scholarly journals Deficient Activity of Mitochondrial Flavine Adenine Dinucleotide-Linked Glycerophosphate Dehydrogenase in Pancreatic Islet Beta Cells as a Determinant of Non-Insulin-Dependent Diabetes Mellitus

2018 ◽  
Vol 8 (2-3) ◽  
pp. 16-26
Author(s):  
Willy J. Malaisse
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Pancreatic Islet ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Islet Beta Cells ◽  
Glycerophosphate Dehydrogenase ◽  
Pancreatic Islet Beta Cells ◽  
Insulin Dependent ◽  
Deficient Activity

scholarly journals Effect of an oral α2-adrenergic blocker (MK-912) on pancreatic islet function in non-insulin-dependent diabetes mellitus

Metabolism ◽  
1991 ◽  
Vol 40 (11) ◽  
pp. 1160-1167 ◽  
Author(s):  
F.Javier Ortiz-Alonso ◽  
William H. Herman ◽  
Barry J. Gertz ◽  
Vanessa C. Williams ◽  
Marla J. Smith ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Pancreatic Islet ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Islet Function ◽  
Adrenergic Blocker ◽  
Insulin Dependent

scholarly journals Deficient Activity of FAD-Linked Glycerophosphate Dehydrogenase in the Mitochondria of Insulin-Producing Pancreatic Islets B-Cells: A Possible Cause of the Metabolic Syndrome

2020 ◽  
pp. 1-3
Author(s):  
Willy J. Malaisse ◽  
Willy J. Malaisse ◽  
Zoheir Mellouk
Keyword(s):  
Metabolic Syndrome ◽  
B Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Glycerophosphate Dehydrogenase ◽  
The Metabolic Syndrome ◽  
Insulin Dependent ◽  
Deficient Activity

A deficient activity of mitochondrial FAD-linked glycerophosphate dehydrogenase in insulin-producing pancreatic islet B-cells was recently identified in selected animal models of non-insulin-dependent diabetes mellitus. The incidence of this enzymatic defect remains however to be unambiguously documented in type-2 diabetic patients. The present review mainly aims at speculating that the altered recognition of nutrients, especially D-glucose, by pancreatic B-cells, as resulting from the abovementioned enzymatic perturbation could also eventually lead to the development of the metabolic syndrome (MetS).

scholarly journals Endogenous secretion of insulin and its relationship with immunogenetic markers in infants with insulin-dependent diabetes mellitus

1995 ◽  
Vol 41 (1) ◽  
pp. 4-6
Author(s):  
I. V. Osokina ◽  
L. N. Scherbacheva ◽  
N. B. Lebedev ◽  
I. M. Belovalova ◽  
A. P. Knyazeva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
High Risk ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
C Peptide ◽  
Insulin Dependent ◽  
Hla Phenotype

The level of C-peptide is a marker determining the clinical course of insulin-dependent diabetes mellitus (IDDM). The factors influencing the volume of residual endogenous secretion of insulin in IDDM patients are not yet well known. In order to elucidate the effect of HLA-phenotype on the residual function .of pancreatic beta-cells and the course of diabetes, 114 children, 55 boys and 59 girls aged 8 months to 6.5 years, suffering from IDDM, were examined. HLA phenotype was detected by the standard microlymphocytotoxic test. Fifty-nine HLA antigens of classes I and II, locuses A, B, DR, DQ were taken into consideration. Basal and radial C-peptide was assessed by radioimmunoassay. The pancreatic insulin-secretory function was found reduced in young patients with IDDM. The mean values of C- peptide were 0.13 ± 0.01 nmol/liter. Residual secretion of insulin was revealed in 56.2% of children. HLA markers of high risk of IDDM development in the first yeais of life were revealed: DQw3. DR3/4. DR4, DR3, B8 antigens. The markers of high risk of diabetes DR3 and DR4, and moreover, DR3/4. as well as the age by the disease onset and duration of IDDM were found to influence the size and duration of functioning of beta-cells.

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