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C Merlet-Bénichou

Publications and source records attributed to C Merlet-Bénichou.

30 records · Page 2Linked to original sources
PubMed1995

Maturation of rat renal phosphate transport: effect of triiodothyronine.

1. Prevention of weaning prevents the increase in the carrier affinity for Na(+)-cotransported phosphate (Pi) and the normal elevation of plasma 3,5,3'-triiodothyronine (T3) which occur between postnatal days 14 and 21. 2. This study examines the possible role of T3 in the control of the maturation process of Pi transport. Clearance experiments and brush-border membrane studies were performed on 14-day-old rats given T3. 3. The fractional excretion of Pi of T3-treated rats was 33% lower compared with controls (P < 0.01). After Pi perfusion, it remained at a lower level, and the amount of Pi reabsorbed per minute, corrected for the glomerular filtration rate (RPi/GFR), was higher. 4. The membrane vesicles from 14-day-old rats given T3 showed a 30% increase in carrier affinity for Na(+)-cotransported Pi. In addition to this maturational effect of T3, a 46% increase in Vmax was also observed. 5. The amount of immunoreactive Pi transporter, detected using anti-(NaPi-2) antiserum, was increased in T3-treated rats. 6. Glucose transport, another Na(+)-dependent transport system, was not altered by T3. 7. It is concluded that exogenous T3 given before the third postnatal week specifically induced precocious maturation of renal Pi transport in 14-day-old rats, suggesting that thyroid hormone is normally involved in this maturation.

Animals↗
PubMed1994

Intrauterine growth retardation leads to a permanent nephron deficit in the rat.

Intrauterine growth retardation (IUGR) was induced in Sprague-Dawley rats by partial artery ligation of one uterine horn in the mother on day 17 of gestation or by feeding the mother a 5% protein diet from day 8 of gestation. The controls were pups of the contralateral uterine horn or pups born to mothers fed a normal (22%) protein diet. The number of nephrons present at birth and the final number of nephrons in 2-week-old rats were counted throughout the entire kidney. The number of nephrons present at birth and the final number of nephrons were significantly correlated with birth weight for growth-retarded rats of both groups and their corresponding controls (P < 0.02 for the poorest correlation). Clearance experiments and morphometric studies of 2-week-old rats born to mothers with uterine artery ligation indicated that, despite a large compensatory hypertrophy of the nephrons in those animals born with a nephron deficit of about 30%, the overall renal function was impaired. We conclude that IUGR is accompanied by a nephron deficit which may not be fully compensated for within the first weeks after birth.

Animals↗
PubMed1993

Lack of control by adrenal steroids of oxidative enzymes and Na/K-ATPase development in the rat proximal tubule.

The activities of citrate synthase, 3-oxoacid CoA-transferase, and Na/K-ATPase were determined in the proximal convoluted tubules (PCT) of midcortical nephrons from 16-, 21- and 30-day-old and adult rats. Enzyme microassays based on NAD amplification were run on tubule segments microdissected from lyophilized tissue sections, and the activities were expressed per unit of tissue dry weight. The activities of 3-oxoacid CoA-transferase (+ 155%) and citrate synthase (+ 44%) increased between 16 and 30 days, while no significant change in Na/K-ATPase activity occurred during this period. The results obtained in PCT from subcapsular nephrons were similar. It is concluded that active transport of Na+ coupled to mitochondrial ATP production might be mature in the PCT by the time of weaning, consistent with data on the development of Na+ reabsorption. Since adrenalectomy on day 16 induced no changes in the activities of oxidative enzymes or Na/K-ATPase on day 21 in midcortical or subcapsular PCT, the physiological rise in circulating glucocorticoids, characteristic of the weaning period, does not trigger the development of oxidative enzymes and Na/K-ATPase in the PCT of the developing rat kidney.

Adrenal Cortex Hormones↗
PubMed1993

Effects of weaning on phosphate transport maturation in the rat kidney. Clearance and brush border membrane studies.

Renal phosphate transport matures via an increase in the carrier affinity for phosphate during the 3rd post-natal week in the rat. This study examines whether weaning, which normally takes place during this period, plays a role in phosphate transport maturation. Early weaning (EW) and prevention of weaning (PW) both increased the fractional excretion of phosphate (EW 26.5 +/- 4.9, PW 26.7 +/- 2.2, controls 11.3 +/- 2.8, P < 0.001 and P < 0.05, n = 6 in each group). EW and PW also decreased the uptake of phosphate into brush border membrane vesicles (BBMV) isolated from the renal cortex of 21-day-old rats. Glucose transport in BBMV was not affected. The kinetics of phosphate uptake, measured in the presence of a sodium gradient, showed lower Vmax (4,112 +/- 362 pmol/mg protein per 10 s) in EW BBMV than in controls (6,030 +/- 200, n = 5, P < 0.001), but the affinity of the carrier for phosphate (1/Km) did not change. The decrease in Vmax may be due to the enhanced phosphate supply. The affinity of the carrier was lower in PW rats (Km = 0.31 +/- 0.04 mM) than in controls (0.18 +/- 0.04, n = 5, P < 0.01) but the Vmax remained unchanged. The low affinity may indicate that normal maturation of tubular transport, in which carrier affinity increases, is altered. The plasma concentrations of corticosterone, parathyroid hormone, insulin and triiodothyronine and their changes during EW and PW are also reported.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Relationship between maternal milk PGE2 and gastric acid secretion in newborn rats.

We previously demonstrated that in rats gastric acid secretion declines after birth and drops steeply on day 12 of life. In the present study, we investigated the part played in this decline by prostaglandin E2 (PGE2) from maternal milk. PGE2 content was first measured in the milk of untreated dams 0, 1, 5, 10, 12, 15, and 18 days after parturition. PGE2 levels were high during the first 5 days (123.5-200.5 pg/ml), declined significantly between days 10 and 15 (56.6-85.4 pg/ml; P less than 0.05), and dropped to 18.4 pg/ml on day 18. We also found that depleting milk of PGE2 prevented drop of acid secretion in 12-day-old suckling rats. Injecting lactating dams with indomethacin significantly reduced milk PGE2 content by 65% vs. milk of untreated dams. Surprisingly, administration of sesame oil, the indomethacin vehicle to the dams, increased milk PGE2 content by 182%. In the pups of the indomethacin-treated dams, acid secretion did not drop. On the contrary, in vivo basal and histamine-induced acid output rose markedly by 40 and 50%, respectively, and in vitro the net movements of 36Cl and 22Na measured in the isolated stomach indicated that active Cl- secretion had resumed. Mucosal PGE2 did not appear to be significantly involved in early development of acid secretion because administration of indomethacin to pups from untreated dams did not significantly modify the secretion measured on day 12. Data indicate that maternal milk depletion of PGE2 prevents the drop of gastric acid secretion previously observed in 12-day-old pups and suggest that in infant rats maternal PGE2 plays a physiological part in regulating acid secretion.

Animals↗
PubMed1988

Light- and electron-microscopic analysis of the kidney in newborn rats exposed to gentamicin in utero.

Kidneys of newborn rats, whose mothers were given 75 mg/kg of gentamicin daily from the tenth day of gestation to its term, were examined by light and electron microscopy, as were kidneys of control rats whose mothers were given saline during the same period. In the gentamicin-treated group, the numbers of differentiated glomeruli and of S-shaped bodies counted in a median cross-section of the kidney were reduced, compared with those in the control group, but the glomerular volume was the same. In newborn rats issued from gentamicin-treated mothers, the proximal tubular lumen of the mature nephron lying in the deepest cortex was dilated, and their proximal tubular cells exhibited extensive damage, resembling that described in tubular cells of adult rats exposed to gentamicin. The subcapsular nephrogenic zone exhibited focal alterations of cytoplasmic organelle membranes, as well as nuclear lesions of several types, in cells of the nephron anlagen of the undifferentiated metanephric blastema, which were otherwise of normal appearance.

Animals↗
PubMed1975

Dependence of 2,3-DPG and oxygen affinity of haemoglobin on sex and pregnancy in the guinea-pig.

Oxygen half-saturation of blood (P50), 2,3-diphosphoglycerate concentration (2,3-DPG) and Bohr effect were determined in male, and nonpregnant and pregnant female guinea pigs, according to a randomized block design. P50 was significantly higher in the female group (26.3 Torr plus or minus 0.22 SEM) than in the male group (24.8 Torr plus or minus 0.26 SEM) and was significantly lower in both these groups than in the pregnant group (27 Torr plus or minus 0.35 SEM). This difference in oxygen affinity was explained by differences in 2,3-DPG: 1.08 plus or minus 0.02 SEM in males, 1.24 plus or minus 0.03 in non-pregnant females and 1.34 plus or minus 0.03 mol/mol HB in pregnant females P50, 2,3-DPG and haemoglobin concentrations were significantly correlated for the ensemble of the 3 groups. There was no significant difference in Bohr effect between the 3 groups.

Adenosine Triphosphate↗
PubMedDate not supplied

The number of nephrons in the mammalian kidney: environmental influences play a determining role.

Several lines of evidence, mostly derived from animal studies, indicate that changes in the fetal environment may affect the renal development. Fetal growth retardation is associated with a nephron deficit in both humans and animals. Changes in the supply of vitamin A to the fetus may be responsible for the variations in the number of nephrons in the human kidney. In utero exposure to hyperglycemia or drugs may also cause a nephron deficit.

Animals↗
PubMedDate not supplied

Effect of glucocorticoids on mitochondrial oxidative enzyme and Na-K-ATPase activities in the rat proximal tubule and thick ascending limb of Henle.

The activities of three mitochondrial oxidative enzymes (citrate synthase, 3-ketoacid-CoA transferase, beta-hydroxyacyl-CoA dehydrogenase) and Na-K-ATPase were microassayed in isolated segments of the rat proximal convoluted tubule (PCT) and medullary thick ascending limb of the loop of Henle (mTAL). The effects of adrenalectomy (ADX) and ADX plus exogenous glucocorticoids were analyzed. The hormonal replacement was daily injections of dexamethasone (10 micrograms/100 g body weight/24 h) for 5 days. ADX lowered the activity of all oxidative enzymes studies in the mTAL, but not in the PCT and led to a decrease in Na-K-ATPase in both nephron segments. Dexamethasone restored the normal level of oxidative enzymes and Na-K-ATPase in the mTAL and of Na-K-ATPase in the PCT. We conclude that the activities of citrate synthase, 3-ketoacid-CoA transferase and beta-hydroxyacyl-CoA dehydrogenase and of Na-K-ATPase are coordinately regulated in the mTAL and that glucocorticoids are essential for the long-term regulation of these enzyme activities in this nephron segment. In contrast, the activities of mitochondrial oxidative enzymes are not influenced by glucocorticoids in the PCT. This study presents the first evidence for a cell-specific regulation by glucocorticoids of oxidative metabolism in the nephron of adult rat kidney.

3-Hydroxyacyl CoA Dehydrogenases↗