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M Burtin

Publications and source records attributed to M Burtin.

35 records · Page 2Linked to original sources
PubMed1990

Adverse effects of sucrose-rich diets on uraemic rats.

The nature of carbohydrate may affect the tolerance and progression of uraemia. The effects of three diets differing only in their carbohydrate source: namely corn starch (C), glucose (G) or sucrose (S) were examined. Study 1 examined the effects of the three carbohydrate diets on unilaterally nephrectomised control rats and severely uraemic rats. The three carbohydrates produced similar nutritional effects in uninephrectomised rats, whereas sucrose rapidly induced anorexia, stunting and slightly accelerated renal damage in uraemia. Study 2 examined the long-term effects of the three carbohydrates in moderate uraemia under conditions of high and identical carbohydrate intakes. Hyperphagic Zucker uraemic rats (F rats) received a daily allotment of each diet plus pure carbohydrate. Lean uraemic rats (L rats) received the same dietary allotment without the carbohydrate supplement. The F rats fed sucrose showed greater morbidity and mortality but little renal deterioration. Their plasma triglycerides increased dramatically. The L rats fed sucrose had the greatest urinary protein, the least creatinine clearance and the most severe renal damage. Thus, sucrose-rich but not glucose-rich diets have two adverse effects in uraemia: a deterioration in nutritional status, perhaps related to abnormal fructose utilisation, and a long-term effect on the kidney, resulting in accelerated renal deterioration.

Animals↗
PubMed1990

[Kidney functional reserve. An experimental study].

The renal functional reserve (RFR), the increase in glomerular filtration rate (GFR) induced by a protein load, seems to be diminished or even lost in renal failure. Our experimental study was undertaken to determine whether the RFR is lost beyond a given level of nephron reduction, using different protein loads. In the first two studies, RFRs were evaluated during an oral protein load consisting in a high-protein diet (30% casein) compared to a low-protein diet (7% casein). Each diet was given to SD rats (200 g) either for three weeks immediately after nephrectomy (Nx) or for four days one month after Nx. Nx was subtotal and consisted in removal of 65 to 85% of the mass of the renal parenchyma. The GFR evaluated by inulin clearance measurements increased considerably after a prolonged (+188%) or short-lived (+35%) oral protein load if less than 70% of the renal mass had been removed. Beyond this threshold of nephron amputation, the high-protein diet had no effect on the GFR, despite an increase in the residual renal mass (+200% in moderate and severe Nxs). In a third study, the GFR was measured one month after Nx and the effects of an infusion of amino acids (vamine) or of a placebo were compared, each rat serving as his own control. Extent of Nx was 0%, 50%, 65-70%, and 80%. Regardless of the extent of nephron reduction, the GFR increased under vamine, but interindividual variations in each group were marked (+5 to +70%).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1985

Prostaglandin E2-like activity of 20:3n-9 platelet lipoxygenase end-product.

5,8,11-Icosatrienoic acid (20:3n-9), a fatty acid associated with platelet hyperactivity, was oxygenated by platelet lipoxygenase. The end-product of this pathway was purified by high-performance liquid chromatography (HPLC) and characterized as 12-hydroxy-5,8,10-icosatrienoic acid [12-OH-20:3(5,8,10)] by capillary gas-liquid mass spectrometry. When tested upon platelet aggregation, 12-OH-20:3(5,8,10) exhibited a biphasic effect. At low concentrations (below 5 X 10(-7) M) it potentiated aggregation but inhibited it at higher levels, a pattern similar to that obtained with prostaglandin E2. However, since the amounts of 12-OH-20:3(5,8,10) generated under thrombin stimulation are in the range of concentrations with potentiating effects, it seems that the 12-OH derivative is responsible for the hyperaggrebility of 20:3n-9-rich platelets.

8,11,14-Eicosatrienoic Acid↗
PubMed1983

Potentiating effect of 5,8,11-eicosatrienoic acid on human platelet aggregation.

5,8,11-Eicosatrienoic acid (20:3 omega 9), a fatty acid increased in the platelet phospholipids of man and animals fed saturated fats, was either added to human platelets simultaneously with the aggregating agents, or incorporated into the platelet phospholipids by preincubation. 20:3 omega 9 markedly increased the response of platelets to all aggregating agents tested when added simultaneously with the agent, but solely to thrombin and ionophore, after incorporation into the platelet phospholipids. The potentiating effects of 20:3 omega 9 on thrombin aggregation do not appear to be related to prostaglandin formation, but rather to the production of a monohydroxy derivative through the lipoxygenase pathway.

8,11,14-Eicosatrienoic Acid↗
PubMed1981

Refractoriness of diabetic platelets to inhibitory prostaglandins.

Inhibition of collagen-induced platelet aggregation by either endothelial extracts, prostacyclin, prostaglandin E1 or prostaglandin D2 was investigated. The inhibition was less efficient with diabetic platelets than with platelets from normal donors. The refractoriness of diabetic platelets to inhibitory prostaglandins was observed both with platelet-rich plasma and platelets isolated from their plasma. Moreover levels of cyclic AMP in resting platelets and after stimulation by either PGE1 or PGD2 were lower in diabetic platelets than in normal platelets. It is concluded that the weaker response of diabetic platelets to inhibitory prostaglandins could be related to their content in cyclic AMP.

Adolescent↗
PubMed1980

Dihomogammalinolenic acid (20:3 omega 6) is more anti-aggregatory than eicosapentaenoic (20:5 omega 3) in a platelet-endothelial cell mixture.

The effect of 20:3 omega 6, the precursor of 1 series prostaglandins was to inhibit platelet aggregation more strongly than either 20:5 omega 3, the precursor of 3 series prostaglandins or 20:3 omega 3 which is not a substrate of prostaglandin synthetase. When platelets and dissociated endothelial cells were pretreated with 20:3 omega 6, platelet aggregation in the presence of endothelial cells was much more inhibited than after 20:5 omega 3 pretreatment.

8,11,14-Eicosatrienoic Acid↗
PubMedDate not supplied

Sodium restriction decreases AP-1 activation after nephron reduction in the rat: role in the progression of renal lesions.

Renal hyperplasia and hypertrophy are early events after nephron reduction which precede progressive destruction of the remnant kidney. Restriction of dietary sodium content was shown to reduce renal lesions following nephron reduction. AP-1 is a transcription factor, resulting from heterodimerization of fos and jun proteins, which mediates the effects of mitogenic growth factors. To elucidate the role of AP-1 in growth processes involved in renal deterioration, we evaluated whether restriction of dietary sodium content (0.25 vs. 0.50% sodium w/w) affected AP-1-DNA binding and hyperplasia in the remnant kidney after nephron reduction (70% nephrectomy). Cell proliferation, evaluated by PCNA immunostaining, increased progressively from day 7 to day 60 in glomeruli, proximal and distal tubules and loops of Henle of nephrectomized (Nx) rats compared to control sham-operated (C) animals. AP-1-DNA binding activity increased 7 and 14 days after surgery, but it was reduced below C values at day 60. c-fos and c-jun expression were also reduced in Nx rats at day 60. Sodium restriction significantly reduced the number of PCNA-stained cells in glomeruli and tubules at days 14 and 60, but not at day 7, whereas it decreased AP-1 activation at all times of the study. This effect was associated to a marked reduction of renal lesions in Nx rats. In conclusion, we showed that, after nephron reduction, the beneficial effect of sodium restriction was associated with a reduction of hyperplasia and AP-1 activation, but that the latter did not parallel delayed cell proliferation rate in remaining nephrons. Thus, we propose that different transduction pathways are involved in cell proliferation after nephron reduction, according to the time of evolution of renal lesions.

Animals↗
PubMedDate not supplied

Species differences in mammalian renal function: 5-HIAA, a reported marker of tubular secretion in humans, is handled exclusively by filtration in the rat.

Renal clearance of endogenous 5-HIAA has been shown to be similar to that of PAH in humans. The present study compared 5-HIAA and PAH clearances in rats. It showed that the clearance of 5-HIAA in rats was identical to that of inulin and creatinine. This suggests that in this species, 5-HIAA is only filtered and not secreted by the tubules in contrast to what is observed in humans.

Animals↗