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M Imler

Publications and source records attributed to M Imler.

At least 19 recordsLinked to original sources
PubMed1989

[Diminution of thyroid stimulating hormone level but normal levels of thyroid hormones. Demonstration of occult hyperthyroidism].

The finding of a low basal concentration of thyroid-stimulating hormone (TSH) in the absence of high thyroid hormone levels is difficult to understand. In order to elucidate the meaning of such a dissociation, 22 patients without history of thyroid disease and showing clinical signs compatible with thyrotoxicosis were explored by the thyrotrophin-releasing hormone (TRH) test, by thyroid radioisotope scanning and, in case of high nodular uptake, by the triiodothyronine suppression test. A specific surgical, isotopic or medical treatment was instituted in the 17 patients who had a high nodular uptake unsupressible by triiodothyronine. During a clinicobiological re-evaluation carried out 6 months later, a significant clinical improvement was observed in 8 patients, and 12 patients whose free thyroxine level had decreased showed normal TSH levels. These results underline the value of thyroid radioisotope scanning in patients with isolated diminution of TSH. They confirm the reality of occult hyperthyroidism with normal thyroid hormone levels by the benefits observed after specific treatment.

Aged↗
PubMed1988

Intestinal ammonium production in the rat: the role of the colon, small intestine, and circulating glutamine.

The intestinal ammonium production and the intestinal uptake of circulating glutamine were investigated in anesthetized intact rats and rats with resected small intestine or colon by simultaneous measurements performed on portal and arterial blood. It was shown that ammonium release into the portal blood by the small intestine is of equal magnitude to that released by the colon, and that circulating glutamine participates in ammonium production by the small intestine. Increased levels of circulating glutamine induced by its i.v. infusion to intact rats were not accompanied by an increase in intestinal ammonium production.

Ammonia↗
PubMed1986

Effects of 2,4-dinitrophenol on renal ammoniagenesis in the rat.

Injection of anesthetized rats with the uncoupling agent, 2,4-dinitrophenol (2,4-DNP) 10 or 20 mg/kg induced a systemic hyperammonemia unaccompanied by blood acid-base status changes and related to an increased release of ammonium from the kidney into the renal vein. Ammonium excretion into the urine did not increase. The renal uptake of circulating glutamine rose. The antiepileptic drug sodium valproate (VPA), a short-chain, branched fatty acid, had the same effects on rat and man. These findings suggest that VPA stimulates renal ammoniagenesis by the same mechanisms as 2,4-DNP.

2,4-Dinitrophenol↗
PubMed1986

Arterial ammonemia changes of renal origin induced in the rat by acid and alkaline diets.

The aim of this study was to investigate the influence of acid and alkali food supplementation on systemic ammonemia to explain the hyperammonemia previously observed in rats fed a high protein diet. In normal rats, arterial ammonia concentration significantly increases after 4 days of HCl-supplemented diet. Following a NaHCO3-enriched food, there is only a slight but not significant decrease in arterial ammonia level. These changes occur before any variation in arterial acid-base status and are of renal origin. Indeed, there is a positive linear correlation (r = 0.946; P less than 0.001) between arterial ammonia level and the ammonia concentration difference between the renal vein and artery (which varies proportionally to the urinary ammonium excretion). Hindquarter uptake and intestinal release of ammonia do not significantly participate in the arterial ammonia changes observed. Following HCl-enriched diets, increased renal glutamine uptake, enhanced hindquarter glutamine release, and perhaps decreased intestinal glutamine uptake occur simultaneously. In conclusion, acid and alkali food supplementation intervenes on the renal ammonia release into the circulation with concomitant arterial ammonemia changes.

Ammonia↗
PubMed1986

Cephalic phase insulin secretion in relation to food presentation in normal and overweight subjects.

The existence of a preabsorptive insulin reflex is well known in animals but remains controversial in humans. Glycemia and insulin variations following olfactive and visual presentation of a standard meal were studied in 25 subjects, 10 of them (5 men and 5 women) of normal weight and 15 overweight (7 men and 8 women), after a 15 hour fast. Blood samples were collected continuously, every minute for 16 minutes after the meal was presented. The presentation produced an early blood insulin increment, variable in magnitude and time course and occurring between the 3rd and 9th minute, in both normal and overweight subjects. Glycemia variations were not significant. Our study demonstrated a positive correlation between the reflex insulin release, body weight and a conscious effort to maintain current body weight. However, the differences between overweight and normal subjects remained small. The physiological and psychological determinants of the cephalic phase of insulin secretion are discussed.

Adult↗
PubMed1985

[Treatment of severe hyperthyroidism by plasma exchange. Clinical and biological efficacy. 8 cases].

The effectiveness of plasmapheresis was evaluated in 8 patients with severe thyrotoxicosis of diverse origin and clinical manifestations, who underwent a total of 22 plasma exchanges. The method proved rapidly effective in controlling the symptoms in 6 cases. No adverse reaction was noted. In all patients plasma exchanges significantly reduced plasma concentrations of total thyroxine and triiodothyronine and of thyroxine-binding globulin, without effect on free thyroxine and triiodothyronine fractions. The satisfactory clinical results obtained can only be explained by displacement of thyroid hormones from the intracellular compartment. The hormonal variations observed were proportional to the initial hormone concentrations, to the amount of thyroxine-binding globulin removed and to the plasma volume purified. It is concluded that plasmapheresis rapidly extracts thyroid hormones and is therefore useful in the treatment of acute severe thyrotoxicosis.

Adult↗
PubMed1985

Decrease of valproate-induced hyperammonemia in normal subjects by lipid ingestion.

Sodium valproate (VPA), a branched short-chain fatty acid, always causes a hyperammonemia of renal origin in fasting man. The intake of medium-length, straight-chain fatty acids abolishes the VPA-induced hyperammonemia, and VPA free fraction increases concomitantly. Accordingly, fatty acids could be useful in preventing and treating hyperammonemia-accompanied stuporous states which are complications of VPA medication.

Ammonia↗
PubMed1985

Adaptation of hepatic ammonia metabolism after chronic valproate administration in epileptics treated with phenytoin.

The effects of phenytoin (PHT) on the modifications of ammonia (NH+4) metabolism caused by sodium valproate (VPA) are here studied in order to identify the drug combinations susceptible of evoking stuporous states in epileptics, a rare condition attributed to a hyperammonemic encephalopathy induced by VPA. During chronic treatment with PHT or VPA-PHT, the acute injection of VPA increases the kidney's output of NH+4. During chronic PHT treatments, the acute injection of VPA modifies the liver's NH+4 metabolism and the arterial hyperammonemia is high (mean = 90 mumol/l). During chronic VPA-PHT treatments, the acute injection of VPA does not affect the hepatic NH+4 metabolism, suggesting that adaptation occurs, and the arterial hyperammonemia is moderate (mean = 60 numol/l). Disturbances of the hepatic adaptive mechanisms may explain certain complications observed during multiple-drug regimens.

Adaptation, Physiological↗
PubMed1979

Semiautomated enzymic microassay for plasma L-alanine.

Plasma L-alanine is deaminated by bacterial alanine-dehydrogenase; the resulting ammonia is dialyzed out and measured by use of a continuous flow phenol-hypochlorite colorimetric microassay. Concentrations in the range of 10-1,000 mumol alanine/l can be determined in a 50-microliter sample. The optimal conditions for the assay are specified. Study of the analytical qualities of the technique shows high specificity, good reproducibility , and a detection limit of 6 mumol/l. Usual values in human plasma from arterial or venous blood are respectively 296 +/- 166 and 376 +/- 214 mumol alanine/l (x +/- 2 SD). The usual values in rats are close to those found in man.

Alanine↗
PubMed1979

An automated microassay for blood ammonia.

A microassay for blood ammonia has been developed. After dilution, blood is dialyzed by a continuous flow procedure, and the ammonium ions in the dialysate are assayed colorimetrically by the hypochlorite-phenol Berthelot reaction. Concentrations from 1 to 400 mumol/l NH+4 can be measured in a 50 mul whole blood sample. Using slight modifications, concentrations up to 800 mumol/l NH+4 can be determined. The precision, accuracy, sensitivity, and specificity of the method have been studied. In man, the usual values (mean +/- 2 SD) found are 27.4 +/- 10.2 mumol/l NH+4 in arterial blood, 20.9 +/- 9.8 mumol/l in venous blood. The usual values in rats and mice are very close to those given for man.

Amino Acids↗
PubMed1979

[Changes in cephalic and peripheral use of glucose and glutamine under the influence of hyperammonemia in rats].

Arterio-venous differences of glucose and glutamine were determined across the brain and across the hind limb in normal and ammonium salt infused rats, before and during an insulin tolerance test, in an attempt to study the effect of hyperammonemia on cephalic and muscular metabolism. The results demonstrate that 1) hyperammonemia reduces the hind limb uptake of glucose without affect the cephalic uptake of glucose which is lowered during hypoglycemia, 2) the reduction of the cephalic and muscular glutamine output induced by the hypoglycemia is masked in presence of an hyperammonemia. In conclusion, it may be assume that, at the concentration obtained in this study, hyperammonemia does not act directly in the pathogenesis of hepatic coma in which a decrease in cerebral glucose uptake described; on the other hand, ammonium plays an important role in the muscle metabolism.

Ammonia↗
PubMed1979

Effects of biguanides on the intermediate metabolism of glucose in normal and portal-strictured rats.

Phenformin and metformin treatments may be complicated by lactic adidosis. This metabolic complication seems favoured by preexistent hepatic disease. We have therefore compared the metabolic effects of phenformin and metformin on non fasting normal and portal-strictured rats. The latter group is characterized by impaired hepatic passage of these drugs without hepatocellular lesions. Given orally to normal rats over 5 days, phenformin (20 mg/kg/24 h) and metformin (150 mg/kg/24 h) decreased blood glucose levels and increased blood urea and the substrates of gluconeogenesis (alanine, glutamine, lactic and pyruvic acids), effects more apparent with phenformin than metformin. In non-treated portal strictured rats, blood glucose levels were lower and the intermediate metabolites were higher than in noraml rats, suggesting a modification of gluconeogenesis. Treatment of the portal strictured group by phenformin or metformin induced no changes in the studied parameters. This absence of effect of the biguanides in portal strictured rats supports the postulate that, in normal rats, biguanides act principally on hepatic metabolism by reducing gluconeogenesis and that, in the absence of other hepatic damage, the presence of a peri-hepatic shunt, which, by itself, modifies gluconeogenesis, does not further predispose to lactic acidosis during short term administration of biguanides.

Alanine↗