Erratum to: Review of the nutritional benefits and risks related to intense sweeteners.

[This corrects the article DOI: 10.1186/s13690-015-0092-x.].

Fasting apoprotein B-48 level and coronary artery disease in a population without frank fasting hypertriglyceridemia.

The aim of this study was to test the hypothesis that fasting apoprotein B-48 level might be a surrogate marker of postprandial lipemia in evaluating the risk of coronary artery disease (CAD) in a population without frank abnormality in fasting lipid profile. One hundred twenty-three patients tested by coronary angiography were selected on the criteria of absence of treatment with hypolipidemic drugs, obvious hypertriglyceridemia (>2.85 mmol/L), or other conditions that may interfere with lipoprotein metabolism except diabetes. CAD was defined by more than 50% narrowing of vessel lumen, and its severity is determined by the number of arteries involved. Fasting apoprotein B-48 was measured by a competitive enzyme-linked immunosorbent assay method. There was no difference in fasting apoprotein B-48 levels between the groups with and without CAD (0.123+/-0.096 vs 0.136+/-0.125 microg/mL, respectively), whatever the sex or whether with or without diabetes. The apoprotein B-48 level was not related to the presence or the severity of CAD. There was also no correlation between fasting apoprotein B-48 levels and age, sex, body mass index, and usual fasting lipid parameters in both patients with and without angiographically proven CAD. Finally, among the features of metabolic syndrome, apoprotein B-48 was correlated with fasting triglyceride levels (r=0.357, P<.01) only. In conclusion, the present study shows that in the absence of any major fasting abnormality in plasma lipid parameters, fasting apoprotein B-48 level, which has been associated with postprandial hyperlipidemia, does not predict the risk of CAD.

Logistics and transplant coordination activity in the GRAGIL Swiss-French multicenter network of islet transplantation.

BACKGROUND: Since the Edmonton trial in 2000, increasing numbers of transplant centers have been implementing islet transplantation programs. Some institutions have elected to associate in multicenter networks, such as the Swiss-French GRAGIL (Groupe Rhin-Rhône-Alpes-Genève pour la Transplantation d'Ilots de Langerhans) consortium. METHODS: All pancreata offers to the University of Geneva Cell Isolation and Transplantation Center from within the network in 2002 and 2003 were reviewed. Islet preparations were attributed to the most suitable recipient on a centrally managed waiting list. All shipments were performed by ambulance in less than 5 hr. RESULTS: Over the period of study, 260 pancreata were offered, from a total of 1,304 cadaveric donors in the four allocation regions (20%). Fifty-two patients were on the waiting list at any time during this 2-year period. The percentage of organs offered varied in the range of 0.5% to 42%, depending on region of origin, with a correlation with number of patients on the waiting list in each region. Of these, 104 (40%) were accepted for processing. Ninety-two pancreata were actually processed, resulting in 42 islet preparations being transplanted. The number of international equivalents of transplanted preparations was 378,500+/-16,000 versus 165,400+/-15,400 (P<0.0001) for nontransplanted preparations. Total cold ischemia time was 6+/-0.3 hr for transplanted preparations versus 6.7+/-0.4 hr for nontransplanted preparations (not significant). CONCLUSIONS.: A high rate of pancreas offers, successful isolation, and islet transplantation can be achieved in multicenter networks such as GRAGIL. Such an approach can expand both the donor pool and the recipient population.

Influence of islet transportation on pancreatic islet allotransplantation in type 1 diabetic patients within the Swiss-French GRAGIL network.

BACKGROUND: The influence of islet transportation on pancreatic islet allotransplantation in type 1 diabetic patients was evaluated within the GRAGIL network. PATIENTS AND METHODS: From December 2001 to April 2003, 16 human pancreatic islet transplants were performed in 9 type 1 diabetic patients with an established kidney graft (functioning for at least 6 months) in four centers of the GRAGIL network. Islet isolation was performed in a core laboratory in Geneva, and the islet preparations were shipped by ambulance to each center for transplantation. One month after transplantation, the efficiency of the graft was assessed according to islet transportation time (ITT): ITT less than 2 hours (group 1, n=5), and ITT greater than 4.5 hours (group 2, n=4, mediant 5 hours). RESULTS: Primary graft dysfunction was observed in one patient in group 1 after one month. Two patients became insulin independent in groups 1 and 2. All other patients in both groups had a plasma C-peptide level greater than 0.5 ng/ml. The HbA1c level and the exogenous insulin needs decreased in both groups. CONCLUSIONS: ITT does not seem to influence the efficiency of pancreatic islet allotransplantation in type 1 diabetic patients. These results emphasize the scope for multicenter networks such as the GRAGIL group.

No association between lck gene polymorphisms and protein level in type 1 diabetes.

We previously described a reduced expression of the protein tyrosine kinase Lck in T-cells from type 1 diabetic patients, the origin of which is still unknown. The human lck gene, located on chromosome 1p35-34.3, was evaluated as a candidate susceptibility gene for type 1 diabetes. A molecular scan of the sequence variations in the coding, the relevant promoter, and most of the intronic sequences of the lck gene (representing a total of 10.5 kb fragment) was performed in 187 Caucasian subjects including 91 type 1 diabetic patients and 96 normoglycemic control subjects. We identified 35 sequence variations, including one deletion and 34 single nucleotide polymorphisms (SNPs), 33 of them being new. Four variants were frequent but not significantly associated with diabetes or Lck protein level. Of the SNP variants, 11 were only found within the diabetic population and some were associated with low Lck protein levels. The low frequency of these polymorphisms did not permit any statistically significant correlations with the disease status, suggesting that the lck gene probably does not contribute to genetic susceptibility to type 1 diabetes.