The objective of this study was to determine the effect of body fat distribution and hyperinsulinemia on the occurrence of ovulation. Fifty-six women (20–35 years old) either with overweight or obesity (body mass index ≥25) were studied. They were classified in two groups according to waist/hip ratio (WHR); one with predominance of adiposity in the upper body segment (n = 29, WHR >0.85) and the other with predominant adiposity in the lower body segment (n = 27, WHR ≤0.85). Basal body temperature and serum progesterone were determined in each cycle during 6 months. Serum insulin levels were measured at baseline and 30, 60, 90, 120 and 180 min after a 75-gram oral glucose load. The mean insulin values in response to oral glucose load in patients with upper body segment obesity were significantly higher than those corresponding to women with lower body segment obesity. Furthermore, the ratio between ovulated cycles and all the cycles studied in patients with upper body segment obesity was significantly lower than that observed in patients with lower body segment obesity. Upper body obesity seems to affect the ovulatory process and this may be related to the presence of hyperinsulinemia.
Changes in fetal weight might be explained by the different concentrations of IGF. The structural homology between IGF-1 and insulin could mean that the presence of higher levels of IGF would result in a increased energetic metabolism that could contribute to fetal growth. EGF levels were not related to IUGR, and TGF-beta levels increased only during the first 3 months in the IUGR group. This observation correlates with the in vitro action of TGF-beta as a negative factor of growth, but as a positive support for sustaining early pregnancy. Our data illustrates that low height represents an increased risk factor for IUGR. These data also correlate with the studies involving extrinsic factors.
Our goal in the present work was to determine whether male patients with untreated hypogonadism have an increased risk of developing rheumatic/autoimmune disease (RAD), and, if so, whether there is a relation to the type of hypogonadism. We carried out neuroendocrine, genetic, and rheumatologic investigations in 13 such patients and 10 healthy male 46,XY normogonadic control subjects. Age and body mass index were similar in the two groups. Nine of the 13 patients had hypergonadotropic hypogonadism (five of whom had Klinefelter's syndrome [karyotype 47,XXY]) and 4 of the 13 had hypogonadotropic hypogonadism (46,XY). Of these last four, two had Kallmann's syndrome and two had idiopathic cryptorchidism.
Eight (61%) of the 13 patients studied had RADs unrelated to the etiology of their hypogonadism. Of these, four had ankylosing spondylitis and histocompatibility B27 antigen, two had systemic lupus erythematosus (in one case associated with antiphospholipids), one had juvenile rheumatoid arthritis, and one had juvenile dermatomyositis. In comparison with the low frequencies of RADs in the general population (about 0.83%, including systemic lupus erythematosus, 0.03%; dermatomyositis, 0.04%; juvenile rheumatoid arthritis, 0.03%; ankylosing spondylitis, 0.01%; rheumatoid arthritis, 0.62%; and other RAD, 0.1%), there were surprisingly high frequencies of such disorders in this small group of patients with untreated hypogonadism (
P
< 0.001) and very low serum testosterone levels (
P
= 0.0005). The presence of RADs in these patients was independent of the etiology of their hypogonadism and was associated with marked gonadal failure with very low testosterone levels.
Hypersecretion of both FSH and LH was demonstrated in a man with pituitary macroadenoma, who also presented elevated levels of blood testosterone and an increased sperm count. The patient underwent transsphenoidal surgery followed immediately by cranial irradiation. Immunocytochemical analysis of the tumour revealed the presence of FSH, LH, TSH and the \g=a\-subunit.Gel chromatography of the serum on Sephadex G-100 revealed immunoactive FSH, LH and the \g=a\-subunitwhich coeluted with the labelled standards of corresponding hormones. Blood levels of both the presence of any physical changes or symptoms of
Size heterogeneity of immunoreactive prolactin (PRL) was studied in serum samples obtained from eight normoprolactinemic women during the menstrual cycle and five additional patients at pregnancy and lactation. Gel filtration of sera from women with normal ovarian function tested at day 10-12th of their menstrual cycle showed two predominant PRL forms, approximately 22K and 26K mol wt. In addition two polymeric variants, 50K ("big" PRL) and 100K ("big-big" PRL) were found in less proportion, accounting for approximately 34% of the total PRL immunoreactivity detected in the sera. It was also noted a low mol wt form eluting around the region of 16K mol wt. In pregnant women the major PRL form was the 22K and its proportion showed a gradual increase as progression of gestation. The polymeric PRL forms were found in substantially less amount as gestation progressed. After parturition, in nursing mothers the 22K form remained prominent and in greater concentrations than the 26K monomeric variant. Large and low mol wt PRL forms were constantly detected in sera from women during the lactation period. From these data we confirmed that PRL circulates at various molecular forms and the relative proportion of these molecular variants exhibit changes according to the physiological state. In our study the predominant form was the 22K PRL (nonglycosylated) and it was of interest to discover the presence of a low mol wt PRL which elutes in the 16K area. The significance of this latter finding is not clear at the present.
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