The aim of this paper was to investigate the relationship between sex hormones and fat distribution in premenopausal obese women. Serum concentrations of sex hormones, glucose tolerance and fat distribution were determined in a population of non-diabetic obese women, in the outpatient clinic of University Hospital, Bari, Italy. The subjects were 40 consecutive premenopausal obese women (BMI > 25). The amounts of visceral, abdominal subcutaneous, and femoral subcutaneous fat, and the visceral to abdominal subcutaneous fat ratio were measured by ultrasound techniques. Serum concentrations of total testosterone (T), free testosterone (FT), dehydroepiandrosterone sulphate (DHEAS), delta 4-androstenedione (A), 17-beta-estradiol (E2), sex hormone binding globulin (SHBG), and the FT to DHEAS molar ratio were measured during the follicular phase. Plasma glucose and insulin concentrations were evaluated during an oral glucose tolerance test. Of all sex hormones, the FT/DHEAS molar ratio was the parameter that most closely related to the amount of visceral fat (r: 0.544, P < 0.001), and this positive association was maintained (P < 0.01) after adjustment for age, BMI and insulin levels (fitted model: R2 adjusted: 0.504; F ratio: 14.73; P-value: < 0.0001). DHEAS was inversely correlated with the amount of visceral fat (r: -0.324, P < 0.05). T was inversely correlated with the amounts of both abdominal subcutaneous (r: -0.409, P < 0.01) and visceral fat (r: -0.324, P < 0.05). The FT to DHEAS molar ratio is the androgenic parameter that most closely relates to the accumulation of visceral fat in premenopausal obese women.

It is well-known that the prevalence of hypertension progressively increases with body weight. Since the major physiological activities of atrial natriuretic factor (ANF) are its natriuretic, diuretic and vasodilatory effects, the aim of the present study was to investigate the ANF basal plasma levels and platelet receptor number in 15 young normotensive obese (O) and 12 age-matched normal weight healthy (C) women. ANF effectiveness was also studied in eight of the obese and seven of the control women, after an intravenous bolus of the hormone (human ANF (99-126): 0.5 mg/kg body weight). Results are expressed as means+s.d. Basal ANF plasma levels were similar between obese (18.2 +/- 9.7 pg/ml) and control women (12.3 +/- 7.7 pg/ml), whereas obese patients showed an increase density of platelet ANF-binding sites (clearance receptors) (C: 28.7 +/- 33.5 fmol/10(9) cells; O: 39.6 +/- 4.6 fmol/10(9) cells; P < 0.001), without apparent differences in receptor affinity (Kd) (C: 6.0 +/- 3.0 pM; O: 7.0 +/- 2.0 pM). The biological response to ANF, evaluated by changes of mean blood pressure levels (C: 5 +/- 1 mmHg; O: 1 +/- 1 mmHg; P < 0.001) and the percentage increase of diuresis (C: 159 +/- 52%; O: 81 +/- 62%; P < 0.01) and natriuresis (C: 205 +/- 129%; O: 99 +/- 41%; P < 0.05) was significantly reduced in obese patients. The percentage increase in sodium excretion was inversely related to the basal insulin concentrations in the obese group (r = 0.64, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Lipoprotein(a) (Lp[a]) is generally considered to be a risk factor for the development of cardiovascular disease, but little is known about the possible influence of obesity on the circulating levels of this lipoprotein. The present study was undertaken to examine this aspect in 136 menstrually active women by comparing the serum concentrations of Lp(a) between 72 obese and 64 age-matched nonobese women. Since an adverse effect of androgens and a protective effect of estrogens have been described for plasma lipoprotein profiles in obese women, the relation between the circulating levels of Lp(a) and those of these other hormones was also investigated in obese patients. In addition, other lipoproteins, anthropometric parameters (body mass index and waist-to-hip ratio), and insulin were evaluated. The levels of Lp(a) were not significantly different (Mann-Whitney U test chi 2, 3.59; p = 0.0582 [NS]) between obese (rank sum, 5,367) and control (rank sum, 3,949) women; in addition, the percentage of patients with high Lp(a) levels (cutoff defined at 30 mg/dL) did not differ between the two groups (obese women, 30%; control, 21.8%; chi 2, 0.90; two-sided p = 0.341 [NS]). Moreover, no correlation was found between Lp(a) and body mass index. Lastly, when the Lp(a) prevalence odds ratio for obesity was examined by adjusting the levels of this lipoprotein for age, triglycerides, total cholesterol, and high density lipoprotein cholesterol, the probability value (0.88) was far from significant. In obese women, no correlation was found between the logarithmically transformed Lp(a) concentrations and all the other variables evaluated in the study. In conclusion, the present study shows that the circulating levels of Lp(a) are not influenced by body weight and cardiovascular risk factors commonly associated with obesity, such as enhanced androgenic activity, hyperinsulinemia, adverse lipoprotein profile, and abdominal fat accumulation.

Severe obesity is known to reduce either dehydroepiandrosterone circulating levels or growth hormone (GH) and insulin-like growth factor-1 (IGF-1) secretion. The present study was undertaken to evaluate the possibility of a relationship between the circulating levels of IGF-1 and those of dehydroepiandrosterone sulphate (DHEAS) in 25 fertile obese women. A logarithmic transformation of the values of non-normally distributed variables was performed before statistical analysis. We found a significant positive correlation between DHEAS and IGF-1 (r = 0.615, P < 0.01). In addition, stepwise multiple regression analysis showed that IGF-1 maintained a strong positive relationship with DHEAS (P < 0.01) when adjusted for other variables such as age, body mass index (BMI), waist:hip ratio (WHR) and insulin levels (adjusted R2 = 0.373; P < 0.01). These findings suggest that IGF-1 may independently influence the DHEAS circulating levels. ADG (5 alpha-androstan-3 alpha, 17 beta-diol-glucuronide) was also positively correlated to IGF-1 (r = 0.436, P < 0.05). However, when ADG concentrations were adjusted for DHEAS levels, this metabolite was not significantly correlated with IGF-1, thus excluding a direct influence of IGF-1 on the 5-alpha-reductase activity. Therefore, although our data represent only a preliminary study, they seem to suggest a possible influence of IGF-1 on circulating levels of DHEAS in obese women.

Dehydroepiandrosterone (DHEA) has an anti-obesity effect in rodents and reduces body fat in normal men. Therefore, the plasma levels of DHEA were evaluated in nine premenopausal healthy women and in 13 menstrually active nondiabetic obese women, including patients (n = 6) with body mass index (BMI) over 40. In the obese group, a significant inverse correlation between DHEA levels and BMI was found. These results suggest that patients with severe obesity are unable to increase the DHEA adrenal production rate in order to parallel the increase in the hormone metabolic clearance rate (due to enlargement of body fat mass per se). The deficiency of this mechanism might itself contribute to the progressive fat accumulation in severe obesity.

The aim of the study was to evaluate in eight normotensive obese patients the influence of low sodium intake (9 mEq/day) on the sympathetic activity modifications induced by caloric restriction (2511 kJ/day). As compared to the isocaloric salt balanced diet, 7 days of normosodic underfeeding induced a decrease in the overall norepinephrine turnover (clearance and appearance rate) and 24 hours urinary output, whereas the combined caloric and salt restriction significantly increased the norepinephrine appearance rate and even more the norepinephrine clearance but, on the other hand, decreased the beta-adrenergic receptor number on the lymphomonocyte surface, suggesting a reduced peripheral sensitivity to catecholamines. Therefore, the utility of the combined sodium and caloric restriction in the treatment of the normotensive obese patients remains still questionable.

Catecholamines acutely exert a pronounced insulin-antagonistic effect, which is mediated by beta-adrenergic receptors stimulation. Nevertheless, several patients with pheochromocytoma fail to exhibit an overt diabetic syndrome, in spite of steadily elevated plasma levels of catecholamines. This prompted us to investigate a 16 years old male patient, bearing an extra-adrenal pheochromocytoma, who displayed a slightly impaired glucose tolerance to oral glucose tolerance test, whereas fasting and post-prandial blood glucose, as well as glycaemic response to intravenous glucagon, were in the normal range. Peripheral insulin sensitivity, as evaluated by intravenous insulin tolerance test, was slightly decreased. Supine norepinephrine plasma levels were steadily upon 9 ng/ml; plasma insulin, both fasting and post-prandial, was within the normal range. beta-adrenergic receptors density of peripheral mononuclear cells was strongly reduced when compared to controls (0.97 +/- 0.08 vs 2.82 +/- 0.37 fmol/10(6) cells), without any concomitant change of affinity. Insulin binding to circulating monocytes was reduced as well (2.38 +/- 0.27 vs 5.1 +/- 0.4%/10(7) monocytes); insulin receptor affinity was quite normal (1.7 ng/ml) and total receptor number was 9,200 sites/cell. In desensitization experiments, 1 microM isoproterenol caused only a 20% decrease of beta-adrenergic receptors density in the patient's cells (70% decrease in controls). Six months after surgery, all the above modifications of receptor binding, as well as the mild glucose intolerance, were almost completely reversed. Thus, high levels of norepinephrine were able to induce a decrease of both beta-adrenoceptor and insulin receptor binding, together with a marked reduction of in vitro agonist-induced redistribution of beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Thermocutaneous, vascular, metabolic and hormonal changes were investigated during 11 hot flashes from 6 postmenopausal women. The first detectable change was an increase in finger blood flow with a concomitant enhancement of skin conductance. The increase in skin conductance was followed rapidly by a sharp rise in finger temperature. The main endocrine-metabolic changes associated with the above phenomena were a sharp increase in plasma free fatty acids (approximately 65%), norepinephrine (approximately 100%) and LH (approximately 20%) levels. Plasma glucose and cortisol tended to be increased but did not reach statistical significance; on the other hand, plasma insulin, glucagon, growth hormone, epinephrine and dopamine remained unchanged.

Diabetic MedicineVolume 5, Issue 5 p. 501-502 Responses to Chickling Vetch and Bread Meals in Normal and Type 2 Non-insulin-dependent Diabetic Subjects M. Cignarelli, M. Cignarelli Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorM. R. Cospite, M. R. Cospite Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorM. Rosco, M. Rosco Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorG. Garruti, G. Garruti Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorG. M. Nardelli, G. M. Nardelli Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorG. de Pergola, G. de Pergola Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorR. Giorgino, R. Giorgino Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this author M. Cignarelli, M. Cignarelli Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorM. R. Cospite, M. R. Cospite Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorM. Rosco, M. Rosco Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorG. Garruti, G. Garruti Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorG. M. Nardelli, G. M. Nardelli Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorG. de Pergola, G. de Pergola Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this authorR. Giorgino, R. Giorgino Clinica Medica Generale RR E Terapia Medica, Universita Degli Studi Di Bari, Bari, ItalySearch for more papers by this author First published: July/August 1988 https://doi.org/10.1111/j.1464-5491.1988.tb01041.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume5, Issue5July/August 1988Pages 501-502 RelatedInformation

The arginine-vasopressin (AVP) response to supine-standing postural change was evaluated in eight healthy subjects and in fourteen diabetic patients. Plasma AVP levels were found to increase in the controls and in nine subjects from the diabetic group. In the controls the increase was 139% 5 min. after standing and 275% 120 min. after standing. In four of the diabetics affected by autonomic neuropathy AVP failed to increase in response to standing, thus suggesting lesions of the neurogenic pathways connecting baroreceptors to neurohypophysis. Consequently, a failure of the afferent limb in the baroregulatory system must be taken into account among other localizations of autonomic neuropathy. On this basis, AVP measurement both in supine and erect positions could represent an additional test for assessing the integrity of the autonomic nervous system.

The influence of plasma lipid disorders on red blood cell (RBC) lipid pattern and some related erythrocyte membrane functions, such as glycerol (GLT50) permeability and erythrocyte deformability was studied in diabetes mellitus. Significantly higher red blood cell cholesterol content, GLT50 and erythrocyte filtration time values were found in diabetics. GLT50 values were found closely related to both RBC cholesterol content (r = 0.84, p less than 0.001) and filtration time (r = 0.60, p less than 0.001). Interestingly, six diabetics with retinopathy showed GLT50 values above 60 sec. The RBC Cholesterol/Phospholipids molar ratio was significantly higher in diabetics. The most notable changes of plasma lipid pattern in diabetics were a decrease of both plasma HDL cholesterol, phospholipids and Apolipoprotein A levels with an increase of HDL free cholesterol/phospholipids molar ratio. RBC cholesterol content was found to be inversely related to HDL esterified/free cholesterol molar ratio (r = -0.56, p less than 0.001), while RBC cholesterol/phospholipids molar ratio was significantly related to both HDL free cholesterol/phospholipids (r = 0.51, p. 0.001) and to LDL total cholesterol/phospholipids (r = 0.25, p less than 0.05). Lastly, HDL cholesterol levels were found to inversely relate to glycosylated haemoglobin values (r = -0.54, p less than 0.01).

381 glucose intake normal curves were studied according to the Diabetes Data Group new classification in healthy persons between 10 and 80 years in order to assess the influence of the age upon the normal glucose tolerance. Such an influence, which was evident in all the subjects, turned out to be more important in women with respect to me. In fact, males showed an increase, per decade, of about 1 mg/dl in fasting glycemic levels, of about 6 mg/dl at 60', of 4 mg/dl at 120', while in females there was an increase of about 2 mg/dl in fasting glicemic values, of about 6 mg/dl at 60' and of about 5 mg/dl at 120'. No meaningful correlation between age and insulinemic values was found at all considered points, either in males or in females. The reasons of the decreased glucose tolerance with aging and of its different behavior in the two sexes are discussed.

The study was designed to determine eventual correlation in diabetes mellitus between reduced erythrocyte deformability and red blood cells (RBC) cholesterol content. Significantly higher RBC cholesterol amount was found in 11 diabetics (IDDM) than in 13 controls of similar age (45 +/- 10 yrs) (1.30 mg ml-1 packed cells -1 +/- 0.15 SD vs 1.19 +/- 0.10 SD, p less than 0.05). Blood filterability values have been found significantly higher (p less than 0.025) in the diabetics (42.2 +/- 11.5 SD ml sec. -1) than in controls (33.5 +/- 6.0). Flow time of RBC filterability, measured in erythrocyte saline buffered suspension (40% Hct) in order to eliminate interferences from plasmatic factors, showed a closely correlation with RBC cholesterol content (r = 0.86 p less than 0.01). A significant inverse correlation between RBC cholesterol content and serum ApoA1-HDL levels was also observed (r = -0.58, p less than 0.05). Moreover ApoA1-HDL serum values were significantly (P less than 0.01) lower in diabetics (111.8 +/- 10.1 mg/dl) than in controls (126 +/- 6.6 mg/dl). Our data underline the possible involvement of augmented erythrocyte cholesterol in impairing the microhemologic competence of RBC in diabetes mellitus. A possible relation with lower ApoA1-HDL and lecithin-cholesterol-acyl-transferase (LCAT) is examined.

Pyruvate-dehydrogenase, an enzymatic mitochondrial complex, exists in both inactive and active forms, insulin being the regulating factor of the transformation of a latter into the former. The basal (PDHb) and total (PDHt) activity of this enzyme in adipose tissue mitochondria from obese hyperinsulinemic humans has been found equal to 1014 +/- 459 SD mU respectively. These values are 250% higher than those found in normal subjects (403 +/- 76 SD and 575 +/- 142 SD respectively). Both in normal and obese subjects the PDHb/PDHt percent ratio was equal to about 70. These results show that insulin, undoubtedly hyperactive in obesity, by activating PDH can induce a major synthesis of fat, a high caloric density tissue.

The effect of PEBG on respiration and oxidative phosphorilation (succinate as substrate) has been studied in liver mitochondria of rat treated with glucagon. The results obtained indicate that, while glucagon, as reported by others, induce a significant increase of respiration rate in state 3 (+ ADP), PEBG, at pharmachological dose, antagonizes this effect. The conclusion is that PEBG exertes its hypoglycemic activity by inhibiting the gluconeogenic reactions promoted by glucagon. This is strongly evident in diabetic or starwed conditions.