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Biomedical subjects

F Berthezene

Publications and source records attributed to F Berthezene.

At least 73 records · Page 4Linked to original sources
PubMedDate not supplied

[Metabolic consequences of the nonenzymatic glucosylation of apolipoproteins].

The non enzymatic glucosylation (NEG) of proteins is a complex chemical reaction resulting in the formation of a stable bond between a glucose molecule and a protein aminogroup. In diabetics, hyperglycaemia may induce a large increase of NEG. Although the NEG of apolipoproteins remains moderate because of their short half-life, it may alter some of their properties. The NEG of LDL apo B induces a decrease of their catabolism due to a lowering of their binding to the LDL receptor. Glucosylated LDL can accumulate in macrophages, thereby facilitating the development of foam cells. The LDL NEG may also cause other processes including apo B oxidation and production of anti-LDL antibodies. The HDL NEG which essentially corresponds to that of apo A-I, induces a shortening of their half-life. In vitro, the NEG of apo A-I results in a decrease of its interaction with HDL surface. Finally, the binding of glucosylated HDL3 to HDL receptors is decreased in cultured fibroblasts. Since the level of lipoprotein NEG in vivo is moderate, the question as to whether this process may affect quantitatively the metabolic behaviour of lipoproteins and participate to the development of atheroma in diabetic patients, has not been clearly answered.

Apolipoproteins↗
PubMedDate not supplied

Characterization of the non enzymatic glycation of high density lipoprotein in diabetic patients.

In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins. We studied the glycation of HDL of patients with either type 1 or type 2 diabetes compared with that of control subjects. Although a basal glycation was detectable in HDL of normal individuals, this increased by about 400% in HDL of both groups of diabetic patients. The degree of HDL glycation was positively correlated with blood glucose concentration. All the HDL apoproteins were glycated but the glycation of apo A-I represented about 80% of the total HDL. These data were compared to those obtained in vitro after incubation of normal apo A-I either as free molecular species or as phospholipid/apo A-I complex, in the presence of glucose (0 to 80 mmol/l) at 37 degrees C. The resulting apo A-I glycation was dependent upon both time of incubation and glucose concentration and was largely increased in the presence of phospholipids. These data suggest that the in vivo glycation of HDL apoproteins might depend upon glucose concentration but might also be partly influenced by their lipid environment.

Adult↗
PubMedDate not supplied

Insulin-mediated glucose disposal in type 1 (insulin-dependent) diabetic subjects treated by continuous subcutaneous or intraperitoneal insulin fusion.

In order to determine if intraperitoneal insulin infusion could improve the insulin resistance of type 1 diabetic patients we have used the englycaemic insulin clamp technique in order to study the effects of insulin on glucose disposal in four C peptide negative type 1 diabetic patients treated by continuous subcutaneous or intraperitoneal insulin infusion and in five control subjects. Compared to control subjects, the diabetic patients treated by subcutaneous insulin infusion had a decreased maximal capacity of glucose utilization (diabetics: 12.6 +/- 0.3 mg.kg-1.min-1; controls: 15.7 +/- 0.7 mg/kg-1.min-1, p less than 0.01) and a trend towards higher half-maximally effective insulin concentrations (diabetics: 70 +/- 11 mU/l-1, controls: 48 +/- 4 mU/l-1). Treatment of the diabetic patients by intraperitoneal insulin infusion for 2 months decreased their mean peripheral free insulin levels (during subcutaneous infusion: 23.5 +/- 2.2 mU/l-1; during intraperitoneal infusion: 18.4 +/- 1.4 mU/l-1, p less than 0.05). However, mean daily insulin requirements were not decreased (during subcutaneous infusion: 0.59 +/- 0.05 U/kg-1.day-1; during intraperitoneal infusion: 0.57 +/- 0.03 U/kg-1.min-1). Moreover, the diabetic patients had a consistently lower maximal capacity of glucose utilization (12.6 +/- 0.7 mg kg-1.min-1) than control subjects (p less than 0.01) without modification of the half-maximally effective insulin concentration (62 +/- 10 mU.l-1). In conclusion, the only benefit of intraperitoneal insulin infusion was a reduction of peripheral free insulin levels; this decrease of peripheral insulinaemia was not associated with an improvement in the insulin resistance of diabetic patients.

Adult↗