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T Iwasaka

Publications and source records attributed to T Iwasaka.

At least 19 recordsLinked to original sources
PubMed1999

Angiotensin II-induced transactivation of epidermal growth factor receptor regulates fibronectin and transforming growth factor-beta synthesis via transcriptional and posttranscriptional mechanisms.

The signaling cascade elicited by angiotensin II (Ang II) resembles that characteristic of a growth factor, and recent evidence indicates transactivation of epidermal growth factor receptor (EGF-R) by G protein-coupled receptors. Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and transforming growth factor-beta (TGF-beta) in cardiac fibroblasts. Ang II stimulated fibronectin mRNA levels dose dependently, with a maximal increase (approximately 5-fold) observed after 12 hours of incubation. Fibronectin synthesis induced by Ang II or calcium ionophore was completely abolished by tyrosine kinase inhibitors and intracellular Ca2+ chelating agents. Ang II-induced fibronectin mRNA was not affected by protein kinase C inhibitors or protein kinase C depletion, whereas specific inhibition of EGF-R function by a dominant negative EGF-R mutant and tyrphostin AG1478 abolished induction of fibronectin mRNA. We isolated the rat fibronectin gene, including the 5'-flanking region, and found that the activator protein-1 (AP-1) binding site present in the promoter region was responsible for the Ang II responsiveness of this gene. A gel retardation assay revealed the binding of nuclear protein to the AP-1 site, which was supershifted with anti-c-fos and anti-c-jun but not anti-activating transcription factor (ATF)-2 antibodies. Conditioned medium from Ang II-treated cells contained TGF-beta bioactivity, and addition of neutralizing TGF-beta antibody modestly (46%) inhibited induction of fibronectin. Ang II-induced synthesis of TGF-beta was also abolished by inhibition of EGF-R function. The effect of TGF-beta was exerted by stabilizing fibronectin mRNA without affecting the promoter activity and required de novo protein synthesis. We concluded that Ang II-induced expression of fibronectin and TGF-beta is mediated by downstream signaling of EGF-R transactivated by Ca2+-dependent tyrosine kinase and that Ang II-induced fibronectin mRNA expression is regulated by 2 different mechanisms, which are transcriptional control by binding of the c-fos/c-jun complex to the AP-1 site and posttranscriptional control by mRNA stabilization due to autocrine or paracrine effects of TGF-beta. Thus, this study suggests that the action of Ang II on extracellular matrix formation should be interpreted in association with the EGF-R signaling cascade.

Angiotensin II↗
PubMed1999

Higher heart rate variability of smokers after acute myocardial infarction.

Although cigarette smoking is known to be a strong risk factor for the development of coronary artery disease, several large clinical studies have demonstrated that current smokers had a favorable prognosis compared to nonsmokers after myocardial infarction. This study sought to evaluate the effect of smoking status on heart rate variability after onset of acute myocardial infarction. We studied 52 patients (34 smokers, 18 nonsmokers) with a first myocardial infarction within 24 h of onset. We recorded 24-h ambulatory ECG to calculate very low frequency power (VLF), low frequency power (LF) and high frequency power (HF) 14 days after onset. Although smokers had a tendency to be younger than nonsmokers (mean age 57 versus 62, P = 0.0812), clinical characteristics were not statistically different between smokers and nonsmokers. After adjustment for age, left ventricular ejection fraction, history of diabetes, acute revascularization and use of beta-blockers, VLF (P = 0.0183) of smokers 14 days after onset was significantly higher than for nonsmokers. In conclusion, although smoking reduces heart rate variability in the general population, higher heart rate variability was observed in smokers than nonsmokers after acute myocardial infarction under the condition of smoking cessation.

Aged↗
PubMed1999

Preoperative cervical cytology in endometrial carcinoma and its clinicopathologic relevance.

OBJECTIVE: The aim of this study was to assess the significance of malignant or suspicious cervical cytology in preoperative identification of poor prognostic factors in endometrial carcinoma and to determine whether preoperative abnormal cervical cytology is an independent prognostic factor for endometrial carcinoma. METHODS: We evaluated the correlation between preoperative cervical cytology and postoperative clinicopathologic findings, sites of metastasis, and receptor status from 99 surgically staged patients with endometrial carcinoma. RESULTS: Sixty-eight patients (68.7%) had normal cervical cytology, 1 (1.0%) had atypical cytology suspicious for malignancy, and 30 (30.3%) had malignant cytology on preoperative cervical cytology. Malignant and suspicious cervical smears were statistically correlated with surgical stage (P = 0.001), histopathology (P = 0.010), tumor grade (P = 0.012), depth of myometrial tumor invasion (P = 0.001), cervical involvement (P = 0. 01), lymph node metastases (P = 0.002), adnexal metastases (P = 0. 012), progesterone receptor (P = 0.007), and estrogen receptor (P = 0.031). No association was found between preoperative cervical cytology and patients' age or peritoneal cytology. Univariate analysis showed that cervical cytology was related to survival (P = 0.018). However, multivariate analysis of cervical cytology, stage, grade, and myometrial invasion showed that preoperative cervical cytology was not a significant prognosticator for survival. CONCLUSION: Patients with endometrial carcinoma who have malignant or suspicious cytology detected by preoperative cervical cytology are at increased risk of having known poor prognostic factors. However, positive preoperative cervical cytology itself does not appear to be an independent prognostic factor and probably should not influence treatment decisions in endometrial cancer.

Adult↗
PubMed1999

Prognostic significance of progesterone receptor immunohistochemistry for lymph node metastases in endometrial carcinoma.

OBJECTIVE: The aim of this study was to determine whether progesterone receptor (PR), estrogen receptor (ER), p53 protein, and proliferating cell nuclear antigen (PCNA) expression constitute independent prognostic factors for lymph node metastases in endometrial carcinoma using immunohistochemical techniques on hysterectomy and biopsy specimens. METHODS: We evaluated the correlation between lymph node metastases and PR/ER immunohistochemistry, p53/PCNA expression, age, tumor grade, myometrial tumor invasion, cervical involvement, and ovarian metastases in a series of 99 cases of primary endometrial carcinoma surgically staged with systemic pelvic lymphadenectomy and para-aortic lymph node biopsy. RESULTS: Lymph node metastases from endometrial carcinoma were statistically correlated with negative PR immunohistochemistry (P = 0.001), intense p53 expression (66% or more of the tumor cells stained, P = 0.003), deep myometrial tumor invasion (greater than one-half, P = 0.001), and cervical involvement (P = 0.001). Tumor grade showed borderline statistical significance for lymph node metastases (P = 0.058). On multivariate analysis, negative PR, intense p53 expression, and cervical involvement were significant prognostic variables for lymph node metastases (P = 0.0001, 0.0023, and 0.002, respectively). Immunohistochemical study indicated that the PR status on preoperative biopsy specimens and hysterectomy specimens was in good agreement, but p53 status was not. Age, ovarian metastases, ER immunohistochemistry, and PCNA expression were not significantly related to lymph node metastases. CONCLUSION: PR immunohistochemistry appeared to be the most powerful prognostic factor associated with lymph node metastases in endometrial carcinoma, independent of other clinicopathological parameters.

Adult↗
PubMed1999

Interleukin-1 beta upregulates cardiac expression of vascular endothelial growth factor and its receptor KDR/flk-1 via activation of protein tyrosine kinases.

Vascular endothelial growth factor (VEGF) is not only an endothelial cell-specific angiogenic factor but also a potent mediator of vascular permeability. Interleukin-1 beta (IL-1 beta) is a pro-inflammatory cytokine that has numerous effects on the pathogenesis of the tissue injury. To explore the possible regulation of the VEGF system by IL-1 beta in the heart, we examined the regulation of expression of VEGF and KDR/flk-1 (one of the VEGF receptors) by IL-1 beta using cardiac myocytes and cardiac microvascular endothelial cells (CMEC). Both cardiac myocytes and CMEC substantially expressed VEGF mRNA and its expression was increased 3.6- and 2.4-fold by IL-1 beta, respectively. IL-1 beta-induced accumulations of VEGF mRNA in cardiac myocytes were abolished by the tyrosine kinase inhibitor genistein, whereas inhibition of protein kinase C (PKC) by staurosporin, calphostin C and phorbol ester-induced PKC depletion, and intracellular Ca2+ chelators did not affect the induction of VEGF mRNA by IL-1 beta. Relatively smaller amounts of KDR/flk-1 mRNA were detected in CMEC, but not in cardiac myocytes, and the analysis using quantitative reverse transcription-polymerase chain reaction revealed that IL-1 beta significantly stimulated the accumulation of KDR/flk-1 mRNA 3.0-fold. VEGF protein (23 kDa) levels in Western blot analysis were increased 4.2- and 3.4-fold by IL-1 beta in cardiac myocytes and CMEC, respectively. KDR/flk-1 protein (230 kDa) levels in CMEC were also increased 3.2-fold by IL-1 beta. In addition, pre-treatment of CMEC by IL-1 beta markedly enhanced VEGF-induced tyrosine phosphorylation of focal adhesion kinase compared with that in the unstimulated cells. These findings indicate that cardiac VEGF-KDR/flk-1 system is upregulated by IL-1 beta via activation of tyrosine kinases, suggesting that the IL-1 beta-modulated autocrine and/or paracrine system of VEGF has an important role in the process of angiogenesis in ischemic hearts.

Animals↗
PubMed1999

Early detection of the no-reflow phenomenon in reperfused acute myocardial infarction using technetium-99m tetrofosmin imaging.

Evaluation of myocardial perfusion in the early stage of acute myocardial infarction (MI) is clinically important for adjunctive therapies to minimize infarct size. To determine the role of early scintigraphic detection of impaired myocardial reperfusion after primary coronary angioplasty (PTCA) in patients with acute MI, semiquantitative technetium-99m tetrofosmin single-photon emission tomographic (SPET) imaging was performed before primary PTCA (before; area at risk), 60 min after PTCA (after) and at 1 month (1 M; final infarct) in 35 patients with acute MI. The left ventricle was divided into 13 segments and the defect score was calculated as the sum of the perfusion defect of each segment, from 3 (complete defect) to 0 (normal perfusion). A significant myocardial perfusion change after PTCA was defined as a change in the defect score (before minus after PTCA) of >/=4. The echocardiographic asynergic score was defined as the number of asynergic (severe hypokinetic or akinetic) segments corresponding to the analogous segments on SPET images, and recovery of wall motion was calculated as absolute change in the asynergic score (before PTCA minus 1 M). Among the 35 patients, 15 (43%) had a change in the defect score of <4 (no reflow: group 1) while 20 had a change in the defect score of >/=4 (reflow: group 2). There were no significant differences between the two groups with respect to the time between admission to PTCA, revascularization time, collateral grade or Thrombolysis in Myocardial Infarction (TIMI) flow grade before PTCA. Despite the lack of a difference in area at risk between the two groups (group 1 = 12.8+/-4.3 and group 2 = 15.1+/-4.7), final infarct size in group 1 was significantly larger compared with that in group 2 (8.1+/-4.3 vs 4.9+/-3.0, P<0.001). Recovery of wall motion was significantly smaller in group 1 than in group 2 (4.3+/-1.7 to 3.5+/-1.5 vs 4. 1+/-2.1 to 1.6+/-1.6, P<0.001). In conclusion, a small change (<4) in defect score (scintigraphic no-reflow phenomenon) after primary PTCA indicates persisting impaired myocardial perfusion or irreversible cellular damage just after PTCA which is associated with poor recovery of wall motion, as compared with that observed in cases of reflow (>/=4 in defect score).

Aged↗
PubMed1999

Apoptosis and Ki-67 expression in adenomyotic lesions and in the corresponding eutopic endometrium.

OBJECTIVE: To examine biologic and proliferative properties of adenomyotic lesions and to determine whether adenomyotic lesions originate in the basal layer of the eutopic endometrium. METHODS: We examined eutopic and ectopic endometria from 23 patients with adenomyosis. To obtain evidence for the induction of programmed cell death, apoptotic cells were identified using a modified terminal deoxynucleotidyltransferase-biotin nick end-labeling method. To evaluate cell death repressor activity, bcl-2 gene expression was examined using immunohistochemical staining. As a proliferative marker, Ki-67 expression was also examined immunohistochemically. RESULTS: In the eutopic endometrium, apoptosis was most frequently observed in epithelial cells during mid- to late secretory phases, although it was rarely found during early proliferative through early secretory phases (P<.01). In contrast, bcl-2 gene expression inversely correlated with the appearance of apoptosis. A similar tendency was observed in stromal cells. In the ectopic endometrium of adenomyosis, endometrial dating revealed that secretory change was rare, even in the secretory phase, and that induction of apoptotic cells as well as bcl-2 gene expression showed no cyclic change. In stromal cells of the ectopic endometrium, apoptosis was more frequent than was seen in the eutopic endometrium, in all menstrual phases (P<.05). Ki-67 was constantly expressed in the glandular epithelium of the ectopic endometrium, irrespective of the menstrual phases, whereas in the secretory phase it was less expressed in the eutopic endometrium of functional and basal layers (P<.01). CONCLUSION: The induction of apoptosis seems to be regulated by hormonal changes in the eutopic endometrium and has an inverse correlation with bcl-2 gene expression. The ectopic endometrium in adenomyosis is rarely influenced by hormonal change and has different biologic and proliferative properties than events observed in the eutopic endometrium findings, which strongly suggest that the adenomyotic lesion does not originate in the basal endometrium.

Adult↗
PubMed1999

Long-term administration of atrial natriuretic peptide in patients with acute heart failure.

A short-term treatment of atrial natriuretic peptide (ANP), a circulating hormone of cardiac origin, is reported to improve cardiac performance in patients with chronic heart failure. However, clinical usefulness of long-term administration of ANP in patients with congestive heart failure has not been reported. We studied 36 patients with severe acute heart failure who resisted various therapy. Hemodynamic parameters were measured before and 48 h after initiating ANP infusion (n = 18) or normal saline (n = 18). Mean pulmonary capillary wedge pressure (23-->13 mm Hg), mean right atrial pressure (10-->5 mm Hg), systemic vascular resistance (2,169-->1,307 dyn x s x cm(-5)) and pulmonary vascular resistance (318-->136 dyn x s x cm(-5)) decreased significantly, whereas cardiac index (1.9-->2.6 L/min/m2) and urine volume (1,692-->2,560 ml/day) increased during long-term ANP infusion (before-->48 h). Moreover, in eight patients with long-term ANP infusion, these hemodynamic effects were maintained at 7 days after initiating ANP infusion. Vasodilating, pulmonary vasorelaxant, and diuretic activities of ANP are maintained without tolerance, and thus long-term ANP infusion is clinically useful in patients with severe acute heart failure.

Acute Disease↗
PubMed1999

Clinical significance of denervated but viable myocardium in patients with recanalized acute myocardial infarction.

In patients with acute myocardial infarction (MI), myocardial sympathetic innervation evaluated by 123I-metaiodobenzylguanidine myocardial scintigraphy is more sensitive to ischaemia than the associated perfusion abnormality of 201Tl myocardial scintigraphy. The purpose of this study was to evaluate the scintigraphic indices related to the recovery of left ventricular function after acute MI. 123I-metaiodobenzylguanidine and 201Tl-chloride imaging were performed in 15 patients (mean age 60 years, 13 men and 2 women) 2 weeks after the onset of acute MI. Using a 20-segment visual interpretation of the 201Tl image, myocardial segments were classified into persistent defect, redistribution or reverse redistribution, and normal 201Tl uptake. The extent of denervated segments showed a fair correlation with the ejection fraction on admission (r = -0.53, P = 0.04), whereas the extent of persistent defect had a close correlation with the ejection fraction at 4 months (r = -0.79, P = 0.01). There was a good correlation between the extent of denervated but viable myocardium and the change in ejection fraction from admission to 4 months (r = 0.68, P = 0.01). Thus, denervated but viable myocardium is a scintigraphic index related to the functional recovery of left ventricular pump function after acute MI.

3-Iodobenzylguanidine↗
PubMed1999

Reduced size of liquefaction necrosis of mitral annular calcification in chronic renal failure by using low calcium concentration hemodialysis.

A report is presented of a liquefaction necrosis of mitral annular calcification in a patient with chronic renal failure and secondary hyperparathyroidism who had been managed by hemodialysis for 11 years. The mass was echogenic with an echo-lucent area inside, high density on computed tomography and low intensity on magnetic resonance imaging. The uptake of gallium-67 (67Ga)-citrate and the bone agent technetium-99m-methylene diphosphate (99mTc-MDP) was seen in the mass. These findings were compatible with liquefaction necrosis of the mitral annular calcification. After treatment with low calcium concentration hemodialysis, the size of the mass reduced with disappearance of the echo-lucent area on the echocardiography and there was no uptake of 67Ga-citrate or 99mTc-MDP. Liquefaction necrosis might be the early and reversible form of mitral annular calcification. When a tumorlike echogenic mass at the base of mitral leaflets is seen in patients with predisposing factors for mitral annular calcification, consider the possibility of this specific form of mitral annular calcification in order to avoid any unnecessary surgical intervention.

Calcinosis↗
PubMed1999

Pseudoaneurysm of the left ventricle progressing from a subepicardial aneurysm.

A 56-year-old man presented with an inferior myocardial infarction and a huge pseudoaneurysm below the inferior surface of the left ventricle, which had progressed from a small subepicardial aneurysm over a 6-month period. Transthoracic echocardiography, Doppler color flow images, radionuclide angiocardiography, magnetic resonance imaging and contrast ventriculography all revealed an abrupt disruption of the myocardium at the neck of the pseudoaneurysm, where the diameter of the orifice was smaller than the aneurysm itself, and abnormal blood flows from the left ventricle to the cavity through the orifice with an expansion of the cavity in systole and from the cavity to the left ventricle with the deflation of the cavity in diastole. Coronary angiography revealed 99% stenosis at the atrioventricular nodal branch of the right coronary artery. At surgery the pericardium was adherent to the aneurysmal wall and a 1.5-cm orifice between the aneurysm and the left ventricle was seen. Pathological examination revealed no myocardial elements in the aneurysmal wall. The orifice was closed and the postoperative course was uneventful. Over-intense physical activity as a construction worker was considered to be the cause of the large pseudoaneurysm developing from the subepicardial aneurysm. These findings indicate that a subepicardial aneurysm may progress to a larger pseudoaneurysm, which has a propensity to rupture, however, it can be surgically repaired.

Aneurysm, False↗
PubMed1999

Primary aldosteronism with aldosterone-producing adrenal adenoma in a pregnant woman.

A 30-year-old pregnant woman complained of muscle weakness at 29 weeks' gestation. She was hypertensive with severe hypokalemia. Lower plasma renin activity and higher aldosterone level than the normal values in pregnancy suggested primary aldosteronism. A cesarean delivery was performed at 31 weeks' gestation because of pulmonary congestion. The neonatal course was uncomplicated. The laparoscopic adrenalectomy for a 2.0-cm right adrenal adenoma resulted in normalizing of her blood pressure and serum potassium level. Although primary aldosteronism is rare, especially during pregnancy, it should be always considered as one of etiologies of hypertension in pregnancy.

Adrenal Cortex Neoplasms↗
PubMed1999

Multiple spontaneous small bowel perforations due to systemic cholesterol atheromatous embolism.

A-65-year-old man was admitted for coronary and peripheral angiography to evaluate angina pectoris and peripheral vascular disease. Following angiography, he suffered from blue toes, livedo reticularis and progressive renal failure. The patient's condition continued to deteriorate, including the development of malnutrition. Four months later he suddenly developed panperitonitis, went into shock and died. The autopsy verified multiple perforations of the small bowel with disseminated cholesterol atheromatous embolism. The other organs including kidney were also invaded by atheroembolism. This was a rare case of multiple spontaneous perforations of small bowel due to systemic cholesterol atheromatous embolism.

Acute Kidney Injury↗
PubMed1999

Differential kinetics of circulating angiotensin IV and II after treatment with angiotensin II type 1 receptor antagonist and their plasma levels in patients with chronic renal failure.

BACKGROUND: Angiotensin II (Ang II) C-terminal hexapeptide (referred to as Ang IV) possesses the characteristics of a real hormone with specific receptors and biological effects. Clinical application of Ang II type 1 receptor (AT1-R) antagonists cause an increase in plasma Ang II level, which may result in enhanced production of Ang IV. PATIENTS AND METHODS: In this study, we measured plasma Ang IV and Ang II levels in patients with chronic renal failure (CRF), and also examined the changes in Ang IV and Ang II levels after administration of an ATI-R antagonist. RESULTS: Ang II and Ang IV levels in CRF patients untreated with hemodialysis (n = 16) were 15.8+/-3.6 and 6.0+/-1.1 pg/ml, respectively, which did not differ significantly from Ang II (20.6+/-2.4) and Ang IV levels (8.6+/-1.1) in normal controls (n = 23). The ratio of Ang IV to Ang II was 38%, similar to that in the controls (41%). Ang II or Ang IV levels in CRF patients treated with hemodialysis (n = 12) were also similar to the control values. Ang IV levels had a significant correlation with Ang II levels (r = 0.59). When hypertensive patients were treated with an AT1-R antagonist candesartan for 7 days, Ang II and Ang IV levels were increased 5.5- and 4.1-fold relative to the control levels, respectively. Ang II levels 28 and 56 days after treatment were significantly lower than those 7 days after treatment, whereas Ang IV levels did not differ significantly from those 7 days after treatment. Similar differential kinetics in Ang II and Ang IV levels after long-term (90 days) treatment with an AT1-R antagonist was also confirmed in experiments using rats. Significant decrease in blood pressure continued during long-term treatment with an AT1-R antagonist. CONCLUSION: These findings demonstrated that plasma Ang IV levels in patients with CRF did not differ significantly from those in normal subjects, and that treatment with an AT1-R antagonist caused marked increases in both Ang II and Ang IV levels. In contrast, during long-term treatment plasma Ang II levels were more rapidly decreased than Ang IV levels, suggesting longer-lasting enhancement of the action of Ang IV rather than that of Ang II after treatment with an AT1-R antagonist.

Aged↗
PubMed1999

Optimum threshold values of 201Tl SPET in the determination of the left ventricular border and extent of myocardial infarction.

The aim of this study was to determine the optimum threshold value of the left ventricular border and the extent of myocardial infarction using quantitative 201Tl single photon emission tomography (SPET). We used the unfolded map method to determine the size of the left ventricle and the extent of myocardial infarction in 10 patients, because it has been shown to be superior to the conventional polar map method. The relative differences in the size of the left ventricle and extent of infarction between 201Tl SPET and post-mortem examination were calculated. The optimum threshold value was determined when the relative difference = 0%. There was an excellent correlation between scintigraphic and post-mortem left ventricular size at a threshold value of 53% (r = 0.91, P < 0.001); an excellent correlation was also observed between scintigraphic and post-mortem infarct size at a threshold value of 55% (r = 0.93, P < 0.03). The optimum threshold value in determining left ventricular size using 201Tl SPET is 53% and that in determining infarct size is 55%.

Adult↗
PubMed1999

[Angiotensin II receptor-mediated function unmasked by gene-engineered animals].

The receptors for angiotensin (Ang) II are classified into two subtypes (AT1-R and AT2-R) by the discovery of non-peptidic ligands and AT1-R mediates most of the cardiovascular actions of Ang II. AT2-R is expressed at very high levels in the developing fetus, whereas in the adult its expression in the cardiovascular system is very low. Cardiac myocyte- or vascular smooth muscle-specific overexpression mice of AT2-R display an inhibitory effect on Ang II-induced chronotropic or pressor actions, suggesting the role of AT2-R on the activity of cardiac pacemaker cells or maintenance of vascular resistance. AT2-R also activates the kinin/nitric oxide/cGMP system in the cardiovascular and renal system, resulting in the AT2-R-mediated cardioprotection, vasodilation and pressure natriuresis. These effects transmitted by AT2-R are mainly exerted by stimulation of protein tyrosine or serine/threonine phosphatases in Gi-protein dependent manner. The expression level of AT2-R is much higher in human hearts than in those of rodents, and the AT2-R-mediated actions are likely enhanced, especially by clinical application of AT1-R antagonists.

Adult↗
PubMed1999

Measurement of serum leptin in patients with chronic renal failure on hemodialysis.

BACKGROUND: Leptin, the product of the obese gene, is produced exclusively in fat cells. SUBJECTS, MATERIALS AND METHODS: To evaluate the clinical significance of measuring serum leptin in 56 patients with chronic renal failure on hemodialysis (HD), we measured leptin levels using radioimmunoassay in 34 normal volunteers and in 56 patients on HD. RESULTS: Normal serum leptin averaged 5.7 +/- 0.7 (mean +/- SEM) ng/ml, which correlated significantly (p < 0.001) with the body fat percentage as measured by bioelectrical impedance analysis. Serum leptin in HD patients ranged from 1.3 to 142 ng/ml. The mean serum leptin analyzed after the logarithmic conversion was 5.6 ng/ml, which was not significantly different from the normal control value, although the body fat percentage was significantly lower than normal volunteers. There was a significant (p < 0.01) positive correlation between body fat percentage and serum leptin in both normal controls and HD patients. The slope of the regression curve was steeper in HD patients than in normal controls. CONCLUSION: (1) serum leptin levels to body fat mass are significantly higher in HD patients than controls; (2) the variability is much wider in HD patients; and (3) a significant relation exists between percent body fat and log serum leptin, the relation being steeper in HD patients than in controls.

Adipose Tissue↗