Biomedical subjects

M Fukase

Publications and source records attributed to M Fukase.

At least 109 records · Page 6Linked to original sources

PubMed1990

The cellular mechanism of action by vasoconstrictor hormones in cultured rat vascular smooth muscle cells.

The effects of angiotensin (Ang) II, arginine vasopressin (AVP), and serotonin (5-HT) on inositol trisphosphate (IP3) production, cytosolic Ca2+ concentration [( Ca2+]i), and the phosphorylation of 20 kilodalton myosin light chain (MLC) were examined in cultured rat vascular smooth muscle cells (VSMC). These vasoconstrictors immediately induced dose-dependent and concomitant increases in IP3 production, [Ca2+]i, and phosphorylation of 20 kDa MLC. The agonist-induced increases in IP3 production, [Ca2+]i, and phosphorylation of 20 kDa MLC in VSMC were completely blocked by pretreatment with the receptor antagonists for Ang II, V1, and 5-HT2, respectively. These data suggest that receptor-mediated increases in IP3 production, [Ca2+]i, and phosphorylation of 20 kDa MLC by these vasoconstrictors are closely interrelated.

Angiotensin II↗

PubMed1990

Calcitonin gene-related peptide and induction of hyperglycemia in conscious rats in vivo.

The effect of calcitonin gene-related peptide (CGRP) on glucose metabolism was investigated in conscious and unrestrained rats in vivo. Intravenous injection of rat CGRP (5.67 and 0.567 nmol/kg) caused a significant, dose-dependent increase in plasma glucose concentration and a simultaneous dose-dependent increase in plasma insulin level. In contrast, plasma glucagon level was not changed. On the other hand, intravenous infusion of CGRP (46.6 pmol.kg-1.min-1) decreased tolerance to intragastric administration of glucose (IGGTT). Plasma insulin response to IGGTT, however, was not affected by CGRP infusion. Moreover, although intravenous injection of CGRP (5.67 nmol/kg) elicited a significant increase in plasma epinephrine and norepinephrine concentrations, concomitant administration of epinephrine and norepinephrine, inducing a more prominent rise in plasma catecholamines than those induced by CGRP, affected neither plasma glucose nor insulin levels. Finally, plasma insulin levels obtained by simulating CGRP-induced changes in plasma glucose or glucose plus catecholamine levels by infusion of glucose or glucose plus catecholamines were not different from those induced by CGRP injection. These results suggest that CGRP has a hyperglycemic action that is not mediated by sympathetic outflow in conscious rats, and inhibition of insulin secretion, if any, does not play a major role in this hyperglycemic action of CGRP. We have demonstrated specific CGRP receptors linked to adenylate cyclase activation in rat liver plasma membranes; this hyperglycemic effect of CGRP in vivo may be partly due to its direct action on the liver.

Animals↗

PubMed1989

[Clinical studies using a highly sensitive radioimmunoassay for mid-region and carboxy terminus of parathyroid hormone in normal, hypo- and hypercalcemic states].

Parathyroid hormone radioimmunoassay (RIA), specific for mid-region of the PTH molecule, has been proven to be extremely useful for the differential diagnosis of abnormal calcium metabolism. Recently, we developed a highly sensitive RIA for PTH, consisting of PTH antiserum (CH9), 125I labelled Tyr42 hPTH (43-68) and synthetic hPTH (1-84) as standard. This RIA cross-reacted with mid-region and carboxyl terminals of PTH. The within-assay and between-assay coefficients of variation were less than 4.6% and less than 8.6%, respectively. The limit of detection was 50pg/ml. The levels of serum calcium, serum phosphate, serum creatinine, Tmpo4/GFR and creatinine clearance (Ccr) in normal healthy volunteers aged 20 to 50 years remained almost constant and showed 9.24 +/- 0.34mg/dl (mean +/- SD, n = 242), 3.34 +/- 0.38mg/dl (n = 242), 0.870 +/- 0.121mg/dl (n = 242), 3.20 +/- 0.54mg/dl GF (n = 189) and 103 +/- 17ml/min (n = 137), respectively. All healthy volunteers (n = 326) had measurements of PTH in the blood. From 20 to 50 years, normal PTH mean was 374 +/- 97pg/ml (+/- SD, n = 237) and ranged from 180-568pg/ml, and from 60 to 80 years it was 471 +/- 133pg/ml (n = 34) and ranged from 205-737pg/ml. Since we found that PTH was markedly elevated above normal when Ccr was below 40ml/min, and PTH was very significantly correlated with the reciprocal of Ccr (r = 0.8996, P less than 0.001) using a multivariate analysis, all of the patients whose Ccr was higher than 40ml/min were selected and examined in the following studies. Serum PTH values completely separated patients with surgically proven primary hyperparathyroidism (1 degree HPT) from malignant associated hypercalcemia (MAH), and patients with idiopathic hypoparathyroidism (IHP) from pseudohypoparathyroidism (PHP), both of which were diagnosed by Ellsworth-Howard test. PTH values in all of the patients with 1 degree HPT (n = 23) were above normal, but those with MAH (n = 6) were below the normal or lower normal range. PTH values in patients with PHP (n = 7) showed above normal, while those with IHP (n = 5) were below the normal range. PTH was normalized in post operative status in all patients after parathyroidectomy (n = 6). These results indicate that this PTH RIA is extremely useful for the differential diagnosis in diseases with calcium abnormalities.

Adolescent↗

PubMed1989

Parathyroid hormone degradation by chymotrypsin-like endopeptidase in the clonal osteogenic UMR-106 cell.

Parathyroid hormone (PTH) -degrading activity was studied using osteoblast-like UMR-106 cells. PTH-degrading activity was assessed by the amount of PTH fragments produced in the medium after exposure of intact human PTH-(1-84) to UMR-106 cells. PTH immunoreactivity recovered in trichloroacetic acid-soluble products of the medium and in fractions eluted from reverse-phase high-performance liquid chromatography (HPLC) was measured by radioimmunoassay using an antibody specific for the mid-region and C-terminus of PTH. In this study, intact UMR-106 cells but not extracellular enzymes cleaved human PTH(1-84) into fragments which were released into the medium (in a time- and temperature-dependent fashion). HPLC analysis of the PTH fragments depicted three immunoreactive peaks (peaks 1, 2 and 3) besides intact PTH, indicating a limited PTH-hydrolyzing activity of the cells. Furthermore, a 1000-fold molar excess of either hPTH-(3-34) or [Nle8,Nle18,Tyr34]hPTH-(3-34)amide inhibited PTH-degrading activity by 63% and 80% of control, respectively, whereas neither calcitonin, vasopressin nor growth hormone suppressed it. Additionally, HPLC analysis of the samples treated with [Nle8,Nle18,Tyr34]hPTH-(3-34)amide showed a reduction of the three peaks, suggesting an involvement of PTH receptor in the production of PTH fragments. This PTH-degrading activity was strongly inhibited by phenylmethylsulfonyl fluoride and chymostatin, but not by soybean trypsin inhibitor, elastatinal or inhibitors of cysteine, aspartic or metalloproteinases, indicating that it is due to a seryl chymotrypsin-like endopeptidase. Chymotrypsin-like activity seems to be solely responsible for PTH-degrading activity in intact UMR-106 cells, since all three PTH fragments were predominantly suppressed in the presence of chymostatin. Further analysis of chymotrypsin-digested products of hPTH-(1-84) eluted from HPLC exhibited five fragments detected by ultraviolet absorbance at 210 nm, three of which were measurable by PTH radioimmunoassay, each corresponding to the three PTH fragments produced by UMR-106 cells. To explore the cleavage sites of PTH further, amino acid analysis of chymotrypsin-cleaved products was performed. The results strongly support the view that the chymotrypsin-like enzyme in UMR-106 cells cleaved the hormone between residues 23-24 and 34-35, to produce, at least, hPTH-(24-84) and -(35-84). Our present study indicates that a chymotrypsin-like endopeptidase is solely responsible for limited hydrolysis of PTH by intact UMR-106 cells.

Amino Acids↗

PubMed1989

Cyclooxygenase inhibitors enhance cell growth in an osteoblastic cell line, MC3T3-E1.

To elucidate the significance of endogenous prostaglandin E2 (PGE2) in osteoblastic cell function, we studied the effects of cyclooxygenase inhibitors on cell growth and alkaline phosphatase (ALP) activity in MC3T3-E1 cells. UMR-106 cells were also used as references in our experiments. MC3T3-E1 cells, cultured in alpha-minimal essential medium containing 10% fetal bovine serum, were shown to produce PGE2, which was markedly suppressed in the presence of indomethacin. Addition of indomethacin resulted in an increase in DNA content and [3H]thymidine incorporation. A similar growth stimulatory effect was observed when structurally different cyclooxygenase inhibitors, that is, acetyl salicylic acid (ASA), flurbiprofen, and piroxicam, were added. These cyclooxygenase inhibitors, however, differed in their effects on ALP activity. Indomethacin and ASA enhanced ALP activity, whereas flurbiprofen and piroxicam suppressed it. We then examined the effects of exogenous addition of PGE2. Although exogenous PGE2 at 6 x 10(-6) M slightly stimulated cell growth, it inhibited cell growth at 6 x 10(-8) M and 6 x 10(-7) M. ALP activity was reduced in a dose-dependent fashion by exogenous PGE2. These results suggest that PGE2 produced by MC3T3-E1 may be suppressing cell proliferation and that cyclooxygenase inhibitors, per se, may stimulate cell growth by inhibiting endogenous PGE2 production in MC3T3-E1 cells. UMR-106 cells also produced PGE2, although less than MC3T3-E1 cells. In UMR-106 cells, the cyclooxygenase inhibitors did not influence DNA content or ALP activity as distinctly as in MC3T3-E1 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

PubMed1989

Reciprocal effects of Ca2+ and Mg-ATP on the 'run-down' of the K+ channels in opossum kidney cells.

Using the patch clamp technique, we identified an inwardly rectifying K+ channel in the membrane of opossum kidney cells. The single channel conductance was about 90 pS for inward currents and 30 pS for outward currents under a symmetrical high-K+ condition. The activity of the channel was found to decrease with time during recording from inside-out patches. In the solution with submicromolar Ca2+, the activity disappeared within 4-20 min. Intracellular Ca2+ promoted the run-down of the channel activity at 0.1-1 mM, whereas millimolar Mg-ATP restored the activity after run-down. The run-down channels could never be reactivated by ATP in the absence of Mg2+, or by a nonhydrolyzable ATP analog, AMPPNP, even in the presence of Mg2+.

Adenosine Triphosphate↗

PubMed1989

Arachidonic acid stimulates cell growth in an osteoblastic cell line, MC3T3-E1, by noneicosanoid mechanism.

Arachidonic acid, added to alpha-minimum essential medium containing 10% fetal bovine serum at the final concentration of 10(-4) M, significantly increased DNA content of an osteoblastic cell line, MC3T3-E1, along with an increase of DNA synthesis. No growth-stimulatory effect of arachidonic acid was observed under serum-free condition. alpha-Linolenic acid, which cannot be converted to arachidonic acid, also increased DNA content at 10(-4) M. Additionally, the stimulatory effects of these fatty acids were not inhibited by simultaneous addition of 10(-5) M of indomethacin. Indomethacin, when added to alpha-minimum essential medium with 10% fetal bovine serum, also significantly increased DNA content of MC3T3-E1 cells. These results suggest that arachidonic acid may potentiate the growth-stimulatory effect of serum-derived growth factors probably via noneicosanoid mechanism. Rat osteogenic sarcoma cell line, UMR106, also showed an increase in DNA content with arachidonic acid treatment. Hence, it is suggested that arachidonic acid may stimulate proliferation of cells of osteoblastic lineage. It is also suggested that indomethacin, probably by blocking endogenous prostaglandin E2 synthesis, stimulates cell growth in MC3T3-E1 cells.

Animals↗

PubMed1989

Low levels of intestinal calbindin-D28K in X-linked hypophosphatemic mice.

Using our radioimmunoassay for chick intestinal calbindin-D28K, a protein homologous to that in the chick intestine on the basis of immuno-crossreactivity, molecular weight and charge properties was identified in mouse intestinal mucosa. No such protein, however, was found in the kidney, cerebellum, cerebrum, liver or myocardium of the mice. In X-linked hypophosphatemic mice (Hyp mice) maintained on a standard diet containing vitamin D, the basal level of intestinal calbindin-D28K was much lower (average 65.13 +/- 7.39%) than that in breeding pairs of normal mice maintained under the same conditions. Although the mean intestinal level of calbindin-D28K was as low as 118.23 +/- 20.08 (SD) ng/mg protein in vitamin D-deficient mice (-D), the level of this protein was markedly increased to the control level (198.68 +/- 9.98 vs. 198.49 +/- 14.29 ng/mg protein of control) (P less than 0.001) in response to the administration of vitamin D3 (1000 I.U. s.c. for 10 days) (+D). These results indicate that calbindin-D28K, biochemically indistinguishable from the chick intestinal calbindin-D28K, is present in the mouse intestine, and that the lower amount of this protein in the Hyp mouse intestine may, at least in part, be responsible for the resistance to the effects of vitamin D.

Animals↗

PubMed1989

Effects of human PTH-related peptide and human PTH on cyclic AMP production and cytosolic free calcium in an osteoblastic cell clone.

Recently, human parathyroid hormone-related peptide (hPTHrP) has been purified and its amino acid sequence determined. Within the amino-terminal 13 residues of hPTHrP, 8 amino acids were found homologous between hPTHrP and human PTH (hPTH). This peptide was reported to stimulate cyclic AMP (cAMP) production in osteoblastic cell lines (UMR106 and ROS17/2.8). However, whether or not this peptide affects another second messenger, i.e., cytosolic free calcium ([Ca2+]i), in osteoblasts has not yet been determined. Therefore, in the present study, we examined the effects of synthetic amino-terminal fragments of hPTHrP (Tyr40hPTHrP1-40 and hPTHrP1-34) on intracellular cAMP production and [Ca2+]i in an osteoblastic cell line (MC3T3-E1) and compared them with those of hPTH1-34. Human PTHrP1-34, Tyr40hPTHrP1-40 and hPTH1-34 stimulated cAMP production in an equipotent manner at concentrations ranging from 2.5 x 10(-10) to 1.3 x 10(-6) M. Human PTH1-34 at concentrations from 2.5 x 10(-7) to 1.3 x 10(-6) M significantly (P less than 0.05) increased [Ca2+]i, but hPTHrP1-34 and Tyr40hPTHrP1-40 at the same concentrations did not. These results suggest a different receptor-mediated mechanism for [Ca2+]i increase between hPTHrP and hPTH, although these two peptides appear to share the same receptor site(s) which is coupled to the cAMP system in MC3T3-E1.

Animals↗

PubMed1989

Quantitative computed tomography of lumbar vertebrae in Japanese patients with osteoporosis.

Vertebral trabecular bone mineral density of both healthy Japanese subjects and Japanese patients with osteoporosis was measured by quantitative computed tomography (QCT) technique. The age-related reduction rate in vertebral trabecular bone mineral density of control females averaged 1.1% per year, from age 20 to 80, with an accelerated loss demonstrated after age 40. In the male controls, trabecular bone mineral density declined by an average of 0.9% per year. These values were found to be similar to the University of California at San Francisco (UCSF) QCT data (US Caucasians: 1.2% for female, 0.72% for male). Therefore, it appears that age-related rates of trabecular bone loss in the lumbar vertebrae may be similar for both Japanese and Caucasians. However, when compared to average values in UCSF QCT data of comparable age and sex, the mean values in Japanese appear to be approximately 10-20 mg/cm3 lower than Caucasian counterparts. All female patients with osteoporosis as evidenced by atraumatic vertebral fracture had QCT values below 50 mg/cm3. It is suggested that the Japanese may have lower trabecular bone mineral density than Caucasians but may also have a lower threshold for fracture of the vertebrae. Further studies are needed to establish the possible racial differences in vertebral trabecular bone mineral density, and to determine whether these possible disparities are related to genetic differences, or to differences in body size, dietary intake, physical activity or other lifestyle/environmental factors.

Adult↗

PubMed1989

The effects of human parathyroid hormone-related peptide on cytosolic free calcium and cAMP production in opossum kidney cell.

The effects of three synthetic amino-terminal fragments of human parathyroid hormone-related peptide (hPTHrP) on cytosolic free calcium ([Ca2+]i) mobilization and intracellular cAMP production were investigated and compared with those of human PTH(1-34) in opossum kidney (OK) cells. The mean basal [Ca2+]i in OK cells was 115 +/- 7.8 nM (mean +/- SE, n = 30). Human PTHrP(1-34), [40Tyr]hPTHrP(1-40) and hPTH(1-34) significantly (P less than 0.01) raised [Ca2+]i to 149 +/- 3, 150 +/- 5 and 148 +/- 6% of the basal value, respectively (mean +/- SE, n = 3). These three peptides showed similar dose dependency at concentrations between 10(-10) and 10(-7) M. These increases appeared to be, in part, due to mobilization from intracellular calcium stores. On the other hand, these three peptides also stimulated intracellular cAMP production in an equipotent manner in OK cells. However, both 10(-3) M dibutyryl cAMP and 10(-5) M forskolin failed to cause an increase in [Ca2+]i. Furthermore, [40Tyr]hPTHrP(3-40) neither affected the intracellular cAMP content significantly nor caused an increase in [Ca2+]i. These results indicate that hPTHrP mimics PTH by activating a dual second messenger system ([Ca2+]i and cAMP) in OK cells, and that [Ca2+]i stimulation by hPTHrP and hPTH is independent of cAMP production. Additionally, N-terminal amino acid position 1 to 2 of hPTHrP appears to play a crucial role in both [Ca2+]i stimulation and cAMP production.

1-Methyl-3-isobutylxanthine↗

PubMed1989

Calcitonin gene-related peptide receptor antagonist human CGRP-(8-37).

From this study, we predicted that the human calcitonin gene-related peptide (hCGRP) fragment hCGRP-(8-37) would be a selective antagonist for CGRP receptors but an agonist for calcitonin (CT) receptors. In rat liver plasma membrane, where CGRP receptors predominate and CT appears to act through these receptors, hCGRP-(8-37) dose dependently displaced 125I-[Tyr0]rat CGRP binding. However, hCGRP-(8-37) had no effect on adenylate cyclase activity in liver plasma membrane. Furthermore, hCGRP-(8-37) inhibited adenylate cyclase activation induced not only by hCGRP but also by hCT. On the other hand, in LLC-PK1 cells, where calcitonin receptors are abundant and CGRP appears to act via these receptors, the bindings of 125I-[Tyr0]rat CGRP and 125I-hCT were both inhibited by hCGRP-(8-37). In contrast to liver membranes, interaction of hCGRP-(8-37) with these receptors led to stimulation of adenosine 3',5'-cyclic monophosphate (cAMP) production in LLC-PK1 cells, and moreover, this fragment did not inhibit the increased production of cAMP induced not only by hCT but also by hCGRP. Thus hCGRP-(8-37) appears to be a useful tool for determining whether the action of CGRP as well as that of CT is mediated via specific CGRP receptors or CT receptors.

Adenylyl Cyclases↗

PubMed1988

Control of parathyroid hormone-degrading activity in the opossum kidney cell: possible involvement of protein kinase C.

To clarify the possible role of protein kinase C in the control of parathyroid hormone (PTH)-degrading activity (PTHDA) in a PTH-responsive opossum kidney (OK) cell line, we investigated the effects of protein kinase C activators, 12-O-tetradecanoyl phorbol 13-acetate (TPA), 1-oleoyl-2-acetyl-glycerol (OAG), and 4 beta-phorbol 12, 13-didecanoate (4 beta-PDD). TPA, OAG, and 4 beta-PDD enhanced PTHDA in a dose-dependent fashion (10-50 ng/ml, 10-100 microgram/ml, and 10-50 nM, respectively), whereas 4 alpha-PDD, a non-activator of protein kinase C, did not affect it. HPLC analysis of TPA-treated samples revealed increase of all immunoreactive PTH fragments produced by OK cells. These findings suggested that activation of protein kinase C in OK cells would augment PTHDA in the cells.

Animals↗

PubMed1988

Human parathyroid hormone related protein fragment-(1-34) had glucose-6-phosphate dehydrogenase activity on distal convoluted tubules in cytochemical bioassay.

In the present study, the action of parathyroid hormone related protein (PTHrP) on glucose-6-phosphate dehydrogenase (G6PD) activity of the distal convoluted tubules was examined utilizing cytochemical bioassay (CBA). Recently full amino acid residues of human PTHrP (hPTHrP), one of the causative agents of HHM, was identified based on the cDNA clone using BEN cells. We synthesized hPTHrP-(1-34) and examined the effect of this protein on G6PD activities on the distal convoluted tubules, and compared its bioactivity to that of human parathyroid hormone (hPTH)-(1-84). hPTHrP-(1-34) stimulated G6PD activity in a log linear fashion with equivalent activity to that of hPTH-(1-84) on a molar basis. Conclusively, we found that PTHrP act on distal convoluted tubules similar to hPTH.

Animals↗

PubMed1988

Atrial natriuretic factor inhibits phosphate uptake in opossum kidney cells: as a model of renal proximal tubules.

The cultured renal cell, an opossum kidney (OK) cell line, which contains several features characteristic of proximal tubular cells, was utilized to examine the direct effects of atrial natriuretic factor (ANF) and cyclic GMP (cGMP) on phosphate uptake. ANF at 2 x 10(-7) M significantly inhibited phosphate uptake by 10.1% of control (P less than 0.01). Incubation of the cells with ANF (10(-8) to 10(-6) M) resulted in an increment of intracellular cGMP in a dose dependent fashion. Exogenous addition of 8-bromo-cGMP (10(-4) M) also significantly inhibited phosphate uptake by 14.6%. These results suggest that ANF directly inhibits phosphate transport in renal proximal tubular cells, probably through stimulation of cGMP production.

Animals↗

PubMed1988

Effect of glucocorticoid administration on intestinal, renal, and cerebellar calbindin-D28K in chicks.

A radioimmunoassay for chick intestinal calcium-binding protein (calbindin-D28K, CaBP-28K) has been developed in our laboratory with a detection limit of 0.3 ng/ml. The values for CaBP-28K in vitamin D-deficient (-D) chicks ranged from a high value for the cerebellum (21,400 +/- 580 ng/mg protein) to a scarcely detectable level in the liver (19.6 +/- 2.2 ng/mg protein). After administration of vitamin D (vitamin D3 500 IU p.o. for 7 days) (+D), the levels of CaBP-28K increased in the duodenum (52,300 +/- 5,100 ng/mg protein), ileum (45,200 +/- 740 ng/mg protein), cerebellum (22,000 +/- 470 ng/mg protein), colon (15,200 +/- 330 ng/mg protein), and kidney (13,460 +/- 540 ng/mg protein). However, the increment in the level of CaBP-28K in each tissue after vitamin D administration was different; levels of CaBP-28K in the duodenum, ileum, and colon increased dramatically more than 200 times after vitamin D administration, whereas that in the kidney showed only a 2.5-fold increase and was unaltered in the cerebellum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Parathyroid hormone control of free cytosolic Ca2+ in the kidney.

We have established a perifusion system to monitor free cytosolic calcium concentrations ([Ca2+]i) in mouse kidney slices, which presumably reflects in vivo status more accurately than renal cells in culture, by means of the fluorescent calcium indicators quin-2 and fura-2. An increase in the extracellular calcium concentrations from 0 (no added Ca2+) to 3.0 mM resulted in an increase in [Ca2+]i from 52 to 239 nM. Replacement of 118 mM of extracellular Na+ with choline, or the addition of ouabain, an inhibitor of Na+,K+-ATPase, at 10(-6) M in the perfusate caused an increase in [Ca2+]i from 161 +/- 13 to 873 +/- 78 nM (n = 10) and 161 +/- 13 to 395 +/- 68 nM (n = 4), respectively, suggesting the possible existence of a Na+,Ca2+ exchange mechanism in the kidney slice. We further examined the effects of PTH on [Ca2+]i mobilization in the kidney. Both human PTH-(1-34) and hPTH-(1-84) increased [Ca2+]i within 60 s at physiologic concentrations of 10(-11)-10(-9) M in a dose-dependent manner. On the other hand, an increase in intracellular cAMP in the slice was also detected above 3 X 10(-9) M hPTH-(1-34) [base 2.1 +/- 0.4 pmol/mg, 3.2 +/- 0.6 pmol/mg (p less than 0.05 versus control values) 5 minutes after the application of 3 X 10(-9) M hPTH-(1-34) and 17.3 +/- 4.3 pmol/mg (p less than 0.05 versus control values) 3 X 10(-8) M hPTH-(1-34), mean +/- SEM, n = 7, p less than 0.05 versus control values].(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoquinolines↗

PubMed1988

A case of membranous lipodystrophy complicated by Fanconi's syndrome.

A case of membranous lipodystrophy complicated by Fanconi's syndrome is described. A 40-year old man complaining of pain in his legs was admitted to our hospital. Roentgenograms showed cystic changes in the long bones. Biopsy of the affected lesion of the femur revealed a peculiar membranocystic structure in the marrow that is typical of membranous lipodystrophy. He had a neuropsychiatric disorder which is often associated with this disease. Laboratory studies were remarkable for renal proximal tubular dysfunction, i.e., Fanconi's syndrome. Membranous lipodystrophy is a rare, hereditary disease that has been reported mainly from Japan and Finland. This is the first case of this disease complicated by Fanconi's syndrome. The possible relationship between these disorders is discussed.

Adult↗