Biomedical subjects

M Lage

Publications and source records attributed to M Lage.

At least 19 recordsLinked to original sources

PubMed2006

Comorbid conditions in men with ED before and after ED diagnosis: a retrospective database study.

Although erectile dysfunction (ED) has been considered a complication of other medical conditions, clinicians and researchers suggest that ED may serve as a clinical marker of vascular health. This retrospective claims study examined the prevalence of predefined comorbid conditions in men with ED (N=301 994) in the 12 months before and the 6 months following ED diagnosis. Consistent with previous research, comorbid conditions were prevalent among men with ED. Comorbid conditions were most often diagnosed before an ED diagnosis, although new diagnoses in the 6 months following an ED diagnosis were common and occured more frequently than new diagnoses in a matched sample of men without ED during the same period. Differences by age, region and insurance coverage for ED medications were also examined. Findings support previous research that suggests ED may serve as a marker for previously undetected comorbid conditions.

Adolescent↗

PubMed2004

High leptin levels in women developing postpartum thyroiditis.

BACKGROUND: There is experimental evidence that leptin is required for the development of T helper 1 (Th1)-mediated autoimmune diseases. However, to our knowledge, there are no studies demonstrating such a role in human autoimmune thyroid disease. OBJECTIVE: In the present study we have retrospectively examined patients developing postpartum thyroiditis (PPT), as a model of autoimmune disease, for changes in serum leptin levels during the postpartum period. MATERIALS AND METHODS: The study group included 61 women in the first month postpartum who were positive for thyroid peroxidase antibodies (TPOAb+ve). Twenty TPOAb-negative (-ve), age and body mass index (BMI)-matched, postpartum women were enrolled as the control group. All subjects were evaluated for BMI, serum leptin values, thyroid function [serum free-triiodiothyronine (FT3), free-thyroxine (FT4), thyrotropin (TSH)] and autoimmunity [TPOAb levels and complement activity index (C3 index)] at 4, 12, 16, 20 and 24 weeks' postpartum. During the postpartum period, 32 of 61 TPOAb+ve women (52.4%) showed one or more episodes of thyroid dysfunction (PPTD group), whereas the remaining 29 TPOAb+ve women remained euthyroid throughout the study period (PPTE group). None of the control group developed thyroid dysfunction. RESULTS: Four weeks postpartum, TPOAb+ve women showed higher serum leptin values than TPOAb-ve women, despite comparable BMI. At this time, PPTE and PPTD patients showed no significant differences in leptin levels or leptin/BMI ratio. Throughout the postpartum period, PPTD patients maintained significantly higher leptin values and leptin/BMI ratio compared to the healthy women. In PPTE women, however, a significant reduction in leptin levels and leptin/BMI ratio was seen at 12 weeks' postpartum. This decrease was transient and correlated negatively with the variation in C3 index at the same time. No significant correlation was found between serum leptin variations and FT4 or TSH levels. CONCLUSIONS: This study has demonstrated that women developing postpartum thyroiditis have higher leptin values compared to the healthy women. The higher levels were maintained for 6 months postpartum. This result would suggest an involvement of leptin in the pathogenesis of postpartum thyroid disease, although further studies are needed to characterize the reciprocal effects of leptin, immune system and thyroid hormones during the course of this disease.

Adult↗

PubMed2004

Therapeutic optimization of growth hormone deficiency in children and adolescents.

More than 40 years after the introduction of growth hormone (GH) treatment, many questions remain unanswered. Clearly, with the availability of rhGH and with current treatment protocols, treatment efficacy has improved. However, it still remains unclear whether current treatment protocols are the best possible. Before GH deficiency was recognized as a chronic disease, children only received treatment until normal adult height had been reached. However, it has recently been shown that not all GH-dependent body structures and functions normalize in parallel with height. Furthermore, in adolescents with GH deficiency, the interruption of GH substitution leads to severe hormone deficiency symptoms in adulthood. In the case of an adolescent who meets the biochemical criteria for GH deficiency in adulthood, but does not show alterations of metabolism, body structure, or emotional state, should GH treatment be started in adolescence, or only if and when the clinical syndrome becomes apparent? This is a difficult question to which there is not yet any clear answer, and we suggest that there is a need for further studies in this area. Furthermore, it will be necessary to re-evaluate the situation of patients who have completed their growth, and definitive conclusions will require controlled studies.

Adolescent↗

PubMed2003

Mechanisms underlying the neuroendocrine response to physical exercise.

Exercise initiates a coordinated series of physiological responses, including hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system activation, that, in combination, lead to the appropriate selection and utilization of metabolic substrates. Physical activity acts as a powerful stimulus for the hypothalamic-pituitary axis, leading to the liberation of several neuroendocrine hormones. The nature of this stimulation varies according to the kind of exercise (intensity, duration, aerobic, strength) and subject characteristics (gender, previous training), as well as depending on the time of the day and meal ingestion. As a whole, the neuroendocrine responses to exercise represent an accurate regulator of fuels (glucose, free fatty acids) homeostasis in a special situation characterized by a drastic increase of the energy requirements at muscle level. In this article the current knowledge about this topic is reviewed.

Energy Metabolism↗

PubMed2002

Presence of bovine leptin in edible commercial milk and infant formula.

Leptin is a hormone secreted by the adipocytes that contribute to the control of energy balance, and circulating leptin levels reflect the amount of adipose tissue in the body, helping to regulate food intake and energy expenditure. Since it has been shown that human milk contains immunoreactive leptin, which is identical to intact human leptin, we decided to investigate the possible presence of immunoreactive bovine leptin in different kinds of common commercial milk. To determine the presence or absence of immunoreactive leptin in bovine milk for human consumption, 81 samples (66 commercial pasteurized milk and 15 artificial formulae for new-born babies) of the most common Spanish commercial types of milk were studied. All samples were evaluated before and after centrifugation, and leptin levels were measured by RIA. Leptin was detected in all samples and RIA standard curves were not perturbed when centrifuged and non-centrifuged milk replaced the buffer. Mean values of leptin in full-cream, semi-skimmed and skimmed samples, were: 5.7+/-0.3 ng/ml, 4.1+/-0.1 ng/ml, 3.7+/-0.1 ng/ml (significantly different). Leptin values were reduced after centrifugation. A significant correlation was observed between leptin levels and lipid content (p<0.0005, r=0.67) while no correlation was observed with respect to carbohydrate and protein levels. Interestingly, some preparations of infant formulae present very high leptin values reaching up to 18.9 ng/ml. In conclusion, leptin is present in significant and variable concentrations in edible commercial bovine milk, with higher concentrations in infant formula.

Animals↗

PubMed2002

Effect of long-term strength training on glucose metabolism. Implications for individual impact of high lean mass and high fat mass on relationship between BMI and insulin sensitivity.

The aim of this study was to examine the independent effect of high lean mass on glucose metabolism, as well as its consequences on the classic relationship between BMI and insulin sensitivity (SI) in 3 groups: 1) 8 strength-trained males with BMI >27 kg/m2 (athletes); 2) 10 sedentary males with BMI >27 kg/m2 (obese); and 3) 12 sedentary males with BMI 22-25 kg/m2 (control). Body composition was measured with impedance analysis. Iv glucose tolerance test was performed at 09:00 h after overnight fast. Estimation of insulin sensitivity and glucose effectiveness by Minimal Model Approach. Plasma glucose and insulin determination by glucose-oxidase and RIA respectively. BMI and lean mass (LM) were greater in athletes than in controls, but there were no differences in fat mass (FM), basal glucose (Gb), basal insulin (Ib), glucose tolerance (Kg), SI, glucose effectiveness (Sg), acute insulin response to glucose (AIRG) and leptin. Obese showed greater FM, leptin, lb and AIRG than athletes, while SI was lower; BMI, LM, Gb, Kg and Sg were similar. BMI, FM, LM, Ib, AIRG and leptin were lower in controls than in obese, while SI index was greater; Gb, Sg and Kg were similar. We found that: 1) Resistance exercise does not modify glucose effectiveness, but can improve insulin sensitivity through FM reduction (LM augmentation alone has no effect on glucose metabolism); and 2) High BMI causes insulin resistance only if it depends on adipose tissue hypertrophy.

Adipose Tissue↗

PubMed2002

A single growth hormone (GH) determination is sufficient for the diagnosis of GH-deficiency in adult patients using the growth hormone releasing hormone plus growth hormone releasing peptide-6 test.

BACKGROUND: The diagnosis of GH deficiency in adults is based on the provocative testing of GH secretion. When testing a patient with suspected GH deficiency, clinicians assess the whole secretory curve and select the GH peak as an index of secretory capability. This procedure is time consuming and the determination of GH in several samples is necessary. The combined administration of growth hormone releasing hormone (GHRH) plus growth hormone releasing peptide-6 (GHRP-6) is an effective test of GH secretion, and it has been unambiguously demonstrated that the elicited GH peak is capable of segregating normal GH secretion subjects from GH deficient patients on an individual basis. The GHRH + GHRP-6 test biochemically classifies patients into three groups; those with a stimulated GH peak >/= 20 micro g/l are considered normal and those with peaks at </= 10 micro g/l as GH deficient. The group comprising individuals between these parameters is considered uncertain, and the results are further interpreted according to clinical information, or by other tests. OBJECTIVE: As the GHRH + GHRP-6 test induces GH peaks consistently in the first 30 minutes, the working hypothesis assessed in this study was whether a single determination of GH 30 minutes after stimulus could provide the same clinical classification as the whole secretory curve. PATIENTS AND METHODS: Three hundred and forty-nine adult subjects (146 patients with organic pituitary disease and 203 healthy subjects) were studied. All were administered GHRH 1 micro g/kg i.v. plus GHRP-6 1 micro g/kg i.v. at 0 minutes, and blood samples were obtained at regular intervals. GH was determined in all samples. RESULTS: GHRH + GHRP-6-evoked GH peaks in controls and patients were not correlated with GH basal values, making this determination useless for test validation. In contrast, an excellent correlation was observed between GH values at 30 minutes and the GH peaks (r = 0.994, P < 0.0001). When comparing the 30-minute GH values against the peaks, the biochemical classification changed from normal toward uncertain in only five out of 203 control subjects, which is without clinical relevance according to Bayes theorem. Similarly, when the 30-minute value was used instead of the peak in GH deficient patients, only two out of 146 patients moved from the uncertain area toward the GH deficient one. Thus, better diagnostic classification was provided for patients. CONCLUSIONS: The GHRH + GHRP-6 test is a convenient, safe and reliable, provocative test of GH reserve in adults, which can be reduced to a single fixed GH determination 30 minutes after stimulus.

Adolescent↗

PubMed2001

Retinoic acid and vitamin D(3) powerfully inhibit in vitro leptin secretion by human adipose tissue.

Leptin, the product of the ob gene, is secreted into the circulation by white adipose tissue; its major role being to participate in the regulation of energy homeostasis. Plasma leptin levels are mainly determined by the relative adiposity of the subject; however, the great dispersion of values for any given body mass index and the noteworthy gender-based differences indicate that other factors are operating. Steroid hormones actively participate in the regulation of leptin secretion; however, non-steroid nuclear hormones have either not been studied or have provided contradictory results. In order to understand the role of hormones of the non-steroid superfamily such as 3,5,3'-tri-iodothyronine (T(3)), vitamin D(3) and retinoic acid (RA) in the control of leptin secretion, in the present work doses of 10(-9), 10(-8) and 10(-7) M of these compounds have been studied on in vitro leptin secretion. The organ culture was performed with omental adipose tissue samples from healthy donors (n=28). T(3) was devoid of effect at any dose studied, while an inhibition of leptin secretion was observed with 9-cis-RA (slight) and all-trans-RA (potent). Interestingly, vitamin D(3) exerted a powerfully inhibitory role at the doses studied, and its action was synergistic with all-trans-RA. In conclusion, in vitro leptin secretion by human adipose tissue is negatively controlled by either RA or vitamin D(3). The clinical significance of leptin regulation by this superfamily of nuclear receptors remains to be ascertained.

Adipose Tissue↗

PubMed2000

The in vitro secretion of human leptin is gender-dependent but independent of the body mass index of the donors.

OBJECTIVE: Leptin is an adipocyte-secreted hormone acting as a signal to the central nervous system, where it regulates energy homeostasis and neuroendocrine processes. Leptin plasma levels are mainly regulated by the percentage of body fat, but are also controlled by several metabolic and nutritional variables. Data regarding leptin secretion suggest that it is gender regulated, and higher levels are present in women than men; however, the biological basis for this sex-related difference is unknown. To clarify those points, a systematic study with tissue cultures from human omental adipose tissue was performed. DESIGN AND METHODS: Surgically obtained samples from 137 patients (68 women, 69 men) were evaluated. The assay was standardized in periods of 24 h ending at 96 h. Each adipose tissue sample from a single donor was incubated in triplicate and leptin results expressed as the mean of the integrated secretion into the medium (nanograms of leptin/g tissue per time). RESULTS: Tissue adipose cultures showed a steady leptin secretion throughout the 96 h studied, with the peak of secretory activity reached at 48 h; afterwards, the in vitro secretion reached a plateau state. Spontaneous leptin secretion in the 24 h and 48 h period, as well as the area under the curve analyzed in the 0-48 h period, showed a gender-based difference that was significantly (P<0. 05) higher in women than in men. When data of spontaneous leptin secretion were correlated with the body mass index (BMI) of the donors, no correlation was found. This suggests that in vivo leptin levels are dependent on the total amount of fat of the individual, but independent of the leptin secretory rate by the adipose tissue of the donor. CONCLUSIONS: Leptin secretion from omental adipose tissue in vitro is: (i) significantly higher in samples from women than in samples from men; and (ii) not correlated with the BMI, showing that in vitro leptin secretion is not related to the adiposity of the donor.

Adipose Tissue↗

PubMed1999

Effect of resistance exercise (body building) training on serum leptin levels in young men. Implications for relationship between body mass index and serum leptin.

UNLABELLED: Available data about the influence of exercise on leptin level are controversial, and there are no studies concerning leptin levels in trained men with low fat mass plus large increase of muscle. 65 healthy young male matched for age were separated in three groups. 1) 25 non-professional body builders; 2) 21 mild overweight sedentary subjects; 3) 19 normal weight sedentary controls. Body composition was determined by bioelectrical impedance. Serum leptin was measured in duplicate by RIA. STATISTICS: Student's t and Pearson's test. Athletes showed similar BMI than overweight subjects: 26.98+/-0.49 vs 27.12+/-0.41 but lower fat mass: 12.53+/-0.96 vs 16.16+/-1.01 % (p=0.0064) and lower leptin: 4.66+/-0.51 vs 7.31+/-0.76 microg/l (p=0.014). Athletes showed higher BMI than controls: 26.98+/-0.49 vs 23.08+/-0.30 (p<0.0001) but similar fat mass: 12.53+/-0.96 vs 12.48+/-0.73% and leptin: 4.66+/-0.51 vs 4.79+0.58 microg/l. Overweight subjects showed higher BMI than controls: 27.12+/-0.41 vs 23.08+/-0.30 (p<0.0001), higher fat mass: 16.16+/-1.01 vs 12.48+/-0.73% (p=0.0064) and higher leptin: 7.31+/-0.76 vs 4.79+/-0.589 microg/l (p=0.014). When leptin was calculated by fat mass no differences were observed between the three groups. There was a significant correlation between leptin and fat mass in all groups. Leptin correlated with BMI in overweight subjects (r=0.438, p=0.0463), but this correlation was not observed either in athletes or in controls. In conclusion 1) regardless of the high BMI characteristic of body builders, no correlation was observed with leptin; 2) trained state induced by resistance exercise does not influence leptin production independently of variations in body composition.

Adipose Tissue↗

PubMed1999

Serum leptin levels in women throughout pregnancy and the postpartum period and in women suffering spontaneous abortion.

OBJECTIVE: In pregnancy, important changes occur in the body weight of the mother, caused by sodium and water retention and by an increase in body fat tissue, but the mechanisms that regulate maternal and foetal changes in fat mass are poorly understood. Leptin is a hormone produced by adipocytes in order to regulate food intake and energy expenditure at the hypothalamic level in man. In order to verify whether leptin participates in the changes in body composition during pregnancy and postpartum, 630 healthy women were studied at specific time periods and leptin and auxological parameters were determined. DESIGN: A cross-sectional study in which leptin levels were measured in women at specific time periods related to pregnancy. Each woman was assessed only once. PATIENTS: 630 women participated in the study, and were divided into categories as follows: Group A, 29 internal controls, with no previous or current pregnancy; Group B, 73 women in the first trimester of pregnancy; Group C, 60 women in the 24 h before delivery; Group D, 212 women in the 24 h postpartum; Group E, 93 women in the eightH postpartum week (2 months group); Group F, 71 women in the sixteenth postpartum week (4 months group); Group G, 20 women in the sixth month postpartum; Group H, 23 women one year postpartum; Group I, 20 women two years postpartum; finally Group J, of 29 women who had suffered spontaneous abortion in the first trimester of pregnancy and were studied in the 24 h after the stillborn delivery. MEASUREMENTS: Serum leptin levels were measured in duplicate by radioimmunoassay using commercial kits. Height and weight was measured and BMI (kg/m2) calculated. RESULTS: Compared with serum leptin in the control group (11.7 +/- 1.0 micrograms/l), a non significant (NS) increase was observed in the first trimester of pregnancy (14.3 +/- 1.4 micrograms/l), with no parallel changes in body weight. A reduction in leptin occurred in the 24 h after delivery (9.4 +/- 1.4 micrograms/l, P = 0.02). After delivery a progressive increase in leptin concentrations was observed, 13.3 +/- 1.5 micrograms/l at two months (NS) and 17.4 +/- 2.6 micrograms/l at four months (P = 0.035 vs controls). Afterwards leptin values decreased towards normal values at 6, 12 and 24 months after delivery 14.4 +/- 1.8 micrograms/l; 12.9 +/- 1.6 micrograms/l; and 10.1 +/- 1.1 micrograms/l respectively (all NS). With the exception of the postpartum group, a significant correlation was observed between leptin concentrations and body weight or BMI in each group of women studied. In the women who suffered spontaneous abortion in the first trimester of pregnancy a reduction in leptin levels occurred (8.8 +/- 1.0 micrograms/l, P = 0.001 vs first trimester group). CONCLUSION: Serum leptin concentrations rose slightly during pregnancy, fell following delivery and subsequently increased during the first six months postpartum. These variations were unrelated to changes in body composition, and may be responsible for the postpartum weight gain observed in some women. Abnormally low serum leptin levels were observed in women suffering spontaneous abortion in the first trimester of pregnancy.

Abortion, Spontaneous↗

PubMed1999

High serum leptin levels in children with type 1 diabetes mellitus: contribution of age, BMI, pubertal development and metabolic status.

OBJECTIVE: Children with diabetes mellitus are prone to develop obesity and to experience a delay in onset of the pubertal process. In order to understand the role of leptin in these abnormalities, serum leptin levels were analysed in children with type 1 diabetes mellitus. SUBJECTS: Twenty diabetic girls, 23 diabetic boys and 66 healthy children (selected from a reference population of 706 normal children), age-, sex- and BMI-matched with diabetic patients, were studied. MEASURMENTS: Standing height, weight and BMI were determined in each child. Serum testosterone, oestradiol and leptin were measured by specific radioimmunoassays, and HBA1c by high performance liquid chromatography. RESULTS: Both diabetic girls and boys showed higher leptin levels than the normative healthy population and a group of age-, sex- and BMI-matched normal children. In an age-related analysis, leptin levels in diabetic girls rose from 7.4 +/- 1.2 and 8.1 +/- 2.1 microg/l for the 5-7.99 and 8-10.99 year groups, to 12.6 +/- 2.4 microg/l for the 11-13.99 year group, and to 15.6 +/- 4.0 microg/l in the 14-15.99 year group in parallel with body weight. Leptin concentrations were parallel but higher (P < 0.05) than those of healthy girls. Diabetic boys had lower leptin levels than girls and, in contrast with normal boys, did not show a drop after the 10-year period. Leptin levels were 4.9 +/- 2.2, 3.9 +/- 0.2, 5.5 +/- 0.6 and 5.1 +/- 0.9 microg/l for the 5-7.99, 8-10. 99, 11-13.99 and 14-15.99 year groups, respectively. When divided by pubertal stage, leptin levels in the prepuberty stage of diabetic girls (8.6 +/- 1.0 microg/l) were higher (P < 0.05) than those in the controls (4.1 +/- 0.4 microg/l). In overt puberty girls, leptin was higher (P < 0.05) for diabetic (15.9 +/- 2.9 microg/l) than for healthy girls (9.2 +/- 1.1 microg/l). In prepubertal boys, differences were observed in leptin levels (4.9 +/- 0.5 microg/l for diabetic boys and 3.4 +/- 0.6 microg/l for healthy boys). In the overt puberty stage, diabetic boys showed higher (P < 0.05) levels of leptin (5.2 +/- 0.7 microg/l) than the healthy matched controls (2.1 +/- 0.2 microg/l). A multiple step regression analysis in the diabetic children revealed no associations between leptin and other relevant variables such as glycosylated haemoglobin, daily insulin dose, or years of suffering from the disease. CONCLUSION: Serum leptin levels were higher in diabetic than in healthy children. These differences were not attributable to age, adiposity or stage of pubertal development, and were probably conditioned by the metabolic perturbation intrinsic to the diabetic state, or the chronic hyperinsulinemia.

Adolescent↗

PubMed1999

Dihydrotestosterone, stanozolol, androstenedione and dehydroepiandrosterone sulphate inhibit leptin secretion in female but not in male samples of omental adipose tissue in vitro: lack of effect of testosterone.

Leptin, the product of the Ob gene, is a polypeptide hormone expressed in adipocytes which acts as a signalling factor from the adipose tissue to the central nervous system, regulating food intake and energy expenditure. It has been reported that circulating leptin levels are higher in women than in men, even after correction for body fat. This gender-based difference may be conditioned by differences in the levels of androgenic hormones. To explore this possibility, a systematic in vitro study with organ cultures from human omental adipose tissue, either stimulated or not with androgens (1 microM), was undertaken in samples obtained from surgery on 44 non-obese donors (21 women and 23 men). The assay was standardized in periods of 24 h, ending at 96 h, with no apparent tissue damage. Leptin results are expressed as the mean+/-s.e.m. of the integrated secretion into the medium, expressed as ng leptin/g tissue per 48 h. Spontaneous leptin secretion in samples from female donors (4149+/-301) was significantly higher (P<0.01) than that from male donors (2456+/-428). Testosterone did not exert any significant effect on in vitro leptin secretion in either gender (4856+/-366 in women, 3322+/-505 in men). Coincubation of adipose tissue with dihydrotestosterone (DHT) induced a significant (P<0.05) leptin decrease in samples taken from women (3119+/-322) but not in those taken from men (2042+/-430). Stanozolol, a non-aromatizable androgen, decreased (P<0.05) leptin secretion in female samples (2809+/-383) but not in male (1553+/-671). Dehydroepiandrosterone sulphate (DHEA-S) induced a significant (P<0.01) leptin decrease in female samples (2996+/-473), with no modifications in samples derived from males (1596+/-528). Exposure to androstenedione also resulted in a significant reduction (P<0.01) of leptin secretion in samples taken from women (2231+/-264), with no effect on male adipose tissue (1605+/-544). In conclusion, DHT, stanozolol, DHEA-S and androstenedione induced a significant inhibition of in vitro leptin secretion in samples from female donors, without affecting the secretion in samples from men. Testosterone was devoid of activity in either gender.

Adipose Tissue↗

PubMed1999

Prevalence of pregnancy and postpartum thyroid dysfunction in a homogeneous population of Spain.

To determine the prevalence of pregnancy and postpartum thyroid dysfunction in the Spanish population, 691 women divided into six cohorts were studied. Biochemical hypothyroidism was observed in 9.4%, 4.4%, 1.9%, 4.6% and 4.8% at the first trimester of pregnancy, at delivery and at the second, fourth and sixth to twelfth postpartum months, respectively. Biochemical hyperthyroidism was observed in 6.7%, 0.8%, 1.9%, 4.6% and 2.4% in the same cohorts of subjects. Thyroiditis was observed in 4%, 0%, 0.6%, 6.2% and 7.3% in the cohorts studied. No depression or psychological alterations were detected either in pregnancy or in the postpartum period. Our data suggest that if screening for thyroid dysfunction is to be recommended in the postpartum period, this must be based on biochemical parameters.

Autoantibodies↗

PubMed1998

Isolation of a bioactive Ca(2+)-mobilizing complex lipid from bovine vitreous body.

Vitreous body extracts show a potent Ca(2+)-mobilizing activity on fibroblast cells. This Ca2+ signal is complex, and due to the presence of two different bioactive substances. The first one was identified as acid FGF. The second one was shown to be a low molecular weight substance identified as a complex lipid by a combination of chromatographic and biochemical data. This finding raises the possibility that non-classical substances with growth factor-like activity might play a role in the regulation of proliferative processes in the eye.

Animals↗

PubMed1998

Gender differences in both spontaneous and stimulated leptin secretion by human omental adipose tissue in vitro: dexamethasone and estradiol stimulate leptin release in women, but not in men.

Leptin is a hormone secreted by the adipocytes to serve as a signal to the central nervous system to regulate energy homeostasis. Circulating leptin mainly reflects both total fat mass and the size of constituent adipocytes, although other ancillary hormonal factors may contribute to its blood concentration. Relevant gender differences in leptin concentrations have been reported, but it is not clear whether the elevated leptin levels in women are an intrinsic property of their adipocytes or merely reflect a greater amount of fat reserves. To clarify these points, a systematic study with organ culture from human omental adipose tissue either stimulated or not with steroid hormones was undertaken in samples obtained at surgery from 67 nonobese donors (33 women and 34 men). The assay was standardized in periods of 24 h ending at 96 h, with no apparent tissue damage. Each adipose tissue sample from a single donor was incubated in triplicate, and leptin results are expressed as the mean +/- SEM of the integrated secretion to the medium (area under the curve; nanograms of leptin per g tissue/48 h). Control nonstimulated samples showed a steady leptin secretion along the 96 h studied, with the peak of secretory activity reached at 48 h; afterward, the in vitro secretion reached a plateau state. Spontaneous leptin secretion in samples from 33 women (3904 +/- 347) was significantly higher (P < 0.05) than that in samples from 34 men (2940 +/- 323). Coincubation of adipose tissue with 1 mumol/L dexamethasone induced a clear-cut leptin increase (P < 0.05) in samples from women (5848 +/- 624; n = 12), but did not change the spontaneous release of leptin in samples from men (3353 +/- 741; n = 6). Similarly, coincubation of adipose tissue with 1 mumol/L estradiol induced a notable leptin increase (P < 0.05) in samples from women (5698 +/- 688; n = 9), whereas it did not alter the secretion in the male samples (3373 +/- 444; n = 6). In samples from both sexes, coincubation with 1 mumol/L estrone or progesterone had no effect, whereas 1 mumol/L forskolin significantly (P < 0.05) reduced leptin release. In conclusion, leptin secretion from omental adipose tissue in vitro 1) is significantly higher in samples from women than in samples from men, 2) is stimulated by dexamethasone and estradiol in women but not in men, 3) is not modified by progesterone or estrone in both sexes, and 4) is inhibited by forskolin in both genders. This different response to the stimulation of adipose tissue may be the biological basis for the gender differences observed in circulating levels of human leptin.

Adipose Tissue↗

PubMed1997

cis-FFA do not alter membrane depolarization but block Ca2+ influx and GH secretion in KCl-stimulated somatotroph cells. Suggestion for a direct cis-FFA perturbation of the Ca2+ channel opening.

It has been reported that cis-unsaturated free fatty acids (cis-FFA) block intracellular Ca2+ rise in EGFR T17 and GH3 cells by perturbing the generation of Ins(1,4,5)P3. In the present work, it was found that cis-FFA did not alter potassium-induced cell depolarization in GH3 cells, while blocking Ca2+ rise and GH secretion. Interestingly enough, saturated or trans-unsaturated FFA exert the opposite actions, i.e., they block cell depolarization without altering Ca2+ rise and hormone secretion. As depolarization activates GH3 cells via direct opening of Ca2+ channels with no generation of intracellular mediators, these results suggest that cis-FFA act by a direct perturbation of the Ca2+ channel opening.

Animals↗

PubMed1997

Serum leptin levels in normal children: relationship to age, gender, body mass index, pituitary-gonadal hormones, and pubertal stage.

UNLABELLED: It is commonly accepted that at least in girls puberty starts when a minimum level of body mass or a certain amount of body fat are present. However the precise signal by which adipose stores inform the hypothalamus of the degree of energetic reserves is unknown. Leptin is a hormone produced by the adipocytes to regulate food intake and energy expenditure at the hypothalamic level. To understand whether leptin is the adipose tissue signal that allows puberty, 789 normal children of both sexes, age 5-15 yr, were transversally studied. Leptin levels, as well as gonadal and gonadotropins, levels, were analyzed in addition to the determination of auxological parameters. In an age-related analysis, leptin levels in girls rose from 5-15 yr (from 4.3 +/- 0.4 to 8.5 +/- 0.9 micrograms/L) in parallel with body weight. Boys always had lower leptin levels than girls (3.3 +/- 0.3 micrograms/L at 5 yr), but they rose in parallel with weight until 10 yr (5.3 +/- 0.7 micrograms/L), when a striking decrease was observed until 15 yr (3.0 +/- 0.3 micrograms/L). In girls, leptin was the first hormone to rise followed by FSH and later by LH and estradiol. A similar pattern occurred in boys, despite the fact that leptin dropped after 10 yr when testosterone rises. Divided into three pubertal stages, i.e. P1 = prepuberty, P2 = early puberty, and P3 = overt puberty, in girls the four hormones rose progressively from P1 to P3, but from P2 to P3 the present increment was greater for LH and estradiol. In boys, leptin decreased from P1 to P3, whereas FSH, LH, and testosterone rose. The age-related changes were not caused by adiposity variations, because data did not change when subtracting values of children over 97% of standard deviation score of body mass index. IN CONCLUSION: 1) leptin appears to increase in both boys and girls before the appearance of other reproductive hormones related to puberty; 2) leptin levels in boys are always lower than in girls, although they increase with age until the age 10 yr; 3) leptin in boys declines about the time testosterone increases. Leptin may well be a permissive factor for the initiation of pubertal events.

Adolescent↗