enzyme-linked immunosorbent assay was used to determine levels of whole CTGF and its NH2- and COOH-terminal fragments. Preretinal membranes from three patients with active PDR were stained immunohistochemically for the presence of CTGF and cell type-specific markers.
RESULTS—A significant increase in NH2-terminal CTGF fragment content was found in vitreous samples from patients with active PDR when compared with samples from nondiabetic patients (P &lt; 0.0001) or patients with quiescent PDR (P = 0.02). Levels of NH2-terminal CTGF were also greater in vitreous samples from diabetic patients with vitreous hemorrhage compared with samples from nondiabetic patients with vitreous hemorrhage (P = 0.02). Vitreous levels of whole CTGF were similar in all groups. COOH-terminal fragments of CTGF were not detected. CTGF immunoreactivity was predominantly localized to smooth muscle actin-positive myofibroblasts within active PDR membranes.
CONCLUSIONS—NH2-terminal CTGF fragment content is increased in the vitreous of patients with active PDR, suggesting that it plays a pathogenic role or represents a surrogate marker of CTGF activity in the disorder. The localization of CTGF in myofibroblasts suggests a local paracrine mechanism for induction of fibrosis and neovascularization.
Diabetes and Oral Tumors in Hungary
Authors: Ujpál Márta , Matos Orsolya , Bíbok György , Somogyi Anikó , Szabó György , Suba Zsuzsanna 
Published: March 2007

OBJECTIVE—Numerous publications have already demonstrated that diabetes is a risk factor for the development of periodontal diseases and various inflammatory lesions in the oral mucosa. A possible correlation between diabetes and oral premalignancies and tumors was examined in this study, as no literature data are available concerning this problem.RESEARCH DESIGN AND METHODS—Stomato-oncological screening was carried out on 200 diabetic patients in the medical departments; the control group included 280 adult dentistry outpatients. The lesions found were classified into three groups: inflammatory lesions, benign tumors, and precancerous lesions. A retrospective diabetes screening of 610 inpatients with histologically confirmed oral malignancies was also performed. The control group comprised 574 complaint- and tumor-free adults. Fasting blood glucose levels were determined in both groups, and the tumor location was registered in the cancer patients.RESULTS—Benign tumors were found in 14.5% and precancerous lesions in 8% of diabetic patients. In the control group these values were significantly lower, at 6.4 and 3.2%, respectively (P &gt; 0.01). Earlier Hungarian screening studies indicated similar frequency of these lesions in the general population. The proportion of oral cavity lesions was higher among diabetic patients compared with that of the control patients. In the oral cancer patient group, diabetes was present in 14.6% and an elevated blood glucose level in 9.7%. These values are significantly higher than those for the tumor-free control group (P &lt; 0.01). The gingival and labial tumor location was significantly more frequent among diabetic cancer patients than in the nondiabetic group (P &lt; 0.01). The combination of diabetes and smoking means a higher risk for oral precancerous lesions and malignancies.CONCLUSIONS—Diabetes may be a risk factor for oral premalignancies and tumors.
Cost Analysis of Human Islet Transplantation for the Treatment of Type 1 Diabetes in the Swiss-French Consortium GRAGIL
Authors: Guignard Adrienne P. , Oberholzer José , Benhamou Pierre-Yves , Touzet Sandrine , Bucher Pascal , Penfornis Alfred , Bayle François , Kessler Laurence , Thivolet Charles , Badet Lionel , Morel Philippe , Colin Cyril ,   On behalf of the GRAGIL Group
Published: March 2007

OBJECTIVE—To evaluate the cost of islet transplantation in type 1 diabetic patients with a functional renal graft in a multicenter network.
RESEARCH DESIGN AND METHODS—The study involved nine diabetic patients transplanted in the Swiss-French Groupe Rhône-Alpes, Rhin et Geneve pour la transplantation d’Ilots Langerhans (GRAGIL) consortium between March 1999 and June 2000. The direct medical costs were estimated from Social Security’s perspective from the inclusion of the patient to 1 year after transplantation. All cost components were computed separately and included evaluation, screening and candidacy, organ retrieval, islet processing, pancreas and islet transportation, hospitalization for transplantation, follow-up, medications (immunosuppressive, antidiabetic, and adjuvant drugs), and adverse events requiring hospitalization.
RESULTS—During the study period, 56 pancreata were processed and 14 islet preparations were transplanted. The average cost of an islet transplantation (procedure and 1-year follow-up) was €77,745 (French rate, year 2000). The four main cost components were islet preparation (30% of the total cost), adverse events (24%), drugs (14%), and hospitalization (13%).
CONCLUSIONS—Overall costs of islet transplantation are slightly higher than those of pancreas transplantation. The cell isolation process is a critical point; a reduction in overall cost will require more efficient ways of isolating high yields of viable islets. Costs generated by shipments within the GRAGIL network did not represent an economic burden. It can be expected that the costs will decrease with growing experience and improving technology.
l-Arginine-Induced Vasodilation of the Renal Vasculature Is Preserved in Uremic Type 1 Diabetic Patients After Kidney and Pancreas but not After Kidney-Alone Transplantation
Authors: De Cobelli Francesco , Fiorina Paolo , Perseghin Gianluca , Magnone Marta , Venturini Massimo , Zerbini Gianpaolo , Zanello Alessandro , Mazzolari Gabriella , Monti Lucilla , Di Carlo Valerio , Secchi Antonio , Del Maschio Alessandro 
Published: March 2007

OBJECTIVE—In uremic type 1 diabetic patients, kidney and pancreas transplantation (KP) and kidney-alone transplantation (KD) provide full restoration of normal renal function; however, only KP, i.e., curing diabetes, is expected to prevent endothelial damages. Our aim was to study l-arginine-induced vasodilation of the renal vasculature in uremic type 1 diabetic patients after KP or KD using magnetic resonance (MR).
RESEARCH DESIGN AND METHODS—MR quantitative flow measurements were performed in 15 KP patients (mean age 39.0 ± 1.7 years, 10 men and 5 women), in 11 KD patients (mean age 47.3 ± 1.9 years, 7 men and 4 women), and in 8 nondiabetic kidney transplant patients (mean age 44.0 ± 4.8 years, 7 men and 1 woman), who were used as control subjects, to measure renal blood flow and velocity and renal vascular resistance before and immediately after infusion of l-arginine.
RESULTS—Renal blood flow and velocity were not different at baseline in KP, KD, and control subjects. In contrast, during l-arginine administration renal blood flow increased significantly in KP subjects (basal 8.4 ± 0.6 vs. post 9.6 ± 0.8 ml/s, Δ 14.3 ± 4.4%, P &lt; 0.05) and in control subjects (basal 9.3 ± 0.8 vs. post 9.1 ± 0.8 ml/s, Δ 17.3 ± 6.2%, P &lt; 0.01), while it remained unchanged in KD subjects (basal 10.0 ± 0.8 vs. post 11.6 ± 0.9 ml/s, Δ −1.36 ± 6.9%, NS). Parallel results have been achieved for renal blood velocity (KP subjects: 20.1 ± 4.9%, P &lt; 0.01; control subjects: 23.0 ± 7.99%, P &lt; 0.01; and KD subjects: −0.3 ± 6.5%; NS). A reduction in renal vascular resistance in response to l-arginine was evident in KP and control subjects but not in KD patients.
CONCLUSIONS—l-Arginine vasodilatory response was successfully assessed with MR quantitative flow measurements. KP patients and control subjects, but not those with KD, showed a preserved l-arginine-induced vasodilation of the renal vasculature.
Short-Term Intensive Insulin Therapy in Newly Diagnosed Type 2 Diabetes
Authors: Ryan Edmond A. , Imes Sharleen , Wallace Clarissa 
Published: March 2007

OBJECTIVE—Type 2 diabetes is associated with defects in insulin secretion and insulin action. Hyperglycemia may aggravate these defects, a feature known as glucose toxicity. Previous studies have shown that acute correction of hyperglycemia in subjects with long-standing type 2 diabetes gives only short-term improvement in glycemic control after discontinuation of insulin. The current study attempts to identify any characteristics of patients with newly diagnosed type 2 diabetes (fasting glucose &gt;11.0 mmol/l) who would have a long-term benefit, in terms of glycemic control, from a brief course of insulin therapy.
RESEARCH DESIGN AND METHODS—A total of 16 subjects (52 ± 2 years old [range 36–64], BMI 30.8 ± 1.9 kg/m2) with newly diagnosed type 2 diabetes had a 2–3 week course of intensive insulin therapy that was then discontinued.
RESULTS—Fasting glucose fell from 13.3 ± 0.7 to 7.0 ± 0.4 mmol/l, and this improvement was maintained at the 1-year follow-up (6.7 ± 0.3 mmol/l). The insulin area under the curve for the posttreatment oral glucose tolerance test also improved (8,251 ± 1,880 before therapy, 18,404 ± 4,040 directly after insulin therapy, and 42,368 ± 8,517 pmol · min at the 1-year follow-up). At 1 year, seven of the subjects maintained good glycemic control on diet therapy alone, eight required oral hypoglycemic agent (OHA) therapy, and one required insulin therapy. The distinguishing features of those who did not require OHA or insulin therapy were that they required less insulin during the active insulin therapy phase (0.37 ± 0.05 vs. 0.73 ± 0.07 units · kg−1 · day−1) and were able to attain a lower fasting serum glucose at the end of the period of insulin therapy (5.9 ± 0.3 vs. 7.7 ± 0.4 mmol/l).
CONCLUSIONS—These results demonstrate that in newly diagnosed type 2 diabetes with elevated fasting glucose levels, a 2- to 3-week course of intensive insulin therapy can successfully lay a foundation for prolonged good glycemic control. The ease with which normoglycemia is achieved on insulin may predict those patients who can later succeed in controlling glucose levels with attention to diet alone.
Diabetes, Depression, and Quality of Life
Authors: Goldney Robert D. , Phillips Pat J. , Fisher Laura J. , Wilson David H. 
Published: March 2007

OBJECTIVE—The aim of the study was to assess the prevalence of diabetes and depression and their associations with quality of life using a representative population sample.
RESEARCH DESIGN AND METHODS—The study consisted of a representative population sample of individuals aged ≥15 years living in South Australia comprising 3,010 personal interviews conducted by trained health interviewers. The prevalence of depression in those suffering doctor-diagnosed diabetes and comparative effects of diabetic status and depression on quality-of-life dimensions were measured.
RESULTS—The prevalence of depression in the diabetic population was 24% compared with 17% in the nondiabetic population. Those with diabetes and depression experienced an impact with a large effect size on every dimension of the Short Form Health-Related Quality-of-Life Questionnaire (SF-36) as compared with those who suffered diabetes and who were not depressed. A supplementary analysis comparing both depressed diabetic and depressed nondiabetic groups showed there were statistically significant differences in the quality-of-life effects between the two depressed populations in the physical and mental component summaries of the SF-36.
CONCLUSIONS—Depression for those with diabetes is an important comorbidity that requires careful management because of its severe impact on quality of life.
Atorvastatin Decreases Apolipoprotein C-III in Apolipoprotein B-Containing Lipoprotein and HDL in Type 2 Diabetes
Authors: Dallinga-Thie Geesje M. , Berk-Planken Ingrid I.L. , Bootsma Aart H. , Jansen Hans ,   on behalf of the Diabetes Atorvastatin Lipid Intervention (DALI) Study Group
Published: March 2007

OBJECTIVE—Apolipoprotein (apo)C-III is a constituent of HDL (HDL apoC-III) and of apoB-containing lipoproteins (LpB:C-III). It slows the clearance of triglyceride-rich lipoproteins (TRLs) by inhibition of the activity of the enzyme lipoprotein lipase (LPL) and by interference with lipoprotein binding to cell-surface receptors. Elevated plasma LpB:C-III is an independent risk factor for cardiovascular disease. We studied the effect of atorvastatin on plasma LpB:C-III and HDL apoC-III.
RESEARCH DESIGN AND METHODS—We studied the effect of 30 weeks’ treatment with 10 and 80 mg atorvastatin on plasma apoC-III levels in a randomized, double-blind, placebo-controlled trial involving 217 patients with type 2 diabetes and fasting plasma triglycerides between 1.5 and 6.0 mmol/l.
RESULTS—Baseline levels of total plasma apoC-III, HDL apoC-III, and LpB:C-III were 41.5 ± 10.0, 17.7 ± 5.5, and 23.8 ± 7.7 mg/l, respectively. Plasma apoC-III was strongly correlated with plasma triglycerides (r = 0.74, P &lt; 0.001). Atorvastatin 10- and 80-mg treatment significantly decreased plasma apoC-III (atorvastatin 10 mg, 21%, and 80 mg, 27%), HDL apoC-III (atorvastatin 10 mg, 22%, and 80 mg, 28%) and LpB:C-III (atorvastatin 10 mg, 23%, and 80 mg, 28%; all P &lt; 0.001). The decrease in plasma apoC-III, mainly in LpB:C-III, strongly correlated with a decrease in triglycerides (atorvastatin 10 mg, r = 0.70, and 80 mg, r = 0.78; P &lt; 0.001). Atorvastatin treatment also leads to a reduction in the HDL apoC-III-to-HDL cholesterol and HDL apoC-III-to-apoA-I ratios, indicating a change in the number of apoC-III per HDL particle (atorvastatin 10 mg, −21%, and 80 mg, −31%; P &lt; 0.001).
CONCLUSIONS—Atorvastatin treatment resulted in a significant dose-dependent reduction in plasma apoC-III, HDL apoC-III, and LpB:C-III levels in patients with type 2 diabetes. These data indicate a potentially important antiatherogenic effect of statin treatment and may explain (part of) the triglyceride-lowering effect of atorvastatin.
Changes in Insulin Sensitivity in Response to Troglitazone Do Not Differ Between Subjects With and Without the Common, Functional Pro12Ala Peroxisome Proliferator–Activated Receptor-γ2 Gene Variant
Authors: Snitker Soren , Watanabe Richard M. , Ani Ifeanyi , Xiang Anny H. , Marroquin Aura , Ochoa Cesar , Goico Jose , Shuldiner Alan R. , Buchanan Thomas A. 
Published: March 2007

OBJECTIVE—We have tested whether the Pro12Ala variant of the peroxisome proliferator–activated receptor (PPAR)-γ nuclear receptor involved in thiazolidinedione (TZD) action accounted for the failure of troglitazone to increase insulin sensitivity in nondiabetic Hispanic women with previous gestational diabetes treated in the Troglitazone in Prevention of Diabetes (TRIPOD) study.
RESEARCH DESIGN AND METHODS—Ninety-three women assigned to troglitazone had intravenous glucose tolerance tests at randomization and after 3 months of treatment with troglitazone, 400 mg/day, and were genotyped for the Pro12Ala variant of the PPAR-γ gene. Subjects were divided into tertiles based on their change in minimal model insulin sensitivity (Si) during the first 3 months of troglitazone treatment.
RESULTS—The mean changes in Si in the bottom, middle, and top tertiles of Si response were −0.21 ± 0.57, 0.91 ± 0.26, and 2.58 ± 1.32 min−1 per μU/ml · 10−4, respectively. Frequencies of the Ala/− genotype were 30, 22, and 26% in the same three tertiles (P = 0.77). Analysis of phenotypes by genotype revealed only small differences between the Pro/Pro and Ala/− groups, respectively, in baseline Si (2.76 ± 0.19 vs. 2.33 ± 0.33 × 10−4 min−1 per μU/ml; P = 0.27), the change in Si after 3 months of troglitazone treatment (1.19 ± 0.17 vs. 0.93 ± 0.30; P = 0.46), and the cumulative incidence of diabetes during a median follow-up of 30 months (13 vs. 17%; P = 0.66).
CONCLUSIONS—Among young Hispanic women at high risk for type 2 diabetes, the Pro12Ala variant of the PPAR-γ receptor gene did not explain the failure of ∼1/3 of subjects to increase their insulin sensitivity when placed on troglitazone at a dose of 400 mg/day.
Acute Alcohol Consumption Improves Insulin Action Without Affecting Insulin Secretion in Type 2 Diabetic Subjects
Authors: Avogaro Angelo , Watanabe Richard M. , Dall’Arche Alessandra , Vigili De Kreutzenberg Saula , Tiengo Antonio , Pacini Giovanni 
Published: March 2007

OBJECTIVE—Long-term exposure to alcohol is associated with an improvement in insulin sensitivity. At this time, however, there is no definitive proof that alcohol per se has an effect on the insulin sensitivity index (Si) in type 2 diabetes patients. The aim of the present study was to assess the role of acute moderate alcohol intake on insulin sensitivity and insulin secretion in comparable subjects with and without type 2 diabetes.
RESEARCH DESIGN AND METHODS—Frequently sampled intravenous glucose tolerance tests (FSIGTs) were performed twice on eight healthy and eight type 2 diabetic volunteers. Forty grams of alcohol (vodka 40% wt/vol) or tap water were sipped from time −60 min to the end of the FSIGT.
RESULTS—Lactate area under the curve (AUC) was higher in both groups during the alcohol study than in the control study. Free fatty acid (FFA) AUC was higher in type 2 diabetic subjects than in control subjects; alcohol slightly reduced FFA by 17% in control subjects (34 ± 4 mmol · min−1 · l−1; P = 0.1) but significantly decreased FFA by 23% in type 2 diabetic subjects (54 ± 10; P = 0.007). β-Cell response was markedly reduced in type 2 diabetic subjects regardless of the type of study. Alcohol significantly increased Si in both groups.
CONCLUSIONS—Acute alcohol consumption improves insulin action without affecting β-cell secretion. This effect may be partly due to the inhibitory effect of alcohol on lipolysis. Alcohol intake increases insulin sensitivity and may partly explain both the J-shaped relationship between the prevalence of diabetes and the amount of alcohol consumption and the decreased mortality for myocardial infarction.
Serum γ-Glutamyltransferase and Risk of Metabolic Syndrome and Type 2 Diabetes in Middle-Aged Japanese Men
Authors: Nakanishi Noriyuki , Suzuki Kenji , Tatara Kozo 
Published: March 2007

OBJECTIVE—To investigate the association between serum γ-glutamyltransferase (GGT) and risk of metabolic syndrome and type 2 diabetes in Japanese male office workers.
RESEARCH DESIGN AND METHODS—This study included 2,957 metabolic syndrome-free men and 3,260 nondiabetic men aged 35–59 years who did not have medication for hepatitis, alanine aminotransferase (ALT) levels higher than three times the upper limit of the reference range, or a history of cardiovascular disease at study entry. Subjects were reexamined at periodic annual health examinations over a 7-year period. We used a modified National Cholesterol Education Program definition of metabolic syndrome with BMI instead of waist circumference and the revised criteria of the American Diabetes Association for type 2 diabetes.
RESULTS—With adjustment for age, family history of diabetes, BMI, alcohol intake, cigarette smoking, regular physical activity (fasting plasma glucose for the risk of type 2 diabetes), and white blood cell (WBC) count, the risk of metabolic syndrome and type 2 diabetes increased in correlation with the levels of serum GGT, ALT, aspartate aminotransferase (AST), and alkaline phosphatase. Additional adjustment for all of the other liver enzymes attenuated these associations, but serum GGT remained a significant risk factor for the risk of both metabolic syndrome and type 2 diabetes (P for trend &lt;0.001 for both). Top one-fifth versus bottom one-fifth relative risks of metabolic syndrome and type 2 diabetes were 2.23 (95% CI 1.51–3.30) and 2.44 (1.34–4.46), respectively.
CONCLUSIONS—These results indicate that serum GGT may be an important predictor for developing metabolic syndrome and type 2 diabetes in middle-aged Japanese men.
Insulin Resistance, Impaired Early Insulin Response, and Insulin Propeptides as Predictors of the Development of Type 2 Diabetes
Authors: Zethelius Björn , Hales C. Nicholas , Lithell Hans O. , Berne Christian 
Published: March 2007

OBJECTIVE—Defects in insulin secretion and insulin action are the major abnormalities in the development of type 2 diabetes. In middle-aged subjects, elevated plasma proinsulin has been found to predict type 2 diabetes. Therefore, our aim was to study the longitudinal relationships between baseline determinations of insulin sensitivity index (Si) assessed by euglycemic insulin clamp, the early insulin response (EIR) at an oral glucose tolerance test (OGTT), fasting intact proinsulin, 32–33 split proinsulin and specific insulin, and the development of type 2 diabetes in a population-based cohort of 70-year-old nondiabetic men (n = 667) with 7-year follow-up.
RESEARCH DESIGN AND METHODS—A euglycemic insulin clamp study and a 75-g OGTT were performed at baseline, and fasting peptide concentrations were measured using specific two-site immunometric assays. Results from logistic regression models are presented as odds ratios (ORs) with 95% CIs for a 1-SD increase in the predictor variable.
RESULTS—In separate multivariate analyses adjusted for EIR (OR 0.72, 95% CI 0.59–0.89) and Si (0.68, 0.58–0.88), 32–33 split proinsulin (1.49, 1.18–1.88) or intact proinsulin (1.30, 1.04–1.63) were significantly associated with the development of type 2 diabetes, whereas specific insulin (1.24, 0.91–1.66) was not. The significant associations between 32–33 split or intact proinsulin and the development of type 2 diabetes were unaltered after adjustment for BMI and glucose tolerance.
CONCLUSIONS—Insulin propeptides predicted type 2 diabetes over a 7-year period in elderly men, independent of the EIR and Si.