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Biomedical subjects

L Baillet

Publications and source records attributed to L Baillet.

9 recordsLinked to original sources
PubMed2002

Atrial fibrillation can cause major hyperglycemia.

We report the case of a 66 years old woman with a well controlled, insulin-treated, type 2 diabetes, who experienced a ten-fold increase of her daily insulin needs (from 21 to 215 U/day) after the onset of a symptomatic atrial fibrillation. Check-up for another cause of insulin resistance was negative, and insulin doses could be decreased to preceding values only after electric cardioversion. Symptomatic atrial fibrillation should be considered as a potential cause of hyperglycemia.

Aged↗
PubMed2002

Comparison between monofilament, tuning fork and vibration perception tests for screening patients at risk of foot complication.

OBJECTIVE: To compare normal and pathologic values of three different tests for screening patients at risk of foot complications: mono-filament, tuning fork and vibration threshold perception (VTP). METHODS: Two hundred and fifty consecutive patients followed-up in a diabetic clinic were screened for sensitive polyneuropathy by three different tests in three different examinations in a blind design. The 10 g mono-filament, tuning fork and Horwell neuro-esthesiometer were applied to different sites on the patients' legs and feet. RESULTS: Thirty eight patients were identified having abnormal tests and being at risk of foot complications using the mono-filament test; 33 of them and 9 more (42 patients (33 + 9)) were identified using the tuning fork applied to the malleolus and eight more (50 patients (33 + 9 + 8)) when the tuning fork was applied to the big toe; twenty more patients (70 (33 + 9 + 8 + 20)) were identified as being at risk using the VTP at a cut-off of 25 V. CONCLUSION: The mono-filament test identified patient with the highest risk of foot complications, but 37 more patients were identified to be at risk from a VTP > 25 V. These patients were not detected using the mono-filament test. The VTP test provides numerical values that can help to follow the course of the risk for foot insensitivity by allowing the care team to grade the education and follow-up of the at-risk group.

Adolescent↗
PubMed2001

Energy expenditure following oral glucose load in ten uremic patients before and after three months on a ketoacid-supplemented very-low-protein diet.

We have previously shown that a ketoacid-supplemented very-low-protein diet (KSVLPD), which has been proposed to slow down the rate of progression of chronic renal failure (CRF), improves tissue insulin sensitivity and decreases hyperinsulinemia in predialytic uremic patients. However, this diet may interfere with nutritional status. The aim of this study was to study basal energy expenditure (EE) and EE after an oral glucose load in patients with CRF before and during a KSVLPD (0.3 cal x kg wt(-1) x d(-1) supplemented with aminoacid and ketoanalogs) using oral glucose loading in combination with indirect calorimetry. We also monitored body weight and analyzed body composition by dual-energy x-ray (DEXA) during KSVLPD. In the third month of KSVLPD, no significant change in total body weight was observed, but DEXA showed a decrease in lean tissue mass (LTM; 46.2 +/- 3.6 kg before v 44 +/- 3.4 kg in the third month; P <.01) and an increase in body fat mass (20.1 +/- 2.4 kg before v 21.3 +/- 2.4 kg on KSVLPD; P <.05). Postabsorptive plasma glucose level was significantly lower, and glucose oxidation and energy expenditure per LTM were significantly increased (EE, 20 +/- 0.8 cal x kg LTM(-1) x min(-1) before diet v 21.9 +/- 1.1 cal x kg LTM(-1) x min(-1) after 3 months on KSVLPD; P <.01). Plasma glucose and serum insulin levels were significantly lower after glucose loading, and glucose oxidation increased. EE values were significantly higher after the oral glucose load, and cumulative EE after oral load increased from 20.7 +/- 0.7 cal x kg LTM(-1) x min(-1) before the diet to 22.9 +/- 1.1 cal x kg LTM(-1) x min(-1) in the third month of KSVLPD; P <.001). Glucose oxidation was higher and cumulative glucose storage was decreased after diet (29.6 +/- 4.2 g v 20.9 +/- 3.4 g on KSVLPD; P <.01). We conclude that KSVLPD increases EE in the postabsorptive state and after an oral glucose load with an adaptation of lean tissue mass in the third month of the diet. Therefore, during KSVLPD, strict monitoring of dietetic management is necessary to maintain energy requirements at high levels appropriate to the new EE.

Administration, Oral↗
PubMed2000

Elucidation of the mechanism by which (+)-acylcarnitines inhibit mitochondrial fatty acid transport.

It is well established that medium and long chain (+)-acylcarnitines (i.e. fatty acid esters of the unnatural d-isomer of carnitine) inhibit the oxidation of long chain fatty acids in mammalian tissues by interfering with some component(s) of the mitochondrial carnitine palmitoyltransferase (CPT) system. However, whether their site of action is at the level of CPT I (outer membrane), CPT II (inner membrane), carnitine-acylcarnitine translocase (CACT, inner membrane), or some combination of these elements has never been resolved. We chose to readdress this question using rat liver mitochondria and employing a variety of assays that distinguish between the three enzyme activities. The effect on each of (+)-acetylcarnitine, (+)-hexanoylcarnitine, (+)-octanoylcarnitine, (+)-decanoylcarnitine, and (+)-palmitoylcarnitine was examined. Contrary to longstanding belief, none of these agents was found to impact significantly upon the activity of CPT I or CPT II. Whereas (+)-acetylcarnitine also failed to influence CACT, both (+)-octanoylcarnitine and (+)-palmitoylcarnitine strongly inhibited this enzyme with a similar IC(50) value ( approximately 35 microm) under the assay conditions employed. Remarkably, (+)-decanoylcarnitine was even more potent (IC(50) approximately 5 microm), whereas (+)-hexanoylcarnitine was far less potent (IC(50) >200 microm). These findings resolve a 35-year-old puzzle by establishing unambiguously that medium and long chain (+)-acylcarnitines suppress mitochondrial fatty acid transport solely through the inhibition of the CACT component. They also reveal a surprising rank order of potency among the various (+)-acylcarnitines in this respect and should prove useful in the design of future experiments in which selective blockade of CACT is desired.

Animals↗
PubMed2000

No change of hyperleptinemia despite a decrease in insulin concentration in patients with chronic renal failure on a supplemented very low protein diet.

Chronic renal failure (CRF) is often accompanied by hyperleptinemia caused by deficient renal metabolism of leptin and possibly increased leptin production, which in turn may result from the hyperinsulinemia and increased proinflammatory cytokine levels in patients with CRF. The hyperinsulinemia and insulin resistance observed in patients with CRF improve on supplemented very low protein diets (SVLPDs). The goal of our study is to determine whether the correction of hyperinsulinemia and insulin resistance in patients with CRF by SVLPDs is accompanied by improvement in hyperleptinemia. Thirteen patients were studied before and 1 year after following SVLPDs providing 0.3 g/kg/d of protein, supplemented with amino acids and ketoanalogues. After 1 year, patients showed markedly less hyperinsulinemia (7.4 +/- 1.6 versus 13.8 +/- 2 microU/mL at the start of diet; P: = 0.05) and insulin resistance, whereas serum leptin levels remained unchanged (16.1 +/- 4.7 versus 19.1 +/- 7.4 ng/mL at start of the study; P: = not significant). The initial correlation between serum leptin level and percentage of body fat persisted during follow-up. No correlation was found between insulin and leptin levels or between the variation of these two parameters during the study. Our study shows that the correction of hyperinsulinemia and insulin resistance in patients with CRF by SVLPDs is not accompanied by improvement in hyperleptinemia, which consequently does not appear to result from changes in carbohydrate metabolism.

Dietary Proteins↗
PubMed1999

Composition of insulin-induced body weight gain in diabetic patients: a bio-impedance study.

Although insulin is a well-known cause of body weight gain, it is not clear whether it is due to the accumulation of fat or lean mass. We performed a 3 months Body-Impedance Analysis follow-up in 72 diabetic patients in a wide range of insulin indications: insulin introduction in young inaugural type 1 diabetics (n = 12), late-onset type 1 (n = 12), type 2 affected by intercurrent diseases (n = 12) or microangiopathic complications (n = 12), type 2 with failure of oral antidiabetic agents (n = 12), and insulin withdrawal in type 2 (n = 12). In type 1 patients, insulin led to the most important weight gain, but it was fat-free, with a major benefit on HbA1C. Type 2 patients affected by intercurrent diseases or microangiopathic complications had a mild, also fat-free weight gain, with a clear benefit on HbA1C. In type 2 patients with failure of oral agents, HbA1C declined less, weight gain was intermedia, but predominantly fat, mirrored by a predominant fat loss in type 2 patients whose insulin was stopped (without significant change in HbA1C). Both fat and lean mass contributed to insulin-induced body weight gain, but a significant negative relationship existed between their respective evolution in our patients (r = -0.23, p < 0.05 by linear regression analysis between delta fat mass and delta lean mass). Insulin-induced body weight gain is not univocal: insulin restaures or protects lean mass in its less controversial indications, whereas it leads to fat accumulation in type 2 patients with isolated failure of oral agents.

Adult↗
PubMed1998

Erythropoietin can deteriorate glucose control in uraemic non-insulin-dependent diabetic patients.

Two patients with non-insulin-dependent diabetes mellitus (NIDDM) and moderate chronic renal failure experienced a worsening of glycaemic control when recombinant human erythropoietin (r-HuEPO) was introduced, leading to insulin therapy. A 71-year-old woman with a 20-year history of NIDDM had presented histologically documented diabetic nephropathy for 2 years during which glucose control was stabilized by a diet and glibenclamide 10 mg. In the 6 months following introduction of r-HuEPO, hyperglycaemic symptoms developed, and HbA1C increased from 8.9% to 12.3%. During this period, no intercurrent events occurred, except epistaxis due to accelerated hypertension one month after r-HuEPO was started. A 62-year-old man had a 15-year history of NIDDM, with proliferative retinopathy, macroproteinuria and chronic renal failure for 4 years. The day after the first injection of r-HuEPO, capillary glucose level rose dramatically. In both of these cases, antihypertensive treatment was increased and insulin introduced. The role of r-HuEPO in hyperglycaemia was probable in the first case and highly probable in the second. Reports about the effects of r-HuEPO on glucose metabolism in uraemic patients are conflicting. Short- and long-term effects can differ, although long-term benefit is likely. The fact that our patients were not dialized may have been important. Clinicians should be aware that glucose control may deteriorate with r-HuEPO, requiring some uraemic NIDDM patients to undergo insulin therapy.

Aged↗