Increased oxidative stress and hypozincemia in male obesity.

OBJECTIVES: Antioxidants protect an organism from the detrimental effects of free radicals via scavenging or inhibiting their formation. Alterations in the levels of antioxidants and several essential trace elements in the plasma and various tissues of ob/ob mice have been reported previously. The aim of this study was to investigate oxidative status and trace elements in obese individuals. DESIGN AND METHODS: Seventy-six obese men (body mass index (BMI) > 30 kg/m(2)) and 24 healthy, age-matched male control volunteers were enrolled in the study. Fasting plasma insulin, glucose, triglyceride (TG), total cholesterol, VLDL, and HDL levels, erythrocyte glutathione peroxidase (GSH-Px) and copper zinc-superoxide dismutase (CuZn-SOD) activities, and erythrocyte thiobarbituric acid reactive substances (TBARS) levels were measured in both groups. Erythrocyte copper (Cu), zinc (Zn) and iron (Fe) levels were also measured. RESULTS: We found that the mean Cu and Fe levels in obese individuals were not significantly different than those in the control group, whereas the mean Zn levels were significantly lower than those of the control group (p = 0.023). The mean erythrocyte CuZn-SOD and GSH-Px levels in obese individuals were significantly lower than those in controls (p = 0.001) whereas erythrocyte TBARS levels were significantly higher (p = 0.001) than those of the control group. CONCLUSION: We conclude that male obesity is associated with defective antioxidant status and hypozincemia, which may have implications in the development of obesity related health problems.

Diurnal leptin secretion is intact in male hypogonadotropic hypogonadism and is not influenced by exogenous gonadotropins.

Circulating leptin shows a pulsatile secretory pattern along with a nocturnal rise. We have previously shown that circulating leptin concentrations are high in males with untreated idiopathic hypogonadotropic hypogonadism (IHH). However, circadian leptin secretion in IHH before and after gonadotropin treatment is not known. Thus, we studied 14 adult males with IHH who had no history of previous hormonal therapy, and 12 age- and body mass index-matched healthy men. Plasma leptin concentrations were measured with 1-h intervals for 24 h before and 6 months after gonadotropin treatment. The 24-h mean leptin concentration showed a significant decrease, from 11.78 +/- 1.908 microg/liter at baseline to 10.85 +/- 1.939 microg/liter after 6 months of therapy (z = 3.107; P = 0.002). Before and after treatment, 24-h mean leptin concentrations were also significantly higher in the patient group when compared with controls (4.275 +/- 0.711 microg/liter) (z = 5.938; P = 0.0001). Hourly leptin levels demonstrated a diurnal pattern in hypogonadal patients, a surge in the midday, and a peak just after midnight, and this pattern did not differ before and after treatment. We observed a similar diurnal pattern in the control subjects too. Leptin levels were negatively and significantly correlated with free testosterone and total testosterone levels both before (r = -0.656, P = 0.011; and r = -0.639, P = 0.014, respectively) and after (r = -0.537, P = 0.048; and r = -0.563, P = 0.036, respectively) gonadotropin administration. Our observations suggest that the diurnal rhythm of leptin is intact in males with IHH, and short-term gonadotropin treatment does not effect its diurnal rhythm. Moreover, testosterone produced under the influence of the gonadotropin treatment led to decreases in the leptin levels.

The renin-angiotensin-aldosterone system (RAAS) and its relation with calcium homeostasis in male obesity.

BACKGROUND: The aim of our study was to determine whether alterations of the vitamin D-endocrine system and the renin-angiotensin-aldosterone system occur in male obesity and influence each other. MATERIAL/METHODS: 32 obese male subjects and 21 age-matched healthy male subjects were enrolled in the study. The parameters measured included serum total calcium (Ca), ionized calcium, magnesium (Mg), phosphorus (P), 25-hydroxyvitamin D (25-OHD), supine and upright aldosterone and renin activity, and urinary calcium, magnesium, and phosphorus. RESULTS: Serum total Ca and ionized calcium were slightly, but not significantly lower in obese subjects compared to controls, whereas serum magnesium phosphorus and PTH levels were significantly higher in the obese subjects. Mean urinary calcium and Mg were not significantly different, while urinary P was significantly higher in obese subjects. Mean serum 25OHD was significantly lower in obese subjects. Supine and upright aldosterone and renin were unrelated to BMI or fat mass. Supine aldosterone correlated with serum total calcium, ionized calcium and supine renin activity, but not with other minerals, PTH or 25OHD, whereas upright aldosterone did not correlate with other parameters. Supine renin activity did not correlate with any parameters, whereas upright renin correlated with serum Mg and PTH. There were significant correlations between PTH and BMI or fat mass. Urinary Mg was also related to both BMI and fat mass. CONCLUSIONS: Male obesity is associated with increased serum Mg, P, PTH and urinary P and lower supine aldosterone and 25OHD, but unchanged serum and urinary Ca.

Increased fasting plasma acylation-stimulating protein concentrations in nephrotic syndrome.

Acylation-stimulating protein (ASP) is an adipocyte-derived protein that has recently been suggested to play an important role in the regulation of lipoprotein metabolism and triglyceride (TG) storage. ASP also appears to have a role in the regulation of energy balance. In addition to its role as a hormonal regulator of body weight and energy expenditure, leptin is now implicated as a regulatory molecule in lipid metabolism. However, little is known about the alterations in fasting plasma ASP and leptin concentrations in the nephrotic syndrome. As hyperlipidemia is one of the most striking manifestations of the nephrotic syndrome, we have investigated fasting plasma ASP and leptin levels and their relation to lipid levels in this syndrome. Twenty-five patients with untreated nephrotic syndrome and 25 age-, sex-, and body mass index-matched healthy controls were included in the study. Fasting plasma lipoproteins, TG, total cholesterol, lipoprotein(a), apolipoprotein AI (apoAI), apoB, urinary protein, plasma albumin, third component of complement (C3), ASP, and leptin levels were measured in both groups. Total cholesterol, TG, low and very low density lipoproteins, lipoprotein(a), apoB, and urinary protein levels were increased in the patient group, whereas plasma albumin, high density lipoprotein cholesterol, and apoAI levels were decreased compared with those in the control group (P < 0.001). Plasma ASP levels were significantly higher in the patient group compared with the control subjects (133.72 +/- 65.14 vs. 29.93 +/- 12.68 nmol/liter; P < 0.001), whereas leptin (2.69 +/- 2.06 vs. 3.99 +/- 2.99 ng/ml; P = 0.118) and C3 (1.01 +/- 0.25 vs. 1.06 +/- 0.23 g/liter; P = 0.662) levels were not significantly different between the two groups. Plasma leptin levels were correlated with body mass index in both nephrotic patients (r(s) = 0.86; P < 0.001) and controls (r(s) = 0.98; P < 0.001), but were not correlated with the other parameters. Fasting ASP concentrations showed no correlation with body mass index, proteinuria, plasma albumin, leptin, or any lipid parameter in either group, but C3 levels (in patient group: r(s) = 0.92; P < 0.001; in control group: r(s) = 0.68; P < 0.001). Our findings showed that plasma ASP levels were significantly elevated, whereas leptin levels were normal in the nephrotic syndrome. Increased ASP levels in the setting of dyslipidemia in the nephrotic syndrome raise the possibility of an ASP receptor defect in adipocytes, which also suggests the existence of so-called ASP resistance. Moreover, it is possible that ASP activity is maximal, but cannot keep up with increased rates of lipid production by the liver. Thus, further studies are needed to elucidate the mechanism or source (adipocytes, the liver, or both) of elevated ASP concentrations in the nephrotic syndrome.