Plasma visfatin levels in young male patients with uncomplicated and newly diagnosed hypertension.
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Adult↗
Biomedical subjects
N Bingol
Publications and source records attributed to N Bingol.
Adiponectin level is reduced and inversely correlated with the degree of proteinuria in type 2 diabetic patients.
AIMS: Adiponectin seems to be an important modulator for metabolic and vascular diseases. We aimed to measure plasma adiponectin levels in type 2 diabetic patients and investigate any association with the severity of proteinuria. METHODS: 80 patients (mean age, 46.9 +/- 5.1 years; body mass index (BMI), 25.8 +/- 1.98 kg/m2) and 47 healthy volunteers (mean age, 46.1 +/- 5.5 years; BMI 26.74 +/- 2.23 kg/m2) were included. Plasma adiponectin concentration, insulin levels, homeostasis model assessment (HOMA) indices, calculated glomerular filtration rate (GFR), high sensitive C reactive protein (hsCRP) and biochemistry panel were determined in all subjects. The association between adiponectin concentration and proteinuria was evaluated. Additionally, the relationship between adiponectin and hsCRP and calculated GFR were also investigated. RESULTS: Adiponectin levels in patients were significantly lower than those of controls (n = 80; 8.76 +/- 4.50 microg/ml for patients, n = 47; 24.27 +/- 5.59 microg/ml for controls, p < 0.001). Plasma adiponectin levels in patients with proteinuria were significantly lower than those without proteinuria (n = 43; 6.81 +/- 2.82 microg/ml for proteinuria, n = 37; 11.98 +/- 3.32 microg/ml for no proteinuria, p < 0.001). There was a significant negative correlation between plasma adiponectin concentrations and the degree of proteinuria (r = -0.433, p < 0.001). There were also significant negative correlations between adiponectin concentrations and insulin levels as well as HOMA index in the patient group (r = -0.322, p = 0.004; r = -0.301, p = 0.032). Additionally there was a significant negative correlation between adiponectin and hsCRP levels in the patient group (r = -0.872, p < 0.001). CONCLUSION: The results show that adiponectin is lower in patients with type 2 diabetes and the levels are negatively correlated with the severity of proteinuria.
Adiponectin↗
The effects of metformin and diet on plasma testosterone and leptin levels in obese men.
OBJECTIVE: The aim of this study was to investigate the effects of combined hypocaloric diet and metformin on circulating testosterone and leptin levels in obese men with or without type 2 diabetes. RESEARCH METHODS AND PROCEDURES: Twenty obese men with type 2 diabetes (mean body mass index [BMI]: 35.5 +/- 1.1 kg/m(2)) and 20 nondiabetic obese men were enrolled in the study. We measured serum follicle-stimulating hormone, luteinizing hormone (LH), total testosterone (TT), free testosterone (FT), sex-hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), and plasma leptin levels before and 3 months after metformin treatment. Both groups were placed on a hypocaloric diet and 850 mg of metformin taken orally twice daily for 3 months. RESULTS: Metformin and hypocaloric diets led to decreases in BMI and waist and hip circumferences in both groups. A significant decrease in TT levels in the diabetic group and FT levels in the control group was found, whereas follicle-stimulating hormone, LH, and DHEAS levels were not changed significantly. A significant increase in SHBG levels was observed in the control group but not in the patient group. Leptin levels also decreased after treatment in both groups. Decreased testosterone levels were not correlated to changes in waist and hip circumference, waist-to-hip ratio, BMI, and levels of fasting blood glucose, leptin, SHBG, or DHEAS in the diabetic group. However, a decrease in FT was correlated to changes in the levels of SHBG (r = -0.71, p = 0.001) and LH (r = 0.80, p = 0.001) but not to other parameters. DISCUSSION: We conclude that metformin treatment combined with a hypocaloric diet leads to reduced FT levels in obese nondiabetic men and to reduced TT levels in obese men with type 2 diabetes. Increased SHBG levels may account for the decrease in FT levels in the former group.
Adult↗
Improved glycemic control increases fasting plasma acylation-stimulating protein and decreases leptin concentrations in type II diabetic subjects.
Acylation-stimulating protein is an adipocyte-derived protein that has recently been suggested to play an important role in the regulation of triglyceride storage. To date, little information has been reported with regard to fasting acylation-stimulating protein levels and its relation to metabolic control, leptin, and/or lipids in subjects with diabetes mellitus. We therefore evaluated fasting acylation-stimulating protein, leptin, and lipid levels before and 4 months after improving glycemic control with sulfonylurea treatment in a group of poorly controlled obese women with type 2 diabetes and in age- and body mass index-matched nondiabetic obese women. Fasting plasma acylation-stimulating protein (49.67 +/- 19.73 vs. 48.49 +/- 20.70 nmol/liter) and leptin concentrations (33.7 +/- 23.2 vs. 26.2 +/- 10.6 ng/ml) were not significantly different between the groups. Improvement of glycemic control produced parallel falls in fasting blood glucose and hemoglobin A1c. Plasma leptin concentrations were also significantly reduced (33.69 +/- 23.2 vs. 22.73 +/- 11.26 ng/ml; P = 0.036), whereas fasting acylation-stimulating protein concentrations were significantly increased after treatment (48.49 +/- 20.70 vs. 72,82 +/- 29,72 nmol/liter; P = 0.004). Nevertheless, lipids and apolipoprotein B did not significantly improve. We could not find any correlation between elevated acylation-stimulating protein levels and changes in body mass index, glucose, insulin, hemoglobin A1c, leptin, or lipid levels. Similarly, the decrement in circulating leptin levels observed after treatment did not correlate with changes in the levels of glucose, insulin, hemoglobin A1c, or any lipid parameters. We conclude that improved glycemic control increases fasting acylation-stimulating protein and decreases leptin concentrations, but not corrects critical lipid abnormalities in type 2 obese diabetic subjects. Moreover, altered plasma acylation-stimulating protein levels are not associated with changes in body mass index or lipid, leptin, insulin, or glucose levels. Thus, our findings suggest that improved glycemic control or insulin resistance is not responsible for abnormal fatty acid trapping, and failure of lipids to improve after treatment in our patients is consistent with the acylation-stimulating protein resistance concept.
Apolipoprotein A-I↗
Is leptin associated with hypertensive retinopathy?
Previous studies have demonstrated that elevated plasma leptin concentrations are associated with essential hypertension. It has also recently been shown that leptin plays a promoting role in angiogenesis, and the vascular endothelium expresses the long form of leptin receptor. Those data led us to hypothesize that leptin might contribute to end-organ damage in hypertension. Thus, in the present study we evaluated the relationship between plasma leptin concentrations and hypertensive retinopathy (HR). One hundred and eleven patients newly diagnosed with essential hypertension [EHT; mean age, 43.5 +/-10.7 yr; body mass index (BMI), 28.1 +/- 4.4 kg/m2; male/female ratio, 71/40] and 79 healthy normotensive control subjects (NT; mean age, 43.6 +/- 9.2 yr; BMI, 28.2 +/- 3.3 kg/m2; male/female ratio, 50/29) were enrolled in the study. For the assessment of retinopathy according to the Keith-Wagener classification, direct and indirect ophthalmoscopy were performed in all subjects after dilatation of the pupils. Plasma leptin levels were significantly higher in EHT (11.8 +/- 11.1 ng/mL) than in NT (7.2 +/- 5.1 ng/mL) (P = 0.003). Plasma leptin concentrations were strongly correlated with BMI in both EHT (r = 0.45; P = 0.001) and NT (r = 0.38; P = 0.001) groups. Plasma leptin in patients with grade 2 HR (24.8 +/- 15.8 ng/mL; n = 22) was significantly higher than that in patients with grade 1 HR (16.1 +/- 4.9 ng/mL; n = 29; P = 0.001), grade 0 HR (5.1 +/- 3.1 ng/mL; n = 60; P = 0.001), and NT (P = 0.001). Plasma leptin in patients with grade 1 HR was also significantly higher than that in patients without retinopathy (P = 0.001) or in NT (P = 0.001). The estimated threshold of plasma leptin concentration for HR was 10.2 ng/mL. This critical leptin level served largely to separate patients with retinopathy from those without retinopathy. In summary, our results show that plasma leptin concentrations increase progressively with higher grades of hypertensive retinopathy even after correction for BMI, suggesting that a critical leptin level is needed for the development of retinopathy. Elevated concentrations of plasma leptin might be secondary to release of leptin by the vascular endothelium damaged by high blood pressure, as an epiphenomenon. However, a pathogenic role for leptin in hypertensive retinopathy cannot be excluded.
Adult↗
Is leptin associated with diabetic retinopathy?
OBJECTIVE: In advanced stages of diabetic retinopathy, new blood vessels are formed based on undefined mechanisms. Recently, leptin was shown to possess an angiogenic action in vitro and to induce neovascularization in vivo. The aim of the present study was to investigate the relationship between plasma leptin levels and the severity of diabetic retinopathy. RESEARCH DESIGN AND METHODS: There were 70 patients with type 2 diabetes (age 47.9 +/- 9.7 years, BMI 26.4 +/- 3.3 kg/m2) who were seen in a retina outpatient clinic recruited and assigned to subgroups according to the stage of their diabetic retinopathy. There were 66 healthy volunteer subjects matched with the diabetic patients for age, BMI, and sex who served as control subjects (age 46.0 +/- 8.8 years, BMI 27.1 +/- 2.3 kg/m2). Fasting plasma leptin levels were measured. RESULTS: Plasma leptin level of the diabetic patients was not significantly different from the control subjects. In patients with proliferative diabetic retinopathy (n = 17), the mean plasma level of leptin (16.1 +/- 9.2 ng/ml) was significantly higher than that in patients with nonproliferative retinopathy (n = 20) (11.5 +/- 3.5 ng/ml, P = 0.039) or patients without retinopathy (n = 33) (5.8 +/- 3.7 ng/ml, P = 0.001). The mean leptin level in patients with nonproliferative diabetic retinopathy was also significantly higher than that in patients without retinopathy (P = 0.002). CONCLUSIONS: Our results show that the more advanced the diabetic retinopathy, the higher the plasma leptin levels, even after adjusting the leptin levels for BMI. The presence of such a positive correlation need not imply a causal relationship. Nevertheless, previously observed leptin-induced promotion of angiogenesis and neovascularization lends support to the possibility that leptin may play a role in the progression of human diabetic retinopathy to a proliferative phase. This possibility deserves further investigation.
Biomarkers↗
The clinical value of the ratio of free prostate specific antigen to total prostate specific antigen.
OBJECTIVE: To examine the usefulness of the ratio of free prostate specific antigen (FPSA) to total prostate specific antigen (TPSA) in men with serum TPSA concentration of 4 to 10 ng/mL by using the cut off value of 0.15 for avoiding unnecessary biopsies. PATIENTS AND METHODS: Two hundred thirty-six men aged between 52 and 91 with symptoms of prostatism were evaluated with digital rectal examination (DRE), FPSA and TPSA measurements. Patients with TPSA values under 4 ng/mL were biopsied if they had positive DRE and/or a FPSA/TPSA ratio lower than 0.15. All patients with TPSA values higher than 4 ng/mL were also biopsied. The predictive value and sensitivity of FPSA/TPSA ratio and TPSA alone were calculated. RESULTS: Eleven patients out of 170 with a TPSA value lower than 4 ng/mL were biopsied. Fifty-five patients had a value between 4.1 and 10 ng/mL. We performed transrectal ultrasound (TRUS) and prostate biopsy in these men except one patient. Biopsy proven prostate cancer was detected only in 12 patients. In this group of patients the predictive value of TPSA was 21%, but the predictive value of FPSA/TPSA ratio of 0.15 was 78% maintaining at least 90% sensitivity. Eleven of the patients had a prostate specific antigen (PSA) value higher than 10 ng/mL. In 6 of these patients the biopsy result was prostate cancer and 10 of these patients had a FPSA/TPSA ratio lower than 0.15. CONCLUSION: In patients with TPSA values between 4-10 ng/mL the cut off value of FPSA/TPSA ratio of 0.15 can be used to eliminate unnecessary biopsies with minimal loss of cancer patients.
Aged↗
Plasma leptin levels strongly correlate with plasma renin activity in patients with essential hypertension.
Previous studies demonstrated elevated plasma leptin and angiotensinogen (PRA) levels in essential hypertension. However, a few studies investigated the relationship between leptin and angiotensinogen levels in both lean and overweight/ obese hypertensives. The aim of the present study was therefore to examine the relationship between blood pressure, leptin and plasma renin activity in normotensives and in both lean and overweight/obese patients with essential hypertension. Two groups of subjects who were carefully matched for age, gender, waist:hip ratio and body mass index (BMI) were studied: 28 normotensives (NT) (age: 40.1+/-9.1 years old, BMI: 28.1+/-3.6 kg/m2, male/female: 18/10) and 33 newly diagnosed mild to moderate essential hypertensives (EHT) (age: 38.9+/-10 years old, BMI: 27.9+/-4.8 kg/m2, male/female: 22/11). No significant differences in age, gender, waist:hip ratio, fasting blood glucose and BMI were detected between EHT and NT groups. However, systolic and diastolic pressures, mean arterial blood pressures, plasma leptin levels and PRA were significantly higher in EHT group than in NT group (P = 0.001). Plasma leptin levels were strongly correlated with BMI in EHT (r=0.67, P = 0.001) and NT groups (r=0.44, P = 0.001). Plasma leptin levels were correlated with plasma PRA levels in both EHT and NT groups (r = 0.66 and r = 0.44; both P < 0.05, respectively). There was no correlation between leptin or PRA and systolic, diastolic pressures, or mean arterial blood pressures. Furthermore, the patients were divided as lean (n=16) and overweight/obese (n = 17) and compared with BMI-matched controls. In both subgroups, plasma leptin and PRA levels were also higher than those of controls. Our results showed that elevated plasma leptin and PRA are associated with hypertension in both lean and overweight/obese hypertensives. Moreover, plasma leptin was significantly correlated with plasma angiotensinogen levels. These findings suggest that adipose mass is an important determinant of blood pressure, although the mechanism is not clear.
Adult↗
The effects of thyroid status on plasma leptin levels in women.
Leptin, the product of the adipose specific ob gene, regulates food intake and energy expenditure. However, little is known about the effects of thyroid status on plasma leptin levels in women. We determined fasting plasma leptin levels before and 1 month after restoration of euthyroidism in 20 female patients with hypothyroidism, 20 female patients with hyperthyroidism and 20 age and BMI-matched female controls. To restore the normal thyroid function patients with hypothyroidism were treated with levothyroxine, whereas patients with hyperthyroidism were treated with propylthiouracil. Plasma leptin levels were measured by a RIA method with a sensitivity of 0.5 microgram/l. Leptin levels were significantly lower in patients with hypothyroidism before treatment (4.17 +/- 2.58 micrograms/l) than in patients with hyperthyroidism (6.80 +/- 4.3 micrograms/l; z = -2.06, p = 0.037). Leptin levels were significantly higher in hyperthyroid patients than in the control group (3.71 +/- 1.69 micrograms/l, z = -2.44, p = 0.014) whereas leptin levels in the hypothyroid patients were not significantly different from those in control subjects (z = -0.16, p = 0.87). Restoration of euthyroid state was not associated with a significant change in leptin levels either in the hypothyroid (from 4.17 +/- 2.58 to 5.22 +/- 3.4 micrograms/l; z = -1.74, p = 0.08) or in the hyperthyroid group (from 6.80 +/- 4.37 micrograms/l to 7.93 +/- 6.25 micrograms/l z = -0.89, p = 0.37), although a tendency for leptin to increase was observed in both groups. There was no correlation between plasma leptin and FT3, FT4, TSH, or BMI either before or after therapy in both groups. Leptin levels were significantly correlated with BMI in the control group (r = -0.53, p = 0.018). We conclude that plasma leptin levels are increased in hyperthyroidism and unchanged in hypothyroidism. Furthermore, our study demonstrates that mean plasma leptin levels are not influenced by short term restoration of euthyroidism in both hypothyroidism and hyperthyroidism, although an effect of long-term treatment may not be excluded.
Adult↗
Daytime plasma melatonin levels in male hypogonadism.
It has previously been shown that increased nocturnal melatonin (MT) secretion exists in male patients with hypogonadotropic hypogonadism. However, little is known about the effects of gonadotropin and testosterone (T) treatment on early morning plasma MT levels in male hypogonadism. Also, the impact of gonadal steroids on plasma MT levels is an open question. We, therefore, determined early morning plasma MT levels at the same hour before and 3 months after treatment in 21 patients with idiopathic hypogonadotropic hypogonadism (IHH), 10 patients with primary hypogonadism, and 11 male controls. Plasma FSH, LH, PRL, T, and estradiol levels were also determined before and 3 months after treatment. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with primary hypogonadism received T treatment. Short term treatments did not achieve normal T levels, although significant increases in T were observed in both groups. Plasma MT levels were measured by a RIA with a sensitivity of 10.7 pmol/L. Mean plasma MT levels before treatment were significantly higher in IHH (41.8 +/- 24.4 pmol/L) compared with those in the controls (21.7 +/- 10.8 pmol/L; P < 0.05). However, a slight, but not significant, increase in MT (34.2 +/- 21.1 pmol/L) was found in primary hypogonadism. Mean MT levels did not change significantly 3 months after the initiation of gonadotropin (41.7 +/- 22.8 pmol/L) or T (28.4 +/- 12.6 pmol/L) treatment in either IHH or primary hypogonadism, although a tendency for MT to decrease was observed in both groups. No correlation was found between MT and circulating FSH, LH, PRL, and gonadal steroids either before or after therapy. We conclude that male patients with IHH have increased early morning MT levels, although the pathophysiological mechanism is not clear. Furthermore, our study demonstrated that mean plasma MT levels are not influenced by short term gonadotropin or T treatment in male hypogonadism, although a longer time effect of gonadotropins or T treatment may not be excluded. The lack of correlation between plasma MT and circulating gonadal steroids before and after treatment suggests that there is no classic feedback regulation between the pineal gland and the testes.
Adult↗
Teratogenicity of cocaine in humans.
To study teratogenicity of cocaine in humans, we studied three groups of pregnant women and their offspring: group 1, 50 women who abused cocaine only; group 2, 110 women who were polydrug abusers; and group 3, 340 who were drug free. All three groups were similar for socioeconomic status, cigarette smoking, and ethnicity. Maternal age of group 1 was similar to that of group 3, but group 2 mothers were significantly older. Gravidity was significantly higher in groups 1 and 2 compared with group 3. No statistical difference was found in spontaneous abortion rate among the three groups, but the stillbirth rate was significantly higher in group 1 (chi 2 = 6.89, P less than or equal to 0.01). All stillbirths were related to abruptio placentae. Birth weight, length, and head circumference were significantly decreased in infants in groups 1 and 2 compared with group 3 (P less than or equal to 0.0001), but no statistical difference was found between groups 1 and 2. The congenital malformation rate was significantly higher in group 1 compared with group 3 (chi 2 = 7.07, P less than or equal to 0.01). We conclude that cocaine abuse in humans significantly reduces weight of the fetus, increases the stillbirth rate related to abruptio placentae, and is associated with a higher malformation rate.
Abnormalities, Drug-Induced↗
Fetal alcohol syndrome associated with trisomy 21.
Five cases of Down syndrome in association with fetal alcohol syndrome (FAS) are described. Four of the babies were full term, one was premature. Phenotypically these babies (3M:2F) had manifestations of both Down syndrome and FAS; growth deficiency was more pronounced than is expected in Down syndrome. All measurements, birth weight, length and head circumference were below -2 SD. All had congenital heart disease. Chromosome analysis confirmed 21 trisomy in every case. Down syndrome and FAS may occur together, at random, in 1 in 525,0000 newborns in United States but 1 in 200,000 in our institution. Estimated incidence of FAS and Down syndrome in our institution was 1 in 6,600, a 30-fold increase over the chance occurrence of these two conditions together. Mean age of mothers at delivery was 29.6 +/- 9.3, statistically similar to the mean ages of mothers who delivered Down syndrome and FAS babies in our two hospitals, but was significantly higher than the mean age of mothers in our general population (p less than 0.001). All study cases had chronic alcoholic mothers as well as maternal grandmothers, suggesting that there is an increased incidence of trisomy 21 in children of second generation of alcoholic mothers.
Adult↗
The influence of socioeconomic factors on the occurrence of fetal alcohol syndrome.
This study was designed to compare manifestations of FAS in the offspring of lower and upper middle class chronic alcoholic mothers, and to compare these offspring with those of nonalcoholic controls. There was highly significant difference in the incidence of FAS offspring between upper middle and lower class alcoholic mothers, 4.5% versus 70.9% respectively. Mean weight, length, and head circumference at birth in children of upper middle class alcoholic women was -ISD, those of lower class alcoholic women fell into -2SD. All other parameters, congenital malformation rate, failure to thrive, mental retardation were also significantly greater in children of lower class alcoholic women (p less than or equal to .01). Attention deficit disorder was found in 21% of upper middle class offspring of alcoholic women as compared to 71% in the children of the lower socioeconomic group (p less than or equal to .01).
Attention Deficit Disorder with Hyperactivity↗
Palpebral fissure length in black and Hispanic children: correlation with head circumference.
Palpebral fissure length and head circumference were measured in 170 black and 170 Hispanic normal children aged 1 month to 16 years. Eye measurement values were compared with those for white children. It was found that black children have longer palpebral fissures than whites and in certain age groups, than Hispanics. A statistically significant correlation between palpebral fissure length and head circumference was established in black children.
Adolescent↗
Long-term follow-up of three siblings with fetal alcohol syndrome.
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Abnormalities, Drug-Induced↗
Fetal alcohol syndrome revisited.
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Adolescent↗
Palpebral fissure size revisited.
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Anthropometry↗
Chromosomal abnormalities in undescended testes.
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Adolescent↗