Sexual dimorphism on growth hormone secretion after oral glucose administration.

Sexual dimorphism of GH secretion is unclear in humans. There is evidence that oral glucose (OG) administration initially decreases and subsequently stimulates GH secretion. Our aim was to study fasting GH concentrations and their response to OG administration in obese and healthy women and men, in order to elucidate the mechanism of sexual dimorphism of GH secretion and the possible contribution of ghrelin. We selected 33 women and 11 men as obese and healthy subjects. After an overnight fast, 75 g of oral glucose were administered; glucose, insulin, ghrelin, and PYY1-36 were obtained at baseline and during 300 min. Fasting GH (µg/l) was higher in women than men; 1.3 ± 0.3 vs. 0.2 ± 0.1, p=0.009, for women and men, respectively. The area under the curve between 0 and 150 min (AUC) of GH (µg/l · min) was higher in women than men; 98.2 ± 25.9 vs. 41.5 ± 28.6, p=0.002, for women and men, respectively. The AUC of total ghrelin (pg/ml · min, mean ± SEM) between 0 and 150 min was borderline and significantly higher in women than men; 128 562.3 ± 8 335.9 vs. 98 839.1 ± 7 668.6, p=0.069, for women and men, respectively. Several initial time points were higher in women than men. Glucose, insulin, and PYY1-36 were similar in women and men after OG. There were significant correlations between indices of post-oral glucose GH and ghrelin secretion. Fasting and initial GH secretion is higher in women than men, in contrast to peak and late GH secretion, which is similar in both cases. Sexual dimorphism in the regulation of GH secretion probably involves ghrelin.

Growth hormone, ghrelin and peptide YY secretion after oral glucose administration in healthy and obese women.

The mechanism of the altered GH secretion in obesity is unclear. There is evidence that oral glucose (OG) administration initially decreases and subsequently stimulates GH secretion. Ghrelin is a peptide that displays strong growth hormone-releasing activity. Its physiological importance on GH regulation is unclear. Our aim was to study fasting GH concentrations and their response to OG administration in relation with ghrelin secretion in obese and healthy women, in order to elucidate the hypothetical participation of ghrelin on post-oral glucose GH secretion. 36 women were included in the study. After an overnight fast, 75 g of oral glucose was administered; glucose, insulin, ghrelin, and PYY (1-36) were obtained at baseline and during 300 min. The area under the curve between 0 and 300 min (AUC) of GH µ/l·min) was lower in obese patients than in controls; 262.5±57.5 vs. 534.9±95.6, p=0.01, for obese and controls respectively. GH peak (µg/l) was lower in obese patients than in controls; 3.7±0.7 vs. 7.1±1.0, p=0.012, for obese and controls, respectively. The AUC of total ghrelin (pg/ml·min) was lower in obese patients than in controls; 233,032±12,641 vs. 333,697±29,877, p=0.004, for the obese patients and controls respectively. PYY (1-36) was similar in obese and healthy women after OG. There were significant correlations between the different indices of post-oral glucose GH and ghrelin secretion. These data suggest that ghrelin is a physiological regulator of GH in the post-oral glucose state, and the decreased ghrelin secretion could be one of the mechanisms responsible for the altered GH secretion in obesity.

Meaning and diagnostic value of determining the lysozyme level of pleural fluid.

We determined the levels of lysozyme in pleural fluid and serum in 141 patients with the following different causes for their pleural effusions: tuberculosis; neoplasias; transudates; parapneumonic, not complicated; empyemas; and miscellaneous. The lysozyme level of the pleural fluid and the ratio of that level over the serum level of lysozyme (PL/SL ratio) was meaningfully increased in patients with empyema (p less than 0.01). The groups with tuberculous and neoplastic effusions showed significant differences in the PL/SL ratio (p less than 0.01). The existence of a raised PL/SL ratio suggested important local synthesis of lysozyme, and it came up in empyemas and tuberculosis, unlike the other groups. Excluding the patients with empyemas, a PL/SL ratio of 1.2 showed a sensitivity of 100 percent, specificity of 94.9 percent, positive predictive value of 94.7 percent, negative predictive value of 100 percent, and accuracy of 97.3 percent for the diagnosis of tuberculous pleural effusion. All of this suggests that the determination of the lysozyme level can be an easy method of great usefulness in the initial diagnosis of pleural effusions.

Diagnostic value of simultaneous determination of pleural adenosine deaminase and pleural lysozyme/serum lysozyme ratio in pleural effusions.

We have determined simultaneously the ADAp and Lp/Ls ratio in 138 pleural effusions: 61 tuberculous; 42 malignant; 14 transudates; five parapneumonic uncomplicated; six empyematous; and ten cases belonging to a miscellaneous group which included two disseminated lupus erythematosus; two posttraumatic; one pancreatitis; one pleuropericarditis by Mycoplasma; one viral pleuropericarditis; and three pulmonary embolisms. This has allowed us to clear the overlapping for the ADAp activity among tuberculous patients (two cases of lupus and three cases of malignant effusions) in our series. The overlap in the Lp/Ls ratio among tuberculous patients, two malignant, and two parapneumonic uncomplicated cases was also cleared. Fixing the ADAp values at 33 U and the Lp/Ls ratio at 1.2, the tuberculous pleural effusion cases were differentiated from the nontuberculous with a sensibility, positive predictive value, negative predictive value, and safety diagnosis of 100 percent. It has been proven that there is a good correlation between ADAp and Lp/Ls ratio (r = 0.717) and the ADAp and Lp (r = 0.660).

Effect of acute ghrelin administration on glycaemia and insulin levels in obese patients.

OBJECTIVES: Ghrelin is a 28-amino-acid peptide, predominantly produced by the stomach. There are several studies that suggest the importance of ghrelin in obesity. However, the pancreatic endocrine response to ghrelin in obesity is unclear at present. The aim of this study was to clarify whether ghrelin administration influences glucose and insulin levels in obese patients. PATIENTS AND METHODS: Six obese female patients (31 +/- 3.4 year) with a BMI of 36.1 +/- 7.7 kg/m(2) were studied. Three tests were done: placebo, ghrelin (1 microg/kg, intravenously) and growth hormone-releasing hormone (GHRH; 1 microg/kg, iv) plus ghrelin (1 microg/kg, iv). Blood samples were taken at appropriate intervals for determination of glucose and insulin. Statistical analyses were performed by Wilcoxon and Mann-Whitney tests. RESULTS: Glucose (mean peak, mmol/l) level after placebo administration was 4.9 +/- 0.2. Glucose level after the administration of ghrelin was 5.1 +/- 0.2, not significantly different from the response after placebo (p = NS). Glucose level after the administration of ghrelin plus GHRH was 5.1 +/- 0.2, not significantly different from placebo (p = NS). Insulin (mean peak, mU/l) level after placebo administration was 16.1 +/- 6.1. Insulin level after the administration of ghrelin was 12.3 +/- 1.6, not significantly different from placebo (p = NS). Insulin level after the administration of ghrelin plus GHRH was 11.1 +/- 2.7, not significantly different from the response after placebo (p = NS). CONCLUSIONS: In female obese patients, we did not find significant differences in glucose or insulin levels following ghrelin or GHRH plus ghrelin administration.

Hyperleptinemia is not correlated with markers of protein malnutrition in chronic renal failure. A cross-sectional study in predialysis, peritoneal dialysis and hemodialysis patients.

BACKGROUND: Serum leptin levels are increased in chronic renal failure (CRF) and may potentially contribute to protein malnutrition in this disorder. METHOD: Following a cross-sectional design, we performed a nutritional survey in a wide sample of uremic patients treated conservatively (n = 87), with peritoneal dialysis (n = 71) and with hemodialysis (n = 53). Then, we analyzed the correlation between serum leptin levels and markers of protein malnutrition. We used a multivariate approach, taking into consideration the confounding effect of other factors on the correlation between hyperleptinemia and protein malnutrition. MAIN RESULTS: Both univariate and multivariate analysis disclosed a poor correlation between hyperleptinemia and markers of protein malnutrition. In fact, there were trends to a positive correlation between leptinemia and body protein stores, as estimated from the scrutinized markers. Persistence of the basic correlation between general intake, fat mass and leptin in CRF could partially explain these findings, but neither a negative correlation between leptin levels nor protein nutritional state could be disclosed after controlling for this factor. CONCLUSIONS: Our results do not support a first-line role for hyperleptinemia in the genesis of protein malnutrition of uremia.

Hyperleptinemia in uremic patients undergoing conservative management, peritoneal dialysis, and hemodialysis: A comparative analysis.

We performed a cross-sectional study in a wide sample of patients with chronic renal failure undergoing conservative therapy (CTh) (n = 79), peritoneal dialysis (PD) (n = 75), and hemodialysis (HD) (n = 51), with the aim of analyzing the impact of the different modes of therapy on serum leptin levels. We used a multivariate approach, taking into consideration the potential effects of other epidemiological, dialysis-related, nutritional, and hormonal factors on serum leptin. Leptin levels were higher in patients treated with PD (median, 36 ng/mL) than in those undergoing CTh (10.8 ng/mL) or HD (5.4 ng/mL) (P < 0.0005). This difference persisted after controlling for gender, body mass index, and fasting insulin levels, suggesting that imbalances in these factors may only partially explain the differences found between the three modes of therapy. Leptin levels showed a significant negative correlation with peritoneal protein losses in PD patients but were poorly associated with factors such as proteinuria, daily peritoneal glucose absorption (PD), renal function, or adequacy of dialysis. Leptin and insulin-like growth factor-I (IGF-I) were significantly correlated in PD patients, but the study design did not allow for establishing a meaning for this correlation. In conclusion, serum leptin levels are increased in PD patients when compared with CTh or HD patients. Differences in gender distribution, fat mass, and insulin levels may partially explain these findings, but other undefined factors also may have a role in producing these results.