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Biomedical subjects

M Ozata

Publications and source records attributed to M Ozata.

At least 37 records · Page 2Linked to original sources
PubMed2000

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↗
PubMed2000

Plasma leptin concentrations in postmenopausal women with osteoporosis.

BACKGROUND: The obese are usually protected against osteoporosis and have increased bone mineral density and plasma leptin concentrations. A recent in vitro study demonstrated that leptin acts on human marrow stromal cells to enhance differentiation to osteoblasts, suggesting an influence of leptin on bone mass. However, little is known about the relationship between plasma leptin and bone mass in postmenopausal women with osteoporosis. OBJECTIVE: To investigate plasma leptin concentrations in postmenopausal women with osteoporosis to improve the understanding of the role of leptin in determining bone mass. METHODS: Fifty postmenopausal women with osteoporosis (ages 61.18+/-6.51 years; body mass index (BMI) 28. 91+/-3.44kg/m(2), mean+/-s.d.) and 30 age- and BMI-matched healthy postmenopausal women were included in the study. Bone mineral densities (BMD) were measured by dual energy X-ray absorptiometry. Plasma leptin concentrations were determined using an immunoradiometric assay. RESULTS: The median spine BMD value in the patient group (0.695+/-8.26g/cm(2), median+/-s.e.m.) was significantly lower than that in the control group (1.006+/-1. 29g/cm(2), median+/-s.e.m.; z=-7.454, P<0.001). The median plasma leptin concentration in the patient group (18.70+/-1.78ng/ml, median+/-s.e.m.) was not significantly different from that in the control group (22.35+/-2.20ng/ml, median+/-s.e.m.; z=-1.630, P=0. 103). Plasma leptin concentrations were correlated with BMI in both groups (r(s)=0.394, P=0.031 in controls and r(s)=0.404, P=0.004 in the patient group). There was no correlation between plasma leptin concentrations and BMD values in controls (r(s)=-0.107, P=0.575) but a weak correlation was observed in the patient group (r(s)=0.285, P=0.045). CONCLUSION: Our data suggest that circulating plasma leptin does not have a significant direct influence on bone mass in postmenopausal women.

Aged↗
PubMed2000

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↗
PubMed1999

Iodine and zinc, but not selenium and copper, deficiency exists in a male Turkish population with endemic goiter.

Although endemic goiter has been shown to have a high prevalence in Turkey, little is known about the concentration of urinary iodine, plasma selenium (Se), copper (Cu), and zinc (Zn) in these patients. We studied on 140 male patient with endemic goiter (mean age: 22.2 +/- 0.19 yr) and 140 healthy male subjects (mean age: 21.8 +/- 0.28 yr). Daily urinary iodine excretion was determined by the ionometric method. Plasma Se, Zn, and Cu were determined by using atomic absorption spectrometry. Daily urinary iodine excretion was found to be significantly lower in the patient group (38.7 +/- 2.26 microg/d) than that of controls (50.73 +/- 2.56 microg/day, p = 0.001). Plasma Zn concentrations were also found to be significantly lower in the patient group (1.04 +/- 0.03 microg/mL) than that of controls (1.16 +/- 0.02 microg/mL, p = 0.001). No significant difference was determined in Se and Cu concentrations between the patient and control groups. Our study shows that a moderate iodine deficiency exists in both patients with endemic goiter and control subjects, which indicates the important role of iodine deficiency in the etiopathogenesis of endemic goiter in Turkey. Zinc deficiency may also contribute to the pathogenesis of endemic goiter. However, Se and Cu do not seem to have any role in the etiopathogenesis of endemic goiter in Turkey. A community-based iodine fortification program throughout the country may be proposed to take over the problem, which also can prevent the contributing effects of other element deficiencies that occur when iodine deficiency is the prevailing factor.

Adult↗
PubMed1999

Plasma leptin levels in male patients with idiopathic central diabetes insipidus.

Leptin is known to regulate food intake and energy expenditure. Moreover, recent studies in rodents have shown that leptin in high doses decreases urine osmolality and increases water intake, together with renal sodium and water excretion. Since it is not clear whether leptin is involved in either the pathogenesis or in resulting metabolic abnormalities in diabetes insipidus, we measured leptin levels in 16 male patients with idiopathic central diabetes insipidus (DI) in comparison to a group of age- and BMI-matched male control subjects (no.=30). We found that plasma leptin concentration did not differ between patients with DI (4.45+/-3.24 microg/l) and healthy control group (3.69+/-2.81 microg/l; t test, p=0.41). Urine osmolality, plasma osmolality and urine volume of the patients with DI was not correlated to leptin. However, leptin was positively associated with body mass index (r=0.67; p=0.005). We conclude that leptin plasma concentrations are unchanged in diabetes insipidus. Furthermore, the lack of correlation between plasma leptin and urine osmolality, plasma osmolality or urine volume suggests that ADH deficiency does not have any impact on the plasma leptin levels.

Adult↗
PubMed1999

Beneficial effect of thyrotropin-releasing hormone on neuropathy in diabetic rats.

Thyrotropin releasing hormone (TRH) is therapeutically effective in experimental and clinical spinal injury. The effects of TRH on diabetic neuropathy are not known. The aim of the present study was to investigate the electrophysiological effects of TRH in the streptozotocin diabetic rats. Three groups of rats were studied, non-diabetic control (n = 10), diabetic controls (n = 8), and TRH treated diabetic rats (n = 9). Administration of TRH or saline and electrophysiological measurements were performed 4 weeks after induction of diabetes. TRH was given intraperitoneally in a dose of 600 microg (3 ml). Nerve conduction velocity (NCV), measured in caudal nerve, and N1 latency of somatosensory evoked potentials (SEP) were measured 75 min after injection of TRH or serum saline. SEP latencies were 28.1 +/- 0.6, 29.4 +/- 0.8, 27.8 +/- 1.1 ms, in normal, diabetic and diabetic TRH-treated groups, and NCV values were 28.1 +/- 0.8, 23.8 +/- 0.4, and 27.9 +/- 0.7 m/s respectively. NCV was significantly reduced in the diabetic group compared to normals (P < 0.05). but then improved by TRH treatment (P < 0.05). Our findings suggest that TRH has an acute effect on peripheral neuropathy in experimental streptozotocin diabetes in the rat.

Animals↗
PubMed1999

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↗
PubMed1999

Human leptin deficiency caused by a missense mutation: multiple endocrine defects, decreased sympathetic tone, and immune system dysfunction indicate new targets for leptin action, greater central than peripheral resistance to the effects of leptin, and spontaneous correction of leptin-mediated defects.

We have previously demonstrated that genetically based leptin deficiency due to a missense leptin gene mutation in a highly consanguineous extended Turkish pedigree is associated with morbid obesity and hypogonadism. We have now performed detailed assessments of endocrine, sympathetic, and immune function. We have also identified a new adult female homozygous patient in this extended family who is severely obese and amenorrheic. In this family all wild-type and heterozgous individuals have normal body weight. Seven obese members of this family, whom we presume to have been leptin deficient, died during childhood. There are several findings that indicate potentially novel targets for leptin action in humans. Four homozygous patients (1 adult male, 2 adult females, and 1 child) have sympathetic system dysfunction, whereas all heterozygous subjects have normal sympathetic system function. Despite sympathetic system dysfunction and postural hypotension, 1 of 3 homozygous adult patients has impaired renin-aldosterone function. The patients also exhibit alterations in GH and PTH-calcium function, and 1 of them has decreased bone mineral density. Despite their obesity, these patients do not have risk factors for cardiovascular disease, such as hypertension, impairments in lipid metabolism, or hyperleptinemia [corrected]. These data support the hypothesis that the obese may have central, but not peripheral, resistance to the effects of leptin and that hyperleptinemia [corrected] may mediate the cardiovascular morbidity of the obese who are not leptin deficient. Furthermore, these data indicate that there may be several new targets for leptin action in human physiology. Such new targets may lead to novel pharmacological strategies for the use of leptin agonists and antagonists in the treatment of human disease. All 19 normal weight individuals in this family are alive, whereas 7 of 11 obese individuals died in childhood after infections. The odds ratio for mortality in the context of this obesity phenotype is 25.4, indicating that this mutation severely impairs key biological functions during childhood, negatively impacting on survival. We found that only the obese child in this family had thyroid function abnormalities. The oldest homozygous female patient started to menstruate, albeit with a luteal phase defect, 7 months ago, after a delay of over 20 yr, whereas the younger adult subjects are still hypogonadic. Thus, we conclude that due to their long life span, humans who survive the negative effects of leptin deficiency during childhood can, in contrast to ob/ob mice, over decades compensate some of the effects of leptin deficiency on immunity and endocrine function through mechanisms that remain to be elucidated.

Adult↗
PubMed1998

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↗
PubMed1998

The effects of thyroid status on serum apolipoprotein A-I-containing lipoprotein particles.

Alterations of lipid profile are a well-known phenomenon in thyroid dysfunction. However, little is known about the influence of thyroid hormone on Lp A-I and LpA-I:A-II particles. We have, therefore, studied LpA-I and LpAI:A-II concentrations in a group of 20 patients with hyperthyroidism and in a group of 15 patients with hypothyroidism before and one month after attainment of euthyroidism. In hypothyroid patients, LDL-cholesterol and apo B concentrations decrease significantly after L-T4 replacement treatment (from 4.49+/-2.51 to 2.76+/-0.70 mmol/ L, P=0.036 and from 89.4+/-16.1 to 78.3+/-13.3 mg/dL, P=0.05, respectively), whereas no significant change was observed in the total cholesterol, HDL-C, LpA-I, LpA-I:A-II and apo A-I concentrations. In hyperthyroid patients, total cholesterol (from 3.58+/-0.72 to 4.74+/-1.39mmol/L, P=0.0025), HDL-C (from 1.19+/-0.23 to 1.41+/-0.27mmol/L, P=0.0084), LDL-C (from 1.83+/-0.69 to 2.96+/-1.20 mmol/l, P=0.0025), apo A-I (from 85.6+/-12.5 to 91.7+/-18.1 mg/dL, P=0.05) and apo B (from 52.7+/-8.2 to 65.6+/-16.5 mg/dL, P=0.0013) increased after restoration of euthyroidism while triglycerides, LpA-I and LpA-I: A-II concentrations were unchanged. LpA-I and LpA-I:A-II concentrations were not related to thyroid hormones in both groups. Our study suggests that LpA-I and LpA-I:A-II particles are not under the direct control of thyroid hormones.

Adult↗
PubMed1998

Effects of gonadotropin and testosterone treatments on plasma leptin levels in male patients with idiopathic hypogonadotropic hypogonadism and Klinefelter's syndrome.

Since little is known about the effects of gonadotropin and testosterone treatment on leptin levels in male hypogonadism, we determined fasting plasma leptin levels before and 3 months after treatment in 21 patients with idiopathic hypogonadotropic hypogonadism (IHH), 16 patients with Klinefelter's syndrome and 20 male controls. Patients with IHH were treated with hCG/human menopausal gonadotropin, whereas patients with Klinefelter's syndrome received T treatment. Plasma leptin levels were measured by an RIA with a sensitivity of 0.5 microg/L. Mean leptin levels in patients with IHH before treatment (9.23+/-4.09 microg/L) were not significantly different from those in patients with Klinefelter's syndrome (7.29+/-5.05 microg/L; z=-1.41; P=0.15). Leptin levels in both IHH and Klinefelter's syndrome groups were, however, significantly higher than in the normal men (3.91+/-1.67 microg/L) (P<0.001 and P<0.01, respectively). Mean leptin levels did not change significantly 3 months after the initiation of gonadotropin (11.6+/-6.44 microg/L) or T (8.32+/-5.17 microg/L) treatment in either IHH or Klinefelter's syndrome. Our study demonstrated that mean plasma leptin levels are not influenced by short-term gonadotropin or T treatment in male hypogonadism.

Adult↗
PubMed1997

Biochemical composition of benign thyroid cyst fluid.

Although the availability of thyroid cyst fluid is easy by fine-needle aspiration, less is known about the biochemical composition of thyroid cyst fluid. The authors have, therefore, determined the biochemical composition of 18 benign thyroid cyst fluid specimens. They found that the activities of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and the concentrations of total protein, total bilirubin, and uric acid were highly increased in thyroid cyst fluid specimens when compared with normal human serum specimens. The concentrations of glucose, cholesterol, and triglycerides in cyst fluid were within normal serum limits. Selenium (Se) concentrations in most cyst fluids were low. Moreover, there was no correlation between Se and other biochemical parameters. Protein electrophoresis of cyst fluid specimens yielded high concentrations of alpha 1 and especially alpha 2 globulin fractions indicating an inflammation. The concentrations or activities of biochemical analytes were not significantly different in pure and mixed cysts. Those parameters were also not significantly different between cyst fluids of different colors. The gross appearance of the fluid and the presence of certain biochemical analytes were consistent with a hemorrhagic origin of most of the cyst fluid specimens. However, some biochemical markers indicate that autolysis or necrosis of thyroid tissue may also contribute the composition of thyroid cyst fluid. The reason for lower Se concentration in the thyroid cyst fluid may be the lower Se concentration in the Turkish population. These results also suggest that the fluid color or nature of cyst, e.g., pure or mixed cyst, is not a main determinant of biochemical composition of benign thyroid cyst fluid.

Alanine Transaminase↗
PubMed1997

A case of Addison's disease associated with the Lambert-Eaton myasthenic syndrome.

Nonneoplastic Lambert-Eaton Myasthenic Syndrome (LEMS) is rare. A 27-year-old man as initially having the diagnosis of Addison's disease was admitted to the hospital because of fatigue, dry-mouthness and proximal limb weakness for 1 year. A diagnosis of LEMS was made from electrophysiological studies. Clinical and laboratory studies revealed no malignancy. We report the first case of Addison's disease associated with non-neoplastic LEMS. It is possible that subclinical LEMS might be present in patients with Addison's disease more frequently than currently believed, since the prominent symptoms of LEMS may be confused with symptoms of Addison's disease.

Addison Disease↗
PubMed1997

Magnetic resonance imaging of posterior pituitary for evaluation of the neurohypophyseal function in idiopathic and autosomal dominant neurohypophyseal diabetes insipidus.

We investigated the role of MR imaging for evaluation of the functional status of the neurohypophyseal system in both idiopathic central diabetes insipidus (DI) and familial autosomal dominant neurohypophyseal DI. The patients and family with DI were analyzed retrospectively for the presence or absence of posterior pituitary gland hyperintense signal on MR images. A total of 19 adult patients with idiopathic central DI, 7 members of a family with autosomal dominant DI and 20 control subjects were included in the study. Diagnosis of idiopathic DI was based on the presence of central DI in the absence of any alteration that is known to be responsible for DI. The patients were studied retrospectively and the morphology and intensity of the posterior lobe by MR imaging was assessed by blinded reading. In all patients with idiopathic central DI and the affected members of the family, the posterior bright signal was absent while the stalk was normal on MR images. In contrast, normal posterior pituitary bright signal and stalk were found in unaffected members of the family and all control subjects. We conclude that MR imaging of the posterior pituitary lobe can be used to evaluate the functional status of the neurohypophyseal system in idiopathic central DI and familial autosomal dominant DI.

Adolescent↗
PubMed1997

A case of thyrotropin-secreting pituitary microadenoma with normal thyrotropin alpha-subunit level.

We present a 32-year-old male with a thyrotropin (TSH)-secreting pituitary microadenoma with normal alpha-subunit (SU) and/or alpha-SU/TSH molar ratio. An interesting feature of this patient is that the size of the pituitary tumor remained unchanged during a 6-year follow-up without treatment. The tumor was clearly visualized with somatostatin receptor imaging, indicating that it was somatostatin receptor-positive. Subcutaneous injection of 100 microg octreotide acetate three times daily resulted in significant reduction of TSH and free thyroid hormones 6 weeks after initiation of treatment. However, tumor size was not changed 3 months after initiation of octreotide therapy and thyroid hormones, but not TSH level, eventually increased in spite of increasing the octreotide dosage up to 600 microg/day. This led to discontinuation of treatment. The patient responded only temporarily to octreotide in spite of somatostatin receptors. This case further demonstrates that a normal alpha-SU and/or alpha-SU/TSH molar ratio cannot exclude the possibility of a TSH-secreting pituitary adenoma.

Adenoma↗