Objective: To investigate in normal-weight premenopausal women the relationship between circulating leptin and serum gonadotropins and gonadal steroids, during both spontaneous and pharmacologically induced menstrual cycles. Design: Clinical longitudinal study. Methods: Two groups of age-matched, normal-weight premenopausal volunteer women (groups I and II) were enrolled in this study. Women in group I were free of any hormonal treatment, while women in group II were taking a triphasic estrogen-progestin contraceptive preparation. Blood samples were collected daily in both groups after an overnight fast throughout a complete menstrual cycle. Results: In the spontaneously cycling women, serum leptin concentration positively correlated with estradiol (P < 0.03) and progesterone (P < 0.05) and was higher in the luteal than in the follicular phase (P < 0.05). However, a significant (P < 0.03) short-lasting increase in circulating leptin was present in the late follicular phase of all subjects. In the women using hormonal contraception serum leptin remained unchanged throughout the cycle, along with constantly low values of circulating luteinizing hormone and follicle-stimulating hormone. Conclusions: In normal-weight premenopausal women serum leptin concentrations differ during the menstrual cycle in line with changes in gonadotropin and gonadal steroid concentrations, increasing in the luteal phase of the cycle after a peri-ovulatory peak. These findings suggest a permissive role for leptin with regard to the functioning of the corpus luteum.

BACKGROUND:In steady-state conditions serum leptin concentration is directly related to body fat stores, but is also affected by changes in energy balance. This cross-sectional study investigated the serum leptin concentrations of severely obese patients with binge eating disorder (BED), in whom body fat was greater than normal and, because of eating pattern, rapid and repeated changes in energy balances took place. METHODS: A group of BED obese patients was compared to a group of obese patients with a regular eating pattern with the same body weight, body composition and resting energy expenditure. Serum leptin was measured and the eating attitudes were evaluated by Eating Inventory and Eating Disorder Inventory. RESULTS: In these patients serum leptin concentrations were only weakly correlated to body mass. Furthermore, in BED obese patients serum leptin concentration was higher than in their non bingeing counterparts. CONCLUSIONS: In obese patients both body fat size and eating behavior influence serum leptin concentration, but BED patients binge eating is not triggered by a low leptin value.

The insulin-like growth factor-I (IGF-I) plasma concentration was evaluated as a nutritional parameter in 18 patients affected with chronic malnutrition secondary to biliopancreatic bypass and compared with albumin, transferrin, and with body composition parameters: total body water (TBW), total body sodium (TBNa), total body potassium (TBK). Subjects were studied in malnutritional conditions and after 20 to 30 days of parenteral and enteral refeeding treatment. Immunoreactive IGF-I concentration was 0.35 U/ml +/- 0.07 (mean +/- SEM), significantly lower (p less than 0.01) than in age-matched controls (1.14 +/- 0.07 U/ml, n = 29) and rose significantly (0.84 +/- 0.12 U/ml; p less than 0.01) in parallel with the improvement of nutritional status. The ratios TBNa/TBW, TBNa/TBK, and TBK/TBW were then considered as reference parameters for definition of malnutritional state, and compared with IGF-I as well as with the most commonly used parameters, albumin and transferrin. Before treatment, IGF-I evidenced higher specificity (true negative ratios 0.63, 0.43, and 0.40 with regard to TBNa/TBW, TBNa/TBK, and TBK/TBW, respectively) than albumin (0.13, 0.14, and 0.10) and transferrin (0 in all cases), and slightly less sensitivity (true positive ratios for IGF-I 0.80, 0.67, and 0.67; always one for albumin and transferrin). Moreover, IGF-I resulted definitely more sensitive in assessing the effectiveness of the refeeding treatment and, on the basis of the likelihood ratio, it appeared a good discriminator of the nutritional status. The data indicate that different nutritional factors regulate IGF-I, albumin, and transferrin, and suggest that IGF-I can be used as a reliable and specific nutritional parameter, complementary to the others currently used.

OBJECTIVE: To evaluate the in¯uence of body fat and food intake on serum leptin concentration. DESIGN: Longitudinal study of a group of obese patients prior to and at, long term follow-up, after biliopancreatic diversion (BPD), when body weight was steadily reduced and food consumption was similar to or greater than preoperatively. RESULTS: In obese patients, very high serum leptin concentrations were found. Following the operation, with the body weight stable and normalized, a sharp fall of serum leptin concentration had occurred, with values returned to normal range. CONCLUSION: The changes in serum leptin concentration observed in the long term after weight loss are substantially accounted for by the loss of body fat and appear unrelated to the reduction of oral food intake.

In obese subjects multiple factors underlie the metabolic syndrome and therefore more than one mechanism may account for the clustering characteristics. In obese patients leptin loads only one factor, and therefore leptin does not appear to be a key feature in the metabolic syndrome. On the contrary, multiple correlation and factor analysis data give rise to the hypothesis that in obese patients, leptin may play a protective role against cardiovascular risk.

No abstract

The presence of GH, insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF), oestradiol (E2) and progesterone (PG) were investigated in the fluids obtained from various ovarian follicles of seven patients in whom the induction of super-ovulation was achieved only after GH (0.1 U/kg BW/day) was added to the gonadotrophin therapy. The follicular fluids of six patients responsive to treatment with gonadotrophin alone served as a control. In patients treated with combined therapy, the results demonstrated the presence in the follicular fluids of GH (M +/- SEM: 8.5 +/- 0.6 mU/l), E2 (771 +/- 38 nmol/l), and PG (16.4 +/- 0.7 pmol/l) in significantly higher concentrations compared to that in control follicles (6.2 +/- 0.8 mU/l, 681 +/- 30 nmol/l, and 14.4 +/- 0.6 pmol/l; P = 0.002, 0.012, 0.0001 respectively). Acid-extractable IGF-I (143 +/- 9 ng/ml) and EGF (3.9 +/- 0.3 ng/ml) concentrations were similar to those of control fluids (124 +/- 10 ng/ml and 2.9 +/- 0.7 ng/ml respectively) and were highly correlated with each other (P less than 0.001), suggesting a stimulatory effect of EGF on the local IGF-I production. A correlation between GH and IGF-I (n = 51, r = 0.36), as well as between IGF-I and PG (n = 48, r = 0.77) and E2 (n = 48, r = 0.55) was evident only in the follicular fluid of GH-treated subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

OBJECTIVE: To investigate the short-and long-term effects of dietary restriction on serum leptin in obese women and the role of the gastrointestinal system in the short-term regulation of leptin production. DESIGN: Clinical longitudinal study of anthropometric and serum leptin changes induced in obese women by a balanced 300 kcalad very low calorie diet (VLCD), administered either orally or parenterally for 5 d, and by a balanced 900 kcalad low calorie diet (LCD) lasting six months. SUBJECTS: 20 obese women (age: 38.1 AE 12.7 y; body mass index (BMI): 40.2 AE 8.3 kgam 2 ). RESULTS: Five days following VLCD, a modest, even if signi®cant (P`0.0001), fall of both body weight (BW) and BMI was observed, along with a dramatic ( b 50%) highly signi®cant (P`0.0001) reduction of circulating serum leptin. Baseline and ®ve-day anthropometric and biochemical ®ndings were closely similar in the group of orally fed subjects, when compared with those of their parenterally fed counterparts. The baseline positive correlation between serum leptin and BMI (r r 0.533) increased (P`0.05) at the end of the ®ve day VLCD (r r 0.849). A further fall of BW and BMI was observed at day 30 (P`0.001) and day 180 (P`0.01) during the 900 kcalad LCD, while the serum leptin concentration gradually increased until day 180 when it was only slightly but non signi®cantly lower than at baseline. At the end of the study, the correlation between serum leptin and BMI was similar to the baseline (r r 0.562). CONCLUSIONS: Energy restriction causes a fall of serum leptin apparently not mediated by gastrointestinal signals and it seems not to affect the long-term regulatory pathways of circulating leptin.