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Objective: Despite malnutrition being a major problem in hospitalized elderly patients, there is a lack of studies focusing on the comparative value of biological parameters for monitoring renutrition. The aim of this study was to determine which biological parameter(s) could best monitor successful renutrition in hospitalized malnourished elderly patients., Design: The objective of the study was to explore the impact of a 6-week renutrition process on anthropometric and biological parameters in elderly patients and to define the biological parameters associated with weight regain., Patients: A total of 72 hospitalized malnourished elderly patients admitted to a hospital-based geriatric rehabilitation unit., Measurements: Patients were evaluated at admission and at 6 weeks for anthropometric measurements of weight, sum of the four subcutaneous skinfold thicknesses, calf circumference and biological serum parameters including albumin, transthyretin, leptin, IGF-1, IGFBP-1 and IGFBP-3. Renutrition was considered successful if a patient gained at least 5% of body weight over 6 weeks., Results: Leptin was the only biological parameter that increased at 6 weeks in successful renutrition. Leptin variations were not influenced by C-reactive protein variations, in contrast to transthyretin which can be modified by the inflammatory states frequently encountered in geriatric patients., Conclusions: Serum leptin is a more appropriate parameter than transthyretin for monitoring renutrition., (© 2011 Blackwell Publishing Ltd.)

Background: Weight loss is associated with a decrease in both energy expenditure and circulating leptin levels. Whether this holds true when the influence of body composition on energy expenditure and leptin is taken into account remains controversial. The aim of the study was to assess changes in resting metabolic rate (RMR) and serum leptin adjusted for body composition during surgically induced weight loss., Methods: In 36 women (age 42.7+/-8.7 years; BMI 47.2+/-8.5 kg/m(2); mean+/-SD) undergoing laparoscopic adjustable gastric banding (LAGB) for morbid obesity, we measured RMR (by indirect calorimetry), body composition (by dual-energy X-ray absorptiometry) and serum leptin (by immunoradiometry), immediately before and 1 year after surgery., Results: 1 year after LAGB, there were significant decreases in body weight (-23.7+/-11.6 kg, P<0.001), fat mass (FM: -20.9+/-11.3 kg, P<0.0001), lean body mass (LBM: -3+/-5.3 kg, P=0.005), RMR (-298+/-309 kcal/day, P<0.0001), serum leptin (-24.0+/-18.4 ng/ml, P<0.0001), RMR/LBM ratio (-3.9+/-5.8 kcal/kg LBM/day, P<0.01) and leptin/FM ratio (-0.21+/-0.29 ng/kg FM/ml, P<0.001). RMR values after surgery were correctly predicted by the regression equation relating RMR to LBM and FM at baseline, whereas this was not the case for serum leptin (in relation to FM)., Conclusions: Changes in RMR 1 year after LAGB were explained by changes in body composition whereas changes in serum leptin were not. The data provide no evidence for a metabolic adaptation of RMR with weight loss, but suggest that serum leptin is decreased beyond expected values based on body composition, a factor that may favor weight regain after surgically induced weight loss.

Background: Certain adipose-produced signals are secreted in proportion to body fat mass and are involved in regulation of the energy metabolism of the whole body. Leptin, IL6 and adiponectin can be considered as adiposity signals. Several Single Nucleotide Polymorphisms (SNPs) in genes encoding for these molecules are known to influence their concentration in situations of stable weight. We hypothesized that polymorphism effects could be better detected in a situation of negative energy balance and that modified concentrations of adiposity signal genes could change the dynamics of weight gain in obese subjects., Methods: 65 obese patients undergoing gastric banding surgery were genotyped for LEP+19A-->G, LEP-2548G-->C, IL6-174G-->C, APM1-11377C-->G and PM1-11391G-->A common SNPs. BMI and concentrations of leptin, IL6 and adiponectin were measured before surgery and after 1 year., Results: All SNPs except IL6-174G-->C SNP were associated with modifications of the circulating concentrations of signals produced by adipose tissue at baseline. During weight loss, variant genotype carriers of LEP -2548 and +19 SNPs were characterized by a trend towards less decrease in circulating leptin. Weight loss was associated with an increase in IL6 concentration (16.9%+/-12.2) in the IL6-174 C/C genotype carriers, whereas the C/G or G/G genotypes carriers showed a decrease in IL6 (19.9%+/-5.2, P=0.001)., Conclusion: We observed that the SNPs studied could modulate the concentration of adiposity signals not only at baseline but also during weight loss. Such variations may be sensed by the homeostatic feedback system that controls energy balance and may in turn contribute to some disturbances in weight regulation.

Our objectives were to analyse carbohydrate metabolism in a series of ALS patients and to examine potential association with parameters of lipid metabolism and clinical features. Glucose tolerance was assessed by the oral glucose tolerance test in 21 non-diabetic ALS patients and compared with 21 age- and sex-matched normal subjects. Lipids and lactate/pyruvate ratio, levels of pro-inflammatory cytokines (tumour necrosis factor-alpha and interleukin-6) and adipocytokines (leptin and adiponectin) were also measured in ALS patients. Mann-Whitney U-tests analysed continuous data and Fisher's exact tests assessed categorical data. Blood glucose determined 120 min after the glucose bolus was significantly higher in patients with ALS (7.41 mmol/l±1.68) compared to controls (6.05±1.44, p=0.006). ALS patients with impaired glucose tolerance (IGT) according to WHO criteria ( n=7, 33%) were more likely to have elevated free fatty acids (FFA) levels compared to patients with normal glucose tolerance (0.77 nmol/l±0.30 vs. 0.57±0.19, p=0.04). IGT was not associated with disease duration or severity. In conclusion, patients with ALS show abnormal glucose tolerance that could be associated with increased FFA levels, a key determinant of insulin resistance. The origin of glucose homeostasis abnormalities in ALS may be multifactorial and deserves further investigation. [ABSTRACT FROM AUTHOR]