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Biomedical subjects

M Laville

Publications and source records attributed to M Laville.

At least 73 records · Page 4Linked to original sources
PubMed2000

Fuel homeostasis during physical inactivity induced by bed rest.

The consequences of physical inactivity on fuel homeostasis were evaluated during 7 days of head-down bed rest (HDBR), a model mimicking weightlessness. Eight men (32.4 +/- 1.9 yr; body mass index, 23.9 +/- 0.7 kg/m2) and eight women (27.9 +/- 0.9 yr; body mass index, 20.9 +/- 0.6 kg/m2) underwent an oral glucose tolerance test (OGTT; 1 g/kg) before and after HDBR. The glucose load was labeled with 13C and associated with D-[6,6-2H2] glucose infusion, indirect calorimetry, breath tests, and plasma measurements to determine the glucose turnover and biodisponibility, substrate oxidation, and endocrine responses. Body composition was assessed using H2(18)O dilution. In addition, hormones were measured in daily blood and 24-h urine samples. No change in body composition was noted. Daily fasting insulin increased during HDBR (men, 34%; women, 26%), as did the insulin to glucose ratio (men, 30%; women, 25%). The normetanephrine level dropped (men, 30%; women, 16%), but metanephrine was unchanged. During OGTTs, the insulin response was increased after HDBR (men, 47%; women, 67%), whereas plasma glucose levels were similar. Nonesterified fatty acids and beta-hydroxybutyrate levels were lower. Endogenous glucose production dropped (28%), and exogenous glucose oxidation increased (28%) only in men. Resting energy expenditure was unchanged, but nonproteic respiratory quotient increased (men, 10%; women, 14%). Basal levels of lipid oxidation dropped in both sexes (approximately 90%), but those of carbohydrate oxidation increased in men (40%); as did lipogenesis in women (570%). In response to OGTTs, lipid oxidation was 80% reduced in both sexes after HDBR, but carbohydrate oxidation increased (25%) in men. Lipogenesis occurred in men (304%) and women (74%), but the latter had higher absolute levels. Therefore, 7 days of HDBR resulted in 1) reduced sympathetic activity, 2) insulin resistance suggested at the muscle level in men and at both the muscle and liver levels in women, 3) no changes in glucose biodisponibility, suggesting no alterations in the gastrointestinal function, and 4) a shift toward carbohydrate oxidation in men and a net lipogenesis in women. Such results suggest gender differences in response to sedentary life style and warrant further analysis.

3-Hydroxybutyric Acid↗
PubMed2000

Elevated levels of interleukin 6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss.

The aim of this study was to investigate the potential role of adipose cytokines in the obesity-associated insulin resistance. To that end, we compared: 1) serum concentrations of interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), and leptin in eight healthy lean control females and in android obese female without (n = 14) and with (n = 7) type 2 diabetes; and 2) the levels of these cytokines both in serum and in sc adipose tissue in the 14 obese nondiabetic women before and after 3 weeks of a very low-calorie diet (VLCD). As compared with lean controls, obese nondiabetic and diabetic patients were more insulin resistant and presented increased values for leptin, IL-6, TNFalpha, and C-reactive protein. In the whole group, IL-6 values were more closely related to the parameters evaluating insulin resistance than leptin or TNFalpha values. VLCD resulted in weight loss and decreased body fat mass (approximately 3 kg). Insulin sensitivity was improved with no significant change in both serum and adipose tissue TNFalpha levels. In contrast, VLCD induced significant decreases in IL-6 and leptin levels in both adipose tissue and serum. These results suggest that, as for leptin, circulating IL-6 concentrations reflect, at least in part, adipose tissue production. The reduced production and serum concentrations after weight loss could play a role in the improved sensitivity to insulin observed in these patients.

Adipose Tissue↗
PubMed2000

Regulation of uncoupling protein-2 and uncoupling protein-3 mRNA expression during lipid infusion in human skeletal muscle and subcutaneous adipose tissue.

To study the effect of nonesterified fatty acids (NEFAs) on uncoupling protein-2 (UCP-2) and uncoupling protein-3 (UCP-3) gene expression, a triglyceride emulsion was infused for 5 h in 14 healthy volunteers. A euglycemic-hyperinsulinemic clamp was administered concomitantly in 7 of the 14 subjects. The mRNA levels of UCP-2 and of the short (UCP-3S) and long (UCP-3L) isoforms of UCP-3 were quantified by reverse transcription-competitive polymerase chain reaction in tissue biopsies taken before and at the end of the infusion periods. Plasma NEFA concentrations increased from 362+/-52 to 989+/-157 micromol/l (P = 0.018) during triglyceride infusion. UCP-3L (8+/-1 vs. 19+/-2 amol/microg total RNA, P = 0.018) and UCP-3S (11+/-2 vs. 17+/-3 amol/microg total RNA, P = 0.027) mRNA levels increased in skeletal muscle during triglyceride infusion. UCP-3L mRNA levels were positively correlated with plasma NEFA concentrations (r = 0.53, P = 0.005) and with lipid oxidation rates (r = 0.56, P = 0.004) determined by indirect calorimetry. In contrast, the expression of UCP-2 was not affected by lipid infusion in skeletal muscle or in subcutaneous adipose tissue. During the hyperinsulinemic clamp (plasma insulin concentrations 202+/-12 pmol/l), NEFA levels (405+/-49 vs. 648+/-77 micromol/l, P = 0.063) and lipid oxidation rates (0.67+/-0.09 vs. 0.84+/-0.10 mg x kg(-1) x min(-1), P = 0.091) were not significantly increased during triglyceride infusion. Under such conditions, the induction of UCP-3L and UCP-3S mRNA expression was totally prevented (8+/-2 vs. 8+/-1 and 8 +/-2 vs. 9+/-2 amol/microg total RNA, respectively). We conclude that increased plasma NEFA levels by lipid infusion for 5 h induces the expression of UCP-3 but not UCP-2 in humans. During triglyceride infusion, physiological hyperinsulinemia appears to prevent the induction of UCP-3 mRNA levels.

Adipose Tissue↗
PubMed2000

[Mechanisms for weight gain during blood glucose normalization].

Secondary failure to dietary and maximal oral treatment leads to insulin therapy in type 2 diabetic patients. However, weight gain is a frequent side effect of insulin therapy in these patients. Mechanisms for this weight gain are complex. Insulin 1) reduces glycosuria and its caloric expenditure; 2) stimulates the stockage of fatty acids into triglycerides in adipose tissue, thus favoring an increase in adipose mass; 3) yields a positive nitrogen balance through an inhibition of muscle proteolysis, thus favoring an increase in lean mass. Most studies report an average 6 kg weight gain during the first year following the initiation of insulin therapy in type 2 diabetic patients. Analysing body composition variations shows that weight gain results both from an increase in fat mass (mean 63%) and an increase in lean mass (mean 37%). Preexisting obesity does not influence this weight gain. Finally, the 10 year-follow up of UKPDS showed a beneficial effect of insulin therapy on microangiopathy prevention, without increasing cardiovascular mortality as compared with type 2 diabetic patients on oral treatment. Thus, while weight gain seems mandatory, it should not refrain from initiating insulin therapy in poorly controlled type 2 diabetic patients, as its expected beneficial effects on the prevention of microangiopathy seem well established.

Blood Glucose↗
PubMed2000

Insulin sensitivity of glucose and fat metabolism in severe sepsis.

In order to quantify the changes in insulin sensitivity, particularly of endogenous glucose production and fat metabolism, in patients with severe sepsis, a prospective study was conducted in five normal subjects and in five patients with severe sepsis hospitalized in an intensive care unit. The responses of endogenous glucose production, glucose utilization, plasma fatty acids and ketone body concentrations to progressive increase in plasma insulin levels (exogenous insulin infusion rates of 0, 0.5, 1 and 2 m-units x min(-1) x kg(-1)) were measured using the isoglycaemic clamp technique. Total glucose turnover was determined with D-[6,6-(2)H(2)]glucose. In each group, plasma glucose was maintained at basal levels (control subjects, 4.32+/-0.22 mmol x l(-1); patients with sepsis, 7.10+/-2.29 mmol x l(-1); P<0.05). Plasma insulin concentrations were comparable in the two groups at an insulin infusion rate of 0.4 m-unit x min(-1) x kg(-1) for controls and 0.5 m-unit x min(-1) x kg(-1) for patients with sepsis, but differed following infusion at 2 m-unit x min(-1) x kg(-1) (control subjects, 102+/-13.4 m-units x l(-1); patients with sepsis, 124.8+/-19.7 m-units x l(-1); P<0.05). Endogenous glucose production was completely suppressed in control subjects by the first insulin infusion (0.4 m-unit x min(-1) x kg(-1)), but was only suppressed during infusion at 1 m-unit x min(-1) x kg(-1) insulin in patients with sepsis. The glucose utilization rate increased significantly with exogenous insulin infusion in control subjects, but did not increase in patients with sepsis. Plasma non-esterified (free) fatty acid and ketone body levels were significantly decreased in both groups by the infusion of exogenous insulin, but the sensitivity of lipolysis was impaired in patients with sepsis. In conclusion, sepsis impaired to a varying extent the action of insulin on endogenous glucose production, glucose utilization, lipolysis and ketogenesis. Whole-body glucose uptake was the most affected, with a total lack of response to the elevated insulin levels obtained in this study. Suppression of endogenous glucose production and lipolysis could only be achieved with higher doses of insulin than those required in normal subjects.

Adult↗
PubMed2000

[Hypertension and renal insufficiency].

Hypertension is almost an inevitable complication of chronic renal failure and it contributes to the acceleration of its progression to terminal renal failure. Cohort studies and large scale clinical trials carried out in the last 10 years have allowed quantification of the respective influences and interactions of hypertension, proteinuria, and metabolic factors on the rate of degradation of renal function. They have conclusively showed a benefit in normalising the blood pressure in diabetic and nondiabetic renal disease especially when the proteinuria is pronounced and when the treatment includes an angiotensin converting enzyme inhibitor. Hypertension is also an increasingly common cause of renal failure, which may become terminal by its consequences associating vascular and ischaemic lesions of the renal parenchyma. Depending on the country studied, 10 to 25% of new dialysis patients are now classified as hypertensive and vascular renal disease. The individual renal risk of essential hypertension is relatively low except in certain groups, such as the coloured population, especially in the USA. The risk of a significant increase in creatinine is doubled by any increase of 20 mmHg of diastolic blood pressure but long-term studies suggest that the effects of increased systolic blood pressure may be even greater.

Blood Pressure↗
PubMed1999

Defective regulation of phosphatidylinositol-3-kinase gene expression in skeletal muscle and adipose tissue of non-insulin-dependent diabetes mellitus patients.

We investigated the regulation of the mRNA expression of the insulin receptor, insulin receptor substrate-1 (IRS-1) and p85alpha-phosphatidylinositol-3-kinase (PI-3K), three major actors of insulin action, in skeletal muscle from 10 healthy lean volunteers, 13 obese patients with Type II (non-insulin-dependent) diabetes mellitus and 7 non-diabetic obese subjects. The in vivo regulation by insulin was studied using a 3-h euglycaemic, hyperinsulinaemic clamp. There were no differences in the basal concentrations of the three mRNAs in skeletal muscle between groups. Insulin infusion produced a twofold reduction in insulin receptor substrate-1 mRNA expression in the three groups (p<0.02). In contrast, insulin increased p85alpha-phosphatidylinositol-3-kinase mRNA expression in muscle from non-diabetic subjects (+98+/-22% in lean and +127+/-16% in obese, p<0.02) but this effect was totally impaired in Type II diabetic patients (+5+/-12%, NS). A similar defect in insulin action on p85alpha-phosphatidylinositol-3-kinase mRNA expression was observed in abdominal subcutaneous adipose tissue (+138+/-25%, p<0.01 in lean and +46+/-14%, p<0.02 in obese and +29+/-11%, NS in Type II diabetic patients). The lack of action of insulin on p85alpha-phosphatidylinositol-3-kinase mRNA in diabetic subjects was probably not due to a deleterious effect of hyperglycaemia since improvement of the glycaemic control for 10 days did not restore the response in muscle or in adipose tissue. This study provides evidence for a defect in the regulation by insulin of PI-3K gene expression in Type II diabetic patients, thus reinforcing the concept that alterations at the gene expression might be involved in the pathogeny of Type II diabetes.

Adipose Tissue↗
PubMed1999

French mirror site of the NPAC visible human viewer: first year evaluation.

The NPAC visible human viewer (NPAC VHV), graphical interface written in JAVA, freely accessible by the Web, allows the display of anatomic cross-sections of the Visible Human Project developed by the National Library of Medicine. In April 1997, the Medical Media Library of Lyons undertook the construction of a French-language mirror site of the NPAC VHV. The aim of this work is to evaluate first year utilisation of this site. From May 1st, 1997 to April 30th, 1998, the mirror site was consulted 34,752 times. In 45.14% of cases, the request came from France, in 4.42% of cases from Belgium, in 3.98% from Canada and in 2.12% from Switzerland. Other connections came either from a country responsible for fewer than 1% of connections or from unidentified computers. Data analysis showed a peak of connections between 15:00 and 17:00, and an increased number of connections from September to March 1998. The NPAC VHV is housed in 5 sites in the world. It is a software very simple to use. As the figures have no legends, it is more appropriate for group teaching than for self-teaching.

Anatomy, Cross-Sectional↗
PubMed1999

Thermogenic effect of slight hyperglycemia during a lipid infusion.

Resistance to the glucoregulatory action of insulin is a common finding in obesity and may affect thermogenesis. In 13 healthy subjects, we studied the influence of acute insulin resistance induced by a lipid infusion on thermogenesis without any glucose load (n = 4) or during a euglycemic-hyperinsulinemic clamp (n = 5) and an oral glucose tolerance test (OGTT, n = 8). When substrates were not administered at the same time, the energy cost of storage was significantly (P < .05) lower for lipids (3.9%+/-0.9%) than for glucose (11.9%+/-0.5% during the clamp and 14.9%+/-4.0% during the OGTT, NS). The lipid infusion decreased glucose storage during the clamp (control, 3.99+/-0.40 mg x kg(-1) x min(-1); lipid infusion, 0.92+/-0.39; P < .05) but increased it during the OGTT (control, 1.76+/-0.22 mg x kg(-1) x min(-1); lipid infusion, 2.94+/-0.27; P < .05). Infused lipids were stored more (clamp, 3.31+/-0.16; OGTT, 2.65+/-0.11 mg x kg(-1) x min(-1); P < .01) and oxidized less (clamp, 0.64+/-0.21; OGTT, 1.02+/-0.09 mg x kg(-1) x min(-1); P < .05) during the clamp than during the OGTT. When lipids were infused, the energy cost of substrate storage was lower during the clamp versus the OGTT (clamp, 3.2%+/-0.8%; OGTT, 7.3%+/-1.0%; P < .05). This effect was attributed to a lipid-induced impairment of glucose tolerance, which overcomes the inhibitory effect of lipid infusion on glucose storage observed in euglycemia. A slight elevation of plasma glucose in response to a lipid infusion impairs thermogenesis by redirecting the storage of substrates from lipids to glucose, which has a higher energy cost.

Adult↗
PubMed1999

Peritoneal clearance of leptin in continuous ambulatory peritoneal dialysis.

Leptin is a 16-kd protein that increases energy expenditure and limits food intake. Serum leptin (S-leptin) is elevated in dialysis patients, and little data have been reported on leptin clearance (Cl) during dialysis. We analyzed the peritoneal dialysis (PD) Cl of leptin in 15 continuous ambulatory peritoneal dialysis (CAPD) patients and compared the results to beta(2)-microglobulin (beta(2)-m), urea, and creatinine PD Cl. S-leptin was significantly elevated (Kruskal-Wallis, P < 0.005) in CAPD women (58.4 +/- 42.4 [SE] microg/L, n = 5) as compared with CAPD men (13.9 +/- 7.1, n = 10) and with healthy women (11.0 +/- 1.4, n = 13) and men (5.1 +/- 0. 9, n = 14). Correlations were found between percent of fat mass and S-leptin (P < 0.05); between S-leptin and the 24-hour PD leptin (P < 0.05); and between dialysate-to-plasma (D/P) beta(2)-m and D/P leptin (P < 0.01). PD leptin Cl (1.80 +/- 0.43 mL/min/1.73 m(2)) was higher than beta(2)-m Cl (1.22 +/- 0.31) (P < 0.01), but reduced as compared with urea Cl (8.84 +/- 1.20) (P < 0.005) and creatinine Cl (7.71 +/- 0.99) (P < 0.005). These results indicate that leptin is eliminated through the peritoneum membrane. However, peritoneal leptin clearance, as beta(2)-m, appears to be clearly restricted as compared with peritoneal transport of smaller molecules. Hence, leptin could use the same diffusion transport pathway as beta(2)-m. In addition, leptin, which has a higher molecular weight than beta(2)-m, was significantly more eliminated into the peritoneal dialysate. More studies are necessary to clarify whether this is an active leptin elimination process by peritoneal secretion or by a different restriction coefficient of diffusion through the peritoneum membrane.

Aged↗
PubMed1999

Uncoupling protein-2 (UCP2) and uncoupling protein-3 (UCP3) expression in adipose tissue and skeletal muscle in humans.

Uncoupling protein-2 (UCP2) and uncoupling protein-3 (UCP3) are mitochondrial proteins that may play a role in the control of energy expenditure by uncoupling respiration from ATP synthesis. The present review focuses on data obtained in humans. UCP2 is widely expressed in the body, whereas UCP3 expression is restricted to skeletal muscle. Positive correlations have been reported between UCP2 mRNA concentrations in adipose tissue, UCP3 mRNA concentrations in skeletal muscle, and components of the metabolic rate. Fasting induces an up-regulation of UCP2 and UCP3 mRNA expression. In vivo and in vitro studies suggest that fatty acids could modulate uncoupling protein gene expression. The putative relationship between obesity, energy expenditure and uncoupling protein expression, and the unexpected rise in UCP2 and UCP3 mRNA concentrations during short-term fasting, are discussed in view of the recent data obtained in rodents and cell lines.

Adipose Tissue↗
PubMed1999

Cloning and mRNA tissue distribution of human PPARgamma coactivator-1.

OBJECTIVES: To determine human PPARgamma coactivator-1 (PGC-1) amino acid sequence and to study PGC-1 mRNA tissue distribution. PGC-1 is a novel transcriptional coactivator of nuclear receptors that may play a role in the control of thermogenesis. SUBJECTS: Subcutaneous adipose tissue was obtained from six obese and five lean male subjects. Vastus lateralis skeletal muscle was obtained from seven lean and six obese subjects undergoing a 5-day severe calorie restriction. Other tissue biopsies were from nonobese nondiabetic subjects. METHODS: Human PGC-1 was cloned from a skeletal muscle cDNA library. A reverse transcription-competitive polymerase chain reaction assay was developed to determine PGC-1 mRNA levels in human tissues. RESULTS: The human amino acid sequence showed 95% identity with mouse PGC-1. PGC-1 mRNA was expressed at very low levels in the small and large intestines and white adipose tissue. Heart, kidney, liver and skeletal muscle showed higher mRNA levels. The degree of obesity did not affect PGC-1 mRNA levels in adipose tissue while lean subjects expressed more PGC-1 mRNA than obese subjects in skeletal muscle. A 5-day severe calorie restriction induced PGC-1 mRNA expression in skeletal muscle of obese but not of lean subjects. CONCLUSION: PGC-1 shows a restricted tissue expression that suggests a tissue-specific role in the control of gene transcription and possible interaction with various members of the PPAR family. The lower expression of skeletal muscle PGC-1 in obesity could contribute to an alteration of mitochondrial gene expression.

Adipose Tissue↗
PubMed1999

Twenty-five years of experience with out-center hemodialysis.

UNLABELLED: Twenty-five years of experience with out-center hemodialysis. BACKGROUND: Out-center hemodialysis (HD) offers patients a better quality of life, a greater independence, and a better rehabilitation opportunity. A lower mortality than with other modalities of dialysis has been reported. In addition, in France the charges paid depend on the modality of dialysis, out-center HD being the less expensive, and savings are also accomplished through fewer patient transports, which are additionally reimbursed. We present a 25-year experience of out-center HD. METHODS: We retrospectively studied the clinical records of 471 patients treated between 1974 and 1997 in a single nonprofit organization operating regional home HD (H-HD) and facilities for self-care HD (SC-HD). Survival results were analyzed according to: (a) causes of end-stage renal disease, (b) age at the start of HD, (c) period of start of HD, (d) modality of HD (H-HD, SC-HD), and (e) a subgroup of 174 patients defined at risk because they were contraindicated for transplantation. RESULTS: The mean age at the start of HD increased from 31.2 +/- 9.7 (mean +/- SD) years in 1974 to 52.6 +/- 13.5 years in 1997. Causes of the end of treatment were: (a) transplantation (63%), (b) transfer (20%), and (c) death (17%). The overall survival was 90% at 5 years, 77% at 10 years, 62% at 15 years, and 45% at 20 years, and, for the group at risk, 78%, 62%, 46%, and 31%, respectively. Cox proportional hazard analyses showed that risk factors were older age, diabetes, and renal vascular diseases. CONCLUSION: If adequate choice is given, out-center HD offers a reliable and safe modality of dialysis with better survival results than survival in full-care in-center HD. In addition, out-center HD ensures a striking financial benefit as compared with the higher costs if the same patients were treated with full-care in-center HD. These modalities should be encouraged for all HD patients who are able to be treated by out-center modalities.

Adult↗
PubMed1999

Nutritional status of haemodialysis patients: a French national cooperative study. French Study Group for Nutrition in Dialysis.

BACKGROUND: Despite the severity and the prognosis value of undernutrition in haemodialysed patients, no large study is available as yet in Europe. Hence, this French National Cooperative Study aimed to determine the prevalence of undernutrition and its relationship to dialysis efficacy. METHODS: Nutritional status was determined in 7123 patients (i.e. one-third of the French haemodialysis population) using body mass index (BMI), predialysis haemoglobin, albumin, pre-albumin, cholesterol, and also normalized protein catabolic rate (nPCR) and lean body mass (LBM) calculated from pre- and postdialysis urea and creatinine. Dialysis treatment was estimated from weekly dialysis time and KtV determination. RESULTS: Dialysis time was 12.4+/-2.7 h/week and KtV 1.36+/-0.36. BMI was below 20 kg/m2 in 24% and the observed/expected LBM ratio below 90% in 62%. Albumin, pre-albumin and nPCR were below the high-risk thresholds of 35 g/l, 300 mg/l and 1g/kg/day in 20%, 36% and 35% of patients, respectively. Pre-albumin was the most representative nutritional parameter. Albumin, pre-albumin and LBM correlated with nPCR. A dialysis time above 12 h/week was associated with higher BMI, albumin, pre-albumin and LBM. LBM was higher in patients with a KtV value >1.1. CONCLUSION: This study showed life-threatening undernutrition in 20-36% of the studied population, according to nutritional parameters. Protein intake (estimated by nPCR) and dialysis efficacy (estimated by dialysis time and KtV) appeared to be major determinants of nutritional status in this population.

Adult↗
PubMed1999

Effects of rilmenidine on stress-induced peak blood pressure and renal function.

Rilmenidine is an imidazoline I1-receptor agonist that centrally acts by reducing the sympathetic tone. There is strong experimental evidence that natriuresis could be evoked by proximal tubular I1-receptors that have also been isolated in human kidneys. However, in humans, the natriuretic effects of proximal tubular I1-receptors have never been demonstrated. Because stress tests elicited a sympathetically mediated increase in blood pressure and in sodium reabsorption, this study examined whether a short-term infusion of rilmenidine (1 mg) may interfere with stress-induced cardiovascular response and renal sodium handling in normotensive men, in a double-blind, crossover, placebo-controlled study. The stress test used is an efficient and reproducible computerized version of the Stroop's stress test. During the experimental sessions, both basal and stress renal functional parameters were determined: glomerular filtration rate, renal plasma flow, filtration fraction, sodium excretion, and segmental sodium tubular reabsorption (lithium clearance). During the placebo phase, stress induced a significant increase in systolic blood pressure (SBP; 22.2+/-10.1 mm Hg) and diastolic blood pressure (DBP; 11.0+/-5.0 mm Hg). During stress, glomerular filtration rate and renal plasma flow tended to decrease, resulting in a nonsignificant increase in filtration fraction. Despite the increase in BP, stress induced a significant decrease in sodium excretion that was due mainly to a nonsignificant increase in sodium reabsorption in the proximal parts of the tubules. Rilmenidine significantly reduced rest and stress BP, but the cardiovascular reactivity to stress was not altered. The treatment slightly decreased basal glomerular filtration rate and increased renal plasma flow, so that the filtration fraction significantly decreased. The treatment-related decrease in BP was associated with a significant increase in basal sodium reabsorption. Stress-induced modifications in renal function and sodium handling were not altered by the treatment. In conclusion, rilmenidine reduced rest BP and preserved stress-induced reactivity in BP and heart rate. Renal effects of rilmenidine are characterized by a decrease in glomerular filtration rate and in filtration fraction and an increase in sodium reabsorption. The study failed to demonstrate any effect of rilmenidine on stress-induced increase in sodium reabsorption.

Adrenergic alpha-Agonists↗
PubMed1999

Lack of skeletal muscle uncoupling protein 2 and 3 mRNA induction during fasting in type-2 diabetic subjects.

Skeletal muscle uncoupling protein 2 and 3 (UCP-2 and UCP-3) mRNA levels are increased during calorie restriction in lean and nondiabetic obese subjects. In this work, we have investigated the effect of a 5-day hypocaloric diet (1,045 kJ/day) on UCP-2 and UCP-3 gene expression in the skeletal muscle of type-2 diabetic obese patients. Before the diet, UCP-2 and UCP-3 mRNA levels were more abundant in diabetic than in nondiabetic subjects. The long (UCP-3(L)) and short (UCP-3(S)) forms of UCP-3 transcripts were expressed at similar levels in nondiabetic subjects, but UCP-3(S) transcripts were twofold more abundant than UCP-3(L) transcripts in the muscle of diabetic patients. Calorie restriction induced a two- to threefold increase in UCP-2 and UCP-3 mRNA levels in nondiabetic patients. No change was observed in type-2 diabetic patients. Variations in plasma nonesterified fatty acid level were positively correlated with changes in skeletal muscle UCP-3(L) (r = 0.6, P < 0.05) and adipose tissue hormone-sensitive lipase (r = 0.9, P < 0.001) mRNA levels. Lack of increase in plasma nonesterified fatty acid level and in hormone-sensitive lipase upregulation in diabetic patients during the diet strengthens the hypothesis that fatty acids are associated with the upregulation of uncoupling proteins during calorie restriction.

Carrier Proteins↗