Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by J Peter
Total Records ( 2 ) for J Peter
  A. P Beigneux , R Franssen , A Bensadoun , P Gin , K Melford , J Peter , R. L Walzem , M. M Weinstein , B. S.J Davies , J. A Kuivenhoven , J. J.P Kastelein , L. G Fong , G. M Dallinga Thie and S. G. Young

Objective— GPIHBP1 is an endothelial cell protein that binds lipoprotein lipase (LPL) and chylomicrons. Because GPIHBP1 deficiency causes chylomicronemia in mice, we sought to determine whether some cases of chylomicronemia in humans could be attributable to defective GPIHBP1 proteins.

Methods and Results— Patients with severe hypertriglyceridemia (n=60, with plasma triglycerides above the 95th percentile for age and gender) were screened for mutations in GPIHBP1. A homozygous GPIHBP1 mutation (c.344A>C) that changed a highly conserved glutamine at residue 115 to a proline (p.Q115P) was identified in a 33-year-old male with lifelong chylomicronemia. The patient had failure-to-thrive as a child but had no history of pancreatitis. He had no mutations in LPL, APOA5, or APOC2. The Q115P substitution did not affect the ability of GPIHBP1 to reach the cell surface. However, unlike wild-type GPIHBP1, GPIHBP1-Q115P lacked the ability to bind LPL or chylomicrons (d < 1.006 g/mL lipoproteins from Gpihbp1–/– mice). Mouse GPIHBP1 with the corresponding mutation (Q114P) also could not bind LPL.

Conclusions— A homozygous missense mutation in GPIHBP1 (Q115P) was identified in a patient with chylomicronemia. The mutation eliminated the ability of GPIHBP1 to bind LPL and chylomicrons, strongly suggesting that it caused the patient’s chylomicronemia.

  J. A Dave , M. E Engel , R Freercks , J Peter , W May , M Badri , L Van Niekerk and N. S. Levitt

Background: Non-diabetic patients presenting with an acute stroke often have hyperglycaemia. In most populations it is unknown whether the hyperglycaemia is transient and due to the acute stress response or whether it represents undiagnosed abnormal glucose metabolism.

Aim: To evaluate the prevalence and predictors of persistent hyperglycaemia in non-diabetic patients with an acute stroke.

Design: Prospective observational study.

Methods: Non-diabetic patients over 40 years old with an acute stroke were enrolled over a 2-year period. On admission patients were evaluated with an HbA1c and a 75 g oral glucose tolerance test (OGTT). The OGTT was repeated 3 months later. A meta-analysis was performed to interpret our results in the context of published data.

Results: One hundred and seven patients were analysed. On admission 26 (24%) patients had diabetes, 39 (37%) had impaired glucose tolerance and 42 (39%) had normal glucose tolerance. Forty-four (68%) patients with hyperglycaemia on admission were re-investigated at least 3 months after discharge. Of these, 6 (14%) had diabetes, 12 (27%) had impaired glucose tolerance and 26 (59%) had normal glucose tolerance. A 2-h post-load glucose value ≥10 mmol/l predicted persistent hyperglycaemia with 72.2% sensitivity, 65.4% specificity and a positive predictive value and negative predictive value of 59.1 and 77.3%, respectively. A meta-analysis of prevalence data of impaired glucose metabolism in non-diabetic individuals 3 months after having had an acute stroke revealed a combined prevalence of 58% (95% confidence interval 25.4–90.5%).

Conclusion: In this study hyperglycaemia in the setting of an acute stroke was transient in the majority of patients.

Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility