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See detailGenetic polymorphism of transforming growth factor-β1 and microvascular complications in type 1 diabetes
Weekers, Laurent ULg; Hadjadj, Samy; Bouhanick, Béatrice et al

in Diabetologia (2000), 43(1), 137

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See detailDiabetogenic coxsackievirus B4 modifies cytokine secretion by human thymic epithelial cells
Brilot, Fabienne; Chehadeh, Wassim; Renard, Chantal et al

in Diabetologia (2000), 43 (Suppl. 1)

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See detailA potent diazoxide analogue activating ATP-sensitive K+ channels and inhibiting insulin release
Lebrun, P.; Arkhammar, P.; Antoine, M.-H. et al

in Diabetologia (2000), 43

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See detailLack of contribution of two endotelial nitric oxide synthase (eNOS) gene polymorphisms to diabetic nephropathy in type 1 diabetes
Weekers, Laurent ULg; Hadjadj, S.; Belloum, R. et al

in Diabetologia (1999), 42(Sup. 1), 226

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See detailThymic insulin-related polypeptides in diabetes-prone Bio-Breeding rats
Kecha, Ouafae; Winkler, Rose ULg; Martens, Henri ULg et al

in Diabetologia (1999), 42 (Suppl. 1)

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See detailVerapamil, a phenylalkylamine Ca2+ channel blocker, inhibits ATP-sensitive K+ channels in insulin-secreting cells
Lebrun, P.; Antoine, M.-H.; Ouedraogo, R. et al

in Diabetologia (1997), 40

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See detailMolecular dissection of the insulin-like growth factor axis in the human thymus
Geenen, Vincent ULg; Kecha, Ouafae; Achour, Imane et al

in Diabetologia (1997), 40

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See detailIA-2-autoantibodies complement GAD65-autoantibodies in new-onset IDDM patients and help predict impending diabetes in their siblings. The Belgian Diabetes Registry.
Gorus, F. K.; Goubert, P.; Semakula, C. et al

in Diabetologia (1997), 40(1), 95-9

IA-2 has been identified as an autoantigen that is recognized by immunoglobulins from insulin-dependent diabetic (IDDM) patients. Using a liquid phase radiobinding assay, we performed an IA-2-autoantibody ... [more ▼]

IA-2 has been identified as an autoantigen that is recognized by immunoglobulins from insulin-dependent diabetic (IDDM) patients. Using a liquid phase radiobinding assay, we performed an IA-2-autoantibody (IA-2-Ab) assay in 474 IDDM patients and 482 non-diabetic control subjects aged 0-3 years. IA-2-Ab were detected in 58% of the patients and 0.8% of control subjects. Their prevalence in patients was lower than that of islet cell autoantibodies (ICA; 73%) or glutamic acid decarboxylase (M(r) 65 kDa)-autoantibodies (GAD65-Ab; 82%) but higher than that of insulin autoantibodies (IAA; 42%). IA-2-Ab were more frequent in patients under age 20 years (70%) than between 20 and 40 years (45%; p < 0.001). In the whole IDDM group, 92% of patients were positive for at least one of the three molecular assays, which is higher than the positivity for the ICA assay (73%). Only 1% was negative in the molecular assays and positive in the ICA assay. IA-2-Ab levels were positively correlated with ICA titres (p < 0.001) and HLA DQ A1*0301-DQ B1*0.02 (p < 0.003) by multivariate analysis. In a group of 481 non-diabetic siblings (age 0-39 years) of IDDM patients only 7 were IA-2-Ab positive (1.5%). All seven were under age 20 years and positive for at least two other autoantibodies and for DQ A1*0301-DQB1*0302. Four of these seven developed IDDM during the 6-70-month follow-up period. The positive predictive value of IA-2-Ab (57%) was higher than that of ICA, GAD65-Ab or IAA alone, or in combination (< or = 20%) but these calculations are restricted by the relatively short observation period and the small number of cases. The only IA-2-Ab-negative case of pre-diabetes was also negative for IAA and GAD65-Ab, while it was strongly positive for ICA. In conclusion, IA-2-Ab show a high diagnostic specificity for IDDM and are predictive markers of impending diabetes in siblings of patients. In combination with other molecular antibody assays they may replace ICA testing in future. Our data also indicate that other autoantibodies than IA-2-Ab, GAD65-Ab and IAA contribute to ICA. [less ▲]

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See detailEffects of Ingested Fructose and Infused Glucagon on Endogenous Glucose Production in Obese Niddm Patients, Obese Non-Diabetic Subjects, and Healthy Subjects
Paquot, Nicolas ULg; Schneiter, P.; Jequier, E. et al

in Diabetologia (1996), 39(5), 580-6

Increased endogenous glucose production (EGP) and gluconeogenesis contribute to the pathogenesis of hyperglycaemia in non-insulin-dependent diabetes mellitus (NIDDM). In healthy subjects, however, EGP ... [more ▼]

Increased endogenous glucose production (EGP) and gluconeogenesis contribute to the pathogenesis of hyperglycaemia in non-insulin-dependent diabetes mellitus (NIDDM). In healthy subjects, however, EGP remains constant during administration of gluconeogenic precursors. This study was performed in order to determine whether administration of fructose increases EGP in obese NIDDM patients and obese non-diabetic subjects. Eight young healthy lean subjects, eight middle-aged obese NIDDM patients and seven middle-aged obese non-diabetic subjects were studied during hourly ingestion of 13C fructose (0.3 g.kg fat free mass-1.h-1) for 3 h. Fructose failed to increase EGP (measured with 6,6 2H glucose) in NIDDM (17.7 +/- 1.9 mumol.kg fat free mass-1.min-1 basal vs 15.9 +/- 0.9 after fructose), in obese non-diabetic subjects (12.1 +/- 0.5 basal vs 13.1 +/- 0.5 after fructose) and in lean healthy subjects (13.3 +/- 0.5 basal vs 13.8 +/- 0.6 after fructose) although 13C glucose synthesis contributed 73.2% of EGP in lean subjects, 62.6% in obese non-diabetic subjects, and 52.8% in obese NIDDM patients. Since glucagon may play an important role in the development of hyperglycaemia in NIDDM, healthy subjects were also studied during 13C fructose ingestion + hyperglucagonaemia (232 +/- 9 ng/l) and during hyperglucagonaemia alone. EGP increased by 19.8% with ingestion of fructose + glucagon (p < 0.05) but remained unchanged during administration of fructose or glucagon alone. The plasma 13C glucose enrichment was identical after fructose ingestion both with and without glucagon, indicating that the contribution of fructose gluconeogenesis to the glucose 6-phosphate pool was identical in these two conditions. We concluded that during fructose administration: 1) gluconeogenesis is increased, but EGP remains constant in NIDDM, obese non-diabetic, and lean individuals; 2) in lean individuals, both an increased glucagonaemia and an enhanced supply of gluconeogenic precursors are required to increase EGP; this increase in EGP occurs without changes in the relative proportion of glucose 6-phosphate production from fructose and from other sources (i.e. glycogenolysis + gluconeogenesis from non-fructose precursors). [less ▲]

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See detailAlterations in the ultradian oscillations of insulin secretion and plasma glucose in aging.
Scheen, André ULg; Sturis, J.; Polonsky, K. S. et al

in Diabetologia (1996), 39(5), 564-72

Normal insulin secretion includes oscillations with a period length of 80-150 min which are tightly coupled to glucose oscillations of similar period. To determine whether normal aging is associated with ... [more ▼]

Normal insulin secretion includes oscillations with a period length of 80-150 min which are tightly coupled to glucose oscillations of similar period. To determine whether normal aging is associated with alterations in these ultradian oscillations, eight, modestly overweight, older men (65 +/- 5 years) and eight weight-matched young control subjects (25 +/- 4 years) were studied during 53 h of constant glucose infusion. Blood samples were collected every 20 min and insulin secretion rates were calculated by deconvolution. Ultradian oscillations of glucose and insulin secretion were evident in both groups. Pulse frequency was similar for glucose and insulin secretion, and was not affected by age. The absolute amplitude of the glucose oscillations was similar in both groups but their relative amplitude was slightly dampened in the older adults. Both the absolute and the relative amplitudes of insulin secretory oscillations were markedly reduced in the older subjects. The normal linear increase in the amplitude of insulin oscillations occurring with increasing amplitudes of glucose oscillations was still present in the older adults but analysis of covariance indicated that the slope was significantly lower than in the young control subjects (p < 0.0005), reflecting a decreased responsiveness of the beta cell to glucose changes. The temporal concordance between insulin and glucose oscillations, as estimated by pulse concomitancy and cross-correlation, was also lower in older subjects. The similarities between the alterations in the ultradian oscillations of insulin secretion and glucose in older healthy adults and those occurring in diabetic patients suggest that an impairment of beta-cell function may play a primary role in the deterioration of glucose tolerance in aging. [less ▲]

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See detailThymic insulin-like growth factors (IGFs) in man and in an animal model of autoimmune IDDM
Geenen, Vincent ULg; Achour, Imane; Kecha, Ouafae et al

in Diabetologia (1996), 39

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See detailActivation of potassium channels in human and rodent B-cells by BPDZ-44 and BPDZ-62; mechanisms of action and effects in human neonatal nesidioblastosis
Kane, C.; Harding, E. A.; Antoine, M.-H. et al

in Diabetologia (1995), 38

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See detailATP-sensitive K+ channels and insulin release: effect of BPDZ 62
Lebrun, P.; Antoine, M.-H.; Ouedraogo, R. et al

in Diabetologia (1995), 38

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See detailBPDZ 44: a new and potent activator of ATP-sensitive K+ channels
Lebrun, P.; Pirotte, Bernard ULg; Antoine, M.-H. et al

in Diabetologia (1993), 36

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See detailEffects of infused sodium lactate on glucose metabolism in healthy human.
PAQUOT, Nicolas ULg; Tappy, L.; Schneiter, Ph et al

in Diabetologia (1993), 36(suppl 1), 143

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See detailInsulin secretion and action in various populations with type 2 (non-insulin-dependant) diabetes mellitus
Scheen, André ULg; Paolisso, G.; Castillo, M. et al

in Diabetologia (1992), 16 ( suppl 1)(29), 116

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See detailMagnesium and glucose homeostasis.
Paolisso, G.; Scheen, André ULg; D'Onofrio, F. et al

in Diabetologia (1990), 33(9), 511-4

Magnesium is an important ion in all living cells being a cofactor of many enzymes, especially those utilising high energy phosphate bounds. The relationship between insulin and magnesium has been ... [more ▼]

Magnesium is an important ion in all living cells being a cofactor of many enzymes, especially those utilising high energy phosphate bounds. The relationship between insulin and magnesium has been recently studied. In particular it has been shown that magnesium plays the role of a second messenger for insulin action; on the other hand, insulin itself has been demonstrated to be an important regulatory factor of intracellular magnesium accumulation. Conditions associated with insulin resistance, such as hypertension or aging, are also associated with low intracellular magnesium contents. In diabetes mellitus, it is suggested that low intracellular magnesium levels result from both increased urinary losses and insulin resistance. The extent to which such a low intracellular magnesium content contributes to the development of macro- and microangiopathy remains to be established. A reduced intracellular magnesium content might contribute to the impaired insulin response and action which occurs in Type 2 (non-insulin-dependent) diabetes mellitus. Chronic magnesium supplementation can contribute to an improvement in both islet Beta-cell response and insulin action in non-insulin-dependent diabetic subjects. [less ▲]

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See detailPulsatile glucagon has greater hyperglycaemic, lipolytic and ketogenic effects than continuous hormone delivery in man: effect of age.
Paolisso, G.; Buonocore, S.; Gentile, S. et al

in Diabetologia (1990), 33(5), 272-7

The present study aimed at investigating the hyperglycaemic, lipolytic and ketogenic effects of small doses of glucagon delivered continuously or in a pulsatile manner. The study was performed in eight ... [more ▼]

The present study aimed at investigating the hyperglycaemic, lipolytic and ketogenic effects of small doses of glucagon delivered continuously or in a pulsatile manner. The study was performed in eight healthy young volunteers (24.2 +/- 1.2 years) and in eight healthy aged subjects (69.4 +/- 2.0 years). In all the subjects, endogenous pancreatic hormone secretion was inhibited by somatostatin and only glucagon was replaced. Consequently, the effects of pulsatile and continuous glucagon delivery were studied in conditions of progressive somatostatin-induced insulin deficiency. In both the young and the aged subjects, pulsatile glucagon delivery resulted in increases in plasma glucose, non-esterified fatty acid, glycerol and beta-hydroxybutyrate levels greater than those observed when the same amount of glucagon was delivered in a continuous manner. The net increases in plasma glucose, glycerol and non-esterified fatty acid levels were similar between the young and the aged subjects when glucagon was infused continuously; in contrast, the rise in plasma beta-hydroxybutyrate in the aged was only about half that observed in the young subjects. Surprisingly, when glucagon was infused in a pulsatile manner, the rises in plasma glycerol, non-esterified fatty acid and beta-hydroxybutyrate levels were all significantly smaller in the aged subjects, while no significant differences were observed in the blood glucose responses. We conclude that, in the presence of somatostatin-induced insulin deficiency, pulsatile glucagon exerts greater effects on blood glucose, plasma non-esterified fatty acid, glycerol and beta-hydroxybutyrate levels than its continuous delivery. In the elderly, the lipolytic and ketogenic, but not the hyperglycaemic, responses to pulsatile glucagon are significantly reduced. [less ▲]

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