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Background: Serum amyloid A (SAA) is an inflammatory marker associated with cardiovascular disease (CVD) and found to be increased in obesity. Obstructive sleep apnea (OSA) syndrome, a frequent complication of obesity also associated with CVD risk, is improved after surgically-induced weight loss. To explore the potential role of SAA in the relation between OSA and CVD, we investigated relationships between changes in SAA concentrations and nocturnal respiratory events in obese subjects undergoing bariatric surgery. Methods: We measured plasma SAA and used nocturnal respiratory polygraphy to assess the apneahypopnea index (AHI), the oxygen desaturation index (ODI) and the mean and lowest O2 saturation (SaO2 ) in 61 morbidly obese patients before either adjustable gastric banding or gastric bypass. For 35 subjects with OSA, the same data were obtained 1 year after the surgery. Results: Before surgery, SAA concentrations were significantly higher in patients with severe OSA (56.26.4 μg/ml) compared to subjects with moderate OSA (22.93.2 μg/ml) or without OSA (16.22.2 μg/ml). Plasma SAA correlated positively with AHI and ODI, and negatively with mean and lowest SaO2. After surgery, plasma SAA decreased significantly by 41.7%, and changes in plasma SAA correlated with variations in OSA parameters. In multivariate analyses, AHI was a predictor of plasma SAA, independent of BMI, both at baseline and during weight loss. Conclusion: The improvement of OSA after bariatric surgery is associated with a decrease in SAA, independent of the change in BMI. SAA may represent a marker of the improvement in CVD risk profile after surgically-induced weight loss in patients with OSA.

AbstractObjective: Adipocytes secrete a series of acute phase proteins including serum amyloid A (SAA); the link with metabolic status is unknown. We studied the variations of expression of the SAA gene in adipose and liver tissues and of SAA serum levels, as well as their relationships with metabolic features during weight loss.Research Methods and Procedures: Plasmatic variations of SAA, inflammatory markers (high sensitivity C-reactive protein, interleukin-6, fibrinogen, and orosomucoid), and adipokines (adiponectin, leptin) were studied in 60 morbidly obese patients before and after gastric surgery. For 10 subjects, SAA mRNA expression was measured at baseline in subcutaneous white adipose tissue (scWAT) and visceral white adipose tissue (vWAT) and in the liver. The evolution of SAA mRNA expression was also studied after surgery in scWAT.Results: SAA serum concentration displayed a significant reduction 3 months after surgery and remained stable beyond 6 months. mRNA expression of inducible SAA isoforms (SAA 1 and 2) in scWAT was higher than in vWAT (p = 0.01) and the liver (p < 0.01) and correlated significantly with BMI, SAA, and high sensitivity C-reactive protein serum concentrations but not with metabolic markers (glucose, insulin, lipid parameters, adiponectin). SAA serum level and its variation during weight loss significantly correlated with adiposity markers (BMI and adipocyte volume, p < 0.01) and inflammatory markers but not with variations of metabolic parameters. The variations of SAA expression in scWAT after surgery correlated with changes in BMI and SAA protein serum levels (p < 0.05).Discussion: SAA can be considered as a marker of adiposity-induced low-grade inflammation but not of the metabolic status of obese subjects.

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/m2; 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.

The aim of this study was to compare three different culture systems for in vitro follicular growth and oocyte maturation in ovarian follicles of mice in order to assess the technique with the optimal growth and improved rate of meiotic maturation. The three systems tested were culture under oil, on a hydrophobic membrane and on agar respectively. Early preantral follicles were cultured for 12 days in α-MEM GlutaMAX medium. Follicular growth, oocyte meiotic maturation, oocyte extrusion, atresia and estradiol production were analysed. Follicular development showed two phases in the three systems, with slow growth before day 5 and subsequent acceleration. The percentage of follicles transferred into oocyte maturation medium was significantly higher after culture under oil. The proportion of oocytes that achieved nuclear maturation (metaphase II) was higher when follicles were cultured under oil or on a hydrophobic membrane than on agar. Our results support the use of culture under oil for in vitro follicular growth from the early preantral stage in order to obtain metaphase II oocytes. Fertilization ability of these oocytes and the capacity to obtain healthy mice in a reproducible manner warrants further investigation.

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.

The circadian variations in plasma progesterone (P) and LH concentrations were investigated in six women, aged 23-40 years. All were studied in the mid-luteal phase (7 ± 2 days after LH mid-cycle surge). Experiments were conducted in autumn and in spring. Blood samples were obtained every 15 min for 24 hr. Plasma P and LH concentrations were measured by RIA. Each subject's time-series was analysed using three methods; visual inspection (chronogram), spectral analysis to estimate component periods of rhythms (τ) and cosinor analysis to quantify the rhythms parameters.Marked temporal variations in plasma P concentration were observed in each subject. The maximal variations over a 24-hr period, ranged between 13-58.5 mmol/1.Differences related to sampling time were statistically validated by ANOVA (p <0.00001). Significant harmonic periods were detected by spectral analysis but differed among subjects. In all subjects but one, a circadian rhythm was detected. The acrophase location was similar (about 0700 hr) in the four subjects studied in autumn, but ranged from 1940 to 0320 hr in those studied in spring. An ultradian rhythm with r = 8 hr was also validated in six time-series with similar acrophases (about 0200,1000, and 1800 hr). Cosinor analysis of pooled data revealed that the 24-hr, 12-hr, and 8-hr rhythms were statistically significant (p = 0.001) in autumn. The algebraic sum of these three cosine functions yielded a circadian waveform with peak-times occurring near 0300 and 1130 hr and a trough-time about 2200 hr. In spring, the circadian pattern appeared quite different, and peak-times were found near 0700 and 2000 hr, and trough-times near 0300 and 1500 hr. Furthermore, the 24-hr mean of P was higher in autumn (28,9 ± 0.4 nmol/l) than in spring (17.2 ± 0.4 nmol/1), p from Anova < 0.00001. The evidence for a similar circadian LH pattern is not as strong. Seasonal, circadian and ultradian rhythms characterize the physiologic time structure of plasma P concentration in mid-luteal phase.

Postmenopausal biochemical hyperandrogenism occurs rarely. The presence of an underlying tumor in women with this condition may be missed without careful evaluation. Androgen excess in these women is the result of either tumoral or nontumoral causes. Factors that distinguish between tumoral and nontumoral etiology have not been identified.

Some patients with premature ovarian failure (POF) experience intermittent resumption of ovarian function. Up to 10 of these women may conceive spontaneously. Fewer data are available on factors predictive for recovery of ovarian function.