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Biomedical subjects

S K Hong

Publications and source records attributed to S K Hong.

At least 55 records · Page 3Linked to original sources

Sodium sulfate potentiates N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA) nephrotoxicity in the Fischer 344 rat.

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) induces nephrotoxicity as its major toxicity in rats. Previous studies have shown that NDPS induces nephrotoxicity following oxidation of the succinimide ring to form N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and the hydrolysis product of NDHS, N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA). Our recent work found that sodium sulfate potentiated NDPS nephrotoxicity, suggesting that sulfate conjugation of NDPS metabolites might be a bioactivation step mediating NDPS nephrotoxicity. The purpose of this study was to determine if sodium sulfate also potentiated the nephrotoxicity of the two nephrotoxic metabolites of NDPS and further to see if sodium sulfate potentiated NDHS and 2-NDHSA nephrotoxicity to the same degree. Male Fischer 344 rats (4-16 rats/group) received an intraperitoneal (ip) injection of sodium sulfate (10 mg/kg) 20 min before a non-nephrotoxic dose (0.05 mmol/kg, ip) of NDHS or 2-NDHSA, or vehicle (12.5% dimethyl sulfoxide in sesame oil). Renal function was then monitored over 48 h. Sodium sulfate pretreatment potentiated the renal effects of a non-nephrotoxic dose of NDHS and 2-NDHSA to induce nephrotoxicity. Nephrotoxicity was characterized by diuresis, increased proteinuria, elevated blood urea nitrogen (BUN) concentration, increased kidney weight and proximal tubular necrosis. Differences in the potentiation of NDHS and 2-NDHSA nephrotoxicity by sodium sulfate were also observed as NDHS nephrotoxicity was potentiated to a lesser degree than 2-NDHSA-induced nephrotoxicity. These results support the likelihood that one or more sulfate conjugate(s) of NDPS metabolites contribute to NDPS nephrotoxicity.

Animals↗

Localization of calcium-binding protein parvalbumin-immunoreactive neurons in mouse and hamster visual cortex.

Calcium-binding proteins are thought to play important roles in regulating intracellular calcium in the central nervous system. In the present study, we investigated the distribution and morphology of neurons containing parvalbumin in the visual cortex of mouse and hamster. The calcium-binding proteins were localized using immunocytochemistry. Parvalbumin-immunoreactive neurons were located in all layers except layer I. The highest density of parvalbumin immunoreactivity was found in layer V of both mouse and hamster. The labeled neurons varied in morphology. The majority of the parvalbumin-immunoreactive neurons both in mouse and hamster visual cortex was stellate and round, or oval with multipolar dendrites. These results indicate that the calcium-binding protein parvalbumin is contained in specific layers and in selective cell types of the mouse and hamster visual cortex. The distribution of parvalbumin in the mouse visual cortex is very similar to that of hamster.

Animals↗

Electrophysiological evidence for the role of substance P in retinohypothalamic transmission in the rat.

The retinohypothalamic tract (RHT) is a neural pathway through which photic time cues are delivered directly to the mammalian circadian pacemaker in the suprachiasmatic nucleus (SCN). Although the excitatory amino acid glutamate is the primary neurotransmitter in the RHT, other substances such as substance P (SPq also have been suggested to play a role. The present study tested the hypothesis that SP participates in retinohypothalamic transmission and selectively modulates either N-methyl-D-aspartate (NMDA) or non-NMDA receptor-mediated neurotransmission. The SP antagonist L-703,606 depressed the excitatory postsynaptic current (EPSC) evoked by optic nerve stimulation in SCN neurons in rat hypothalamic slices. The SP antagonist also had a similar depressive effect on the NMDA and non-NMDA receptor-mediated components of the EPSC. These results suggest that SP is an excitatory neuromodulator contributing to the expression of both the NMDA and non-NMDA receptor-mediated components of retinohypothalamic transmission.

2-Amino-5-phosphonovalerate↗

Is sympathetic sprouting in the dorsal root ganglia responsible for the production of neuropathic pain in a rat model?

Partial peripheral nerve injury often results in neuropathic pain that is aggravated by sympathetic excitation and induces sympathetic nerve sprouting in both the injured nerve and corresponding dorsal root ganglia (DRGs). Presently, the functional mechanisms of the interactions between the sprouting and injured somatic afferents remain uncertain. This study was performed to see whether the sprouting in the DRGs plays a key role in the development of neuropathic pain. To this aim, we compared two groups of rats, both of which were subjected to unilateral transection of the superior and inferior caudal trunks at the level between the S1 and S2 spinal nerves, with respect to sympathetic fiber sprouting; one group showed well-developed neuropathic pain behaviors (i.e. mechanical, cold and warm allodynia signs) and the other group showed poorly-developed ones. Immuno-histochemical staining with tyrosine hydroxylase (TH) antibody of the injured S1 DRG taken from both groups of rats after behavioral tests revealed that the magnitude of penetration of TH-positive fibers into the S1 DRG was not significantly different between the two groups. These results suggest that sympathetic nerve sprouting in the injured DRG is not a key factor in the development of neuropathic pain.

Animals↗

Effect of sulfation substrates/inhibitors on N-(3,5-dichlorophenyl)succinimide nephrotoxocity in Fischer 344 rats.

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is an acute nephrotoxicant in rats. Our previous studies suggested that sulfate conjugation of NDPS metabolites might be a bioactivation step mediating NDPS nephrotoxicity. In this study, effects of substrates and/or inhibitors of sulfation on NDPS nephrotoxicity were examined to explore further the role of sulfation in NDPS nephrotoxicity. Male Fischer rats (4-8/group) were administered one of the following intraperitoneal (ip) pretreatment (dose, pretreatment time) prior to NDPS (0.6 mmol/kg) or NDPS vehicle (sesame oil, 2.5 ml/kg): (1) no pretreatment, (2) dehydroepiandrosterone (DHEA) (0.5 mmol/kg, 1 h), or (3) 2,6-dichloro-4-nitrophenol (DCNP) (0.04 mmol/kg, 1 h). Following NDPS or NDPS vehicle administration, renal function was monitored at 24 and 48 h. Pretreatment with DHEA, a typical substrate for and an inhibitor of hydroxysteroid (alcohol) sulfotransferase, resulted in marked protection against NDPS nephrotoxicity. A selective inhibitor of phenol sulfotransferase, DCNP, afforded little attenuation in NDPS nephrotoxicity. These results suggest that alcohol sulfate conjugates of NDPS metabolites, rather than phenolic sulfate conjugates, may be a penultimate or ultimate nephrotoxicant species mediating NDPS nephrotoxicity. The marked, but not complete, protection by DHEA also suggests that there are other metabolites or mechanisms responsible for NDPS nephrotoxicity.

Adjuvants, Immunologic↗

Some membrane property changes following axotomy in A delta-type DRG cells are related to cold allodynia in rat.

Numerous studies have suggested that changes in electrophysiological properties of primary sensory neurons after axonal injury contribute to the generation of neuropathic pain. Presently, however, it is unclear which of the changes is important. To address this issue, we performed behavioral and electrophysiological experiments in a double-blind fashion; we made intracellular recordings in the S1 dorsal root ganglia excised from rats exhibiting cold allodynia behavior after chronic S1 spinal nerve transaction (allodynia-positive group) and from rats lacking such behavior after the same nerve injury (allodynia-negative group) or sham injury (sham group). In this study, we sought which of the membrane property changes produced by the spinal nerve injury in each of C-, Adelta- and Aalpha/beta-cell populations was unique to the allodynia-positive group. Analyses of our data revealed that only some changes in Adelta-cells (e.g. the decrease in resting membrane potential and in the threshold of central process) were more pronounced in or unique to the allodynia-positive group. We concluded that certain membrane property changes in the somata and dorsal root axons of Adelta-cells might be important in the generation of cold allodynia.

Action Potentials↗

Nephrotoxic potential of N-(3,5-dichloro-4-fluorophenyl)succinimide in Fischer 344 rats: comparison with N-(3,4,5-trichlorophenyl)succinimide.

Numerous structure-nephrotoxicity relationship studies from our laboratory have demonstrated that N-(3,5-dichlorophenyl)succinimide (NDPS) is one of the most potent nephrotoxicants among the N-arylsuccinimides. The purpose of this study was to extend our previous structure-nephrotoxicity relationship studies by examining the effect of addition of a fluoro verses a chloro group at the 4-phenyl position in NDPS. Male Fischer 344 rats (four rats/group) received a single intraperitoneal (i.p.) injection of N-(3,5-dichloro-4-fluorophenyl)succinimide (NDCFPS) or N-(3,4,5-trichlorophenyl)succinimide (NTCPS)(0.4 or 0.8 mmol/kg) or vehicle, and renal function monitored at 24 and 48 h. NDCFPS did not induce significant nephrotoxicity at either dose tested. In contrast, NTCPS (0.4 or 0.8 mmol/kg) induced marked nephrotoxicity characterized by diuresis, increased proteinuria, glucosuria, elevated kidney weight and increased blood urea nitrogen (BUN) concentration. NTCPS also induced marked proximal tubular necrosis at both doses tested. Neither NDCFPS nor NTCPS induced hepatotoxicity at either dose tested. The results of these experiments indicate that addition of a fluoro group at the 4-position on the phenyl ring of NDPS produces a nonnephrotoxicant NDPS derivative (NDCFPS), while addition of a chloro group at this site produces an NDPS derivative with similar nephrotoxic potential to NDPS. The mechanism for this differential effect between 4-halophenyl substitution is unclear, but may result from increased hydrolysis of the succinimide ring and/or increased clearance of N-arylsuccinimide metabolites when a fluoro group is added to the 4-position of the phenyl ring.

Animals↗

SHC1, a high pH inducible gene required for growth at alkaline pH in Saccharomyces cerevisiae.

In this study, we carried out a large-scale transposon tagging screening to identify genes whose expression is regulated by ambient pH. Of 35,000 transformants, two strains carrying the genes whose expression is strictly dependent on pH of growth medium were identified. One of the genes with 20-fold induction by alkali pH was identified as SHC1 gene in the Yeast Genome Directory and its expression was the highest at alkaline pH and moderately induced by osmotic stress. However, the gene was expressed neither at acidic pH nor by other stress conditions. The haploid mutant with truncated shc1 gene showed growth retardation and an abnormal morphology at alkaline pH. On the other hand, the mutant strain carrying the wild-type SHC1 gene reverted to the mutant phenotype. To confirm that Shc1p is an alkali-inducible protein, a monoclonal antibody to Shc1p was produced. While a 55-kDa protein band appeared on the Western blot of cells grown at alkaline pH, Shc1p was barely detectable on the blots of cells grown in YPD. Our results indicate that yeast cells have an efficient system adapting to large variations in ambient pH and SHC1 is one of the genes required for the growth at alkaline pH.

Amino Acid Sequence↗

The role of glucuronidation in N-(3,5-dichlorophenyl)succinimide (NDPS) nephrotoxicity: nephrotoxic potential of NDPS and NDPS metabolites in Gunn, Wistar, and Fischer 344 rats.

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is an acute nephrotoxicant in rats. Although the mechanism of NDPS nephrotoxicity is not clear, our previous studies have strongly suggested that glucuronide conjugation of NDPS metabolite(s) is an important biotransformation reaction leading to the ultimate nephrotoxicant metabolite(s) mediating NDPS nephrotoxicity. In this study, the nephrotoxic potential of NDPS and its nephrotoxicant metabolites, N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (NDHSA), was examined in Gunn rats, which contain a genetic deficiency in bilirubin uridine diphosphate-glucuronosyltransferase (UDPGT), to explore further the role of glucuronidation in NDPS nephrotoxicity. The nephrotoxic potential of NDPS, NDHS, and NDHSA was also examined in Wistar rats, the parent strain for Gunn rats and which generally have normal UDPGT activity. Comparisons were then made with the nephrotoxicity induced by these compounds in Fischer 344 (F344) rats. Age-matched male F344, homozygous (j/j) Gunn, and Wistar rats were used. Rats (four to eight rats/group) of each strain were administered NDPS (0.4 mmol/kg ip), NDHS (0.1 or 0.2 mmol/kg ip), NDHSA (0.1 mmol/kg ip), or vehicle, and renal effects were monitored functionally and morphologically for 48 h. NDPS and its nephrotoxicant metabolites, NDHS and NDHSA, were much weaker nephrotoxicants in Gunn rats than in F344 rats, while Wistar rats were susceptible to the nephrotoxicity induced by NDPS, NDHS, or NDHSA. These results suggest that the lack of NDPS nephrotoxicity observed in Gunn rats is due to the deficiency in UDPGT in this strain rather than the parent Wistar strain being inherently nonresponsive to NDPS nephrotoxicity. Therefore, it appears that glucuronide metabolite(s) of NDHS and/or NDHSA contribute(s) to NDPS nephrotoxicity, although the exact nature of the nephrotoxicant glucuronide metabolite(s) of NDPS remains to be determined.

Amiloride↗

Effect of glucuronidation substrates/inhibitors on N-(3,5-dichlorophenyl)succinimide nephrotoxicity in Fischer 344 rats.

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is an acute nephrotoxicant in rats. Our previous studies have strongly suggested that glucuronide conjugation of NDPS metabolites might be a bioactivation step mediating NDPS nephrotoxicity. In this study, effects of substrates and/or inhibitors of primarily glucuronidation on NDPS nephrotoxicity were examined to explore further the role of glucuronidation in NDPS nephrotoxicity. Male Fischer 344 rats (4-6/group) were administered one of the following intraperitoneal (i.p.) pretreatments (dose, pretreatment time) prior to NDPS (0.4 mmol/kg) or NDPS vehicle (sesame oil, 2.5 ml/kg): (1) no pretreatment; (2) borneol (900 mg/kg, 30 min); (3) eugenol (500 mg/kg per day, 3 days); (4) clofibric acid (400 mg/kg, 15 min before (1/2 dose) and 3 h after (1/2 dose)), or (5) valproic acid, sodium salt (1.0 mmol/kg, 15 min). Following NDPS or NDPS vehicle administration, renal function was monitored at 24 and 48 h. Pretreatment with borneol or eugenol, substrates for ether glucuronidation and sulfation (mainly glucuronidation), afforded complete protection against NDPS nephrotoxicity. Substrates for acyl glucuronidation, clofibric acid or valproic acid, mildly reduced or had little effect on NDPS nephrotoxicity, respectively. These results suggest that ether glucuronide conjugates of NDPS metabolites, rather than acyl glucuronide conjugates, may be the primary ultimate nephrotoxicant species mediating NDPS nephrotoxicity.

Animals↗

Multicentric juvenile pilocytic astrocytoma occurring primarily in the trigone of the lateral ventricle.

The authors report a juvenile pilocytic astrocytoma (JPA) in the trigone of an 11-year-old girl, apparently with disseminated lesions that disappeared spontaneously after the removal of primary lesion. Gadolinium-enhanced magnetic resonance images (MRIs) showed features suggestive of the development of multicentric spread of the tumor at the initial diagnosis. Histologically the primary tumor showed the typical features of a JPA. Serial postoperative MRIs demonstrated that everything except a remnant of the primary tumor seemed to regress spontaneously without any adjuvant therapy. The site of origin of this tumor is thought to be the subependymal glia of the occipital lobe.

Astrocytoma↗

Elevated plasma proinsulin/insulin ratio is a marker of reduced insulin secretory capacity in healthy young men.

AIM: To examine whether reduced insulin secretory capacity or increased insulin secretory demand is associated with elevated ratio of plasma proinsulin to immunoreactive insulin (PI/IRI ratio) in non-diabetic subjects. SUBJECTS AND METHODS: We measured various indices of insulin secretory function and insulin sensitivity by frequently sampled intravenous glucose tolerance test (FSIGT) and hyerglycemic glucose clamp in 21 healthy young men. We then examined the relationships between these indices and PI, IRI, or PI/IRI ratio in the fasting state. RESULTS: Insulin sensitivity index (SI) measured by FSIGT correlated inversely with basal IRI (r=-0.53, P < 0.01) and PI levels (r=-0.57, P < 0.01), but there was no significant correlation between SI and PI/IRI ratio (r=0.26, NS). On the other hand, PI/IRI ratio correlated inversely with insulin secretory indices, such as acute insulin responses during FSIGT (r =-0.46, P < 0.01) and hyperglycemic glucose clamp (r=-0.54, P < 0.01) and submaximum insulin response during hyperglycemic glucose clamp (r=-0.59, P < 0.01). CONCLUSIONS: These results indicate that elevated PI/IRI ratio may serve as a marker of reduced insulin secretory function in non-diabetic subjects.

Adult↗

Initiation of shoot apical meristem in rice: characterization of four SHOOTLESS genes.

The regulatory mechanism of shoot apical meristem (SAM) initiation is an important subject in developmental plant biology. We characterized nine recessive mutations derived from four independent loci (SHL1-SHL4) causing the deletion of the SAM. Radicles were produced in these mutant embryos. Concomitant with the loss of SAM, two embryo-specific organs, coleoptile and epiblast, were lost, but the scutellum was formed normally. Therefore, differentiation of radicle and scutellum is regulated independently of SAM, but that of coleoptile and epiblast may depend on SAM. Regeneration experiments using adventitious shoots from the scutellum-derived calli showed that no adventitious shoots were regenerated in any shl mutant. However, small adventitious leaves were observed in both mutant and wild-type calli, but they soon became necrotic and showed no extensive growth. Thus, leaf primordia can initiate in the absence of SAM, but their extensive growth requires the SAM. An in situ hybridization experiment using a rice homeobox gene, OSH1, as a probe revealed that shl1 and shl2 modified the expression domain of OSH1, but normal expression of OSH1 was observed in shl3 and shl4 embryos. Accordingly, SHL1 and SHL2 function upstream of OSH1, and SHL3 and SHL4 downstream or independently of OSH1. These shl mutants are useful for elucidating the genetic program driving SAM initiation and for unraveling the interrelationships among various organs in grass embryos.

Gene Deletion↗

Gender differences in acute N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA) nephrotoxicity in Fischer 344 rats.

N-(3,5-Dichlorophenyl)succinimide (NDPS) is an agricultural fungicide that induces nephrotoxicity as its major toxicity. NDPS is also a more potent nephrotoxicant in female than in male rats. The purpose of this study was to examine the nephrotoxic potential of the two NDPS metabolites N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA) in age-matched male and female Fischer 344 rats to determine if gender differences exist for the nephrotoxicity induced by the two NDPS metabolites. Rats (4 per group) were administered a single intraperitoneal (ip) injection of NDHS or 2-NDHSA (0.025 or 0.05 mmol/kg) or vehicle, and renal function was monitored for 48 h. Neither compound induced significant nephrotoxicity in male rats at the doses tested. However, in female rats both metabolites induced marked nephrotoxicity at the 0.05 mmol/kg dose level, and treatment with 0.025 mmol/kg 2-NDHSA induced some changes in renal function (transient diuresis, transient proteinuria, decreased organic ion accumulation). Little effect on renal function was induced in females by treatment with 0.025 mmol/kg NDHS. At toxic levels in female rats, the renal lesions were located primarily in the S2 and S3 segments of the proximal tubule. These results indicate that, like the parent compound, gender differences exist in the nephrotoxic potential of NDHS and 2-NDHSA. The results also suggest that in females, as in males, NDPS nephrotoxicity is mediated via NDHS and/or 2-NDHSA. However, it is not clear if the ultimate nephrotoxicant species following NDPS exposure is different in males and females or if the same ultimate nephrotoxicant species is produced in both species but handled differently by male and female kidneys. Thus, further studies are needed to determine the exact nature of the ultimate nephrotoxicant species and the mechanisms of the observed gender differences.

Animals↗

Supraspinal involvement in the production of mechanical allodynia by spinal nerve injury in rats.

This study examined whether or not the production of mechanical allodynia in a rat model of neuropathic pain required an involvement of supraspinal site(s). To this aim, we assessed the effect of spinal cord section at the L1 segment level on the mechanical allodynia sign (i.e. tail flick/twitch response), which was elicited by innocuous von Frey hair stimulation of the tail after unilateral transection of the tail-innervating nerve superior caudal trunk (SCT) at the level between the S3 and S4 spinal nerves. Cord transection or hemisection of the cord ipsilateral to the injured SCT drastically (though not completely) blocked the behavioral sign of mechanical allodynia (leaving noxious pinprick-elicited tail withdrawal reflex intact), whereas sham section or contralateral hemisection of the cord was without effect. These results suggest that the generation of mechanical allodynia following partial peripheral nerve injury involves transmission of the triggering sensory signal to a site(s) rostral to the L1 segment via an ipsilateral pathway(s).

Animals↗

Amount of sympathetic sprouting in the dorsal root ganglia is not correlated to the level of sympathetic dependence of neuropathic pain in a rat model.

Incomplete peripheral nerve injury often leads to neuropathic pains, some of which are relieved by sympathectomy, and results in sympathetic postganglionic nerve fiber sprouting in the dorsal root ganglion (DRG). This study was performed to see whether the sprouting in the DRG plays a key role in the sympathetic dependence of neuropathic pain. To this aim, we compared two groups of rats, both of which were subjected to unilateral transection of the inferior and superior caudal trunks at the levels between the S1 and S2, S2 and S3, and S3 and S4 spinal nerves, with respect to sympathetic fiber sprouting; one group showed neuropathic pain behaviours (i.e. mechanical and cold allodynia signs) which were very sensitive to phentolamine, alpha adrenergic blocker, and the other group exhibited no sensitivity. Immuno-histochemical staining with tyrosine hydroxylase antibody of the S1-S3 DRGs was not correlated with the sensitivity to phentolamine. These results suggest that the degree of sympathetic dependence of neuropathic pain is not a function of the extent of the sympathetic postganglionic nerve fiber sprouting in the DRG.

Adrenergic alpha-Antagonists↗

Epidemiology of eating disordered symptoms in the Korean general population using a Korean version of the Eating Attitudes Test.

OBJECTIVE: The purposes of the present study were to estimate the proportion of subjects with a high score on the Korean version of Eating Attitudes Test--26 (KEAT-26), which may provide preliminary data regarding the prevalence rate of eating disorders in the Korean general population, and to further examine the sociocultural hypothesis of eating disorders. METHOD: Using a multi-stage questionnaire sampling method, we surveyed 3062 subjects (1249 males, 1813 females) from 3896 Korean adults in a nationwide area. RESULTS: 8.5% (260/3062) of subjects scored above the cut-off on the KEAT-26. Their demographic correlates, eating traits, and other characteristics relating to general psychopathology were similar to those of patients with eating disorders and female Caucasian controls in Western countries. DISCUSSION: These results suggest that changes in various sociocultural aspects have increased the risk of developing eating disorders in Korea, and support the sociocultural hypothesis of eating disorders.

Adult↗

Association of microalbuminuria and atherosclerotic risk factors in non-diabetic subjects in Korea.

Microalbuminuria in non-diabetic subjects is reportedly associated with increased cardiovascular morbidity and mortality. The prevalence of microalbuminuria in non-diabetic subjects varies widely from 5-6% in the UK and USA to 30-55% in Finland, Mexico, or Australian Aborigines. We studied cross-sectionally 497 clinically healthy, non-diabetic subjects more than 40 years of age who were living in Seoul, Korea for the prevalence of microalbuminuria and various cardiovascular risk factors. Urinary albumin-to-creatinine ratio (UACR) was determined in morning spot urine samples. Subjects were divided into normoalbuminuria (UACR < 2 mg/mmol) and microalbuminuria (UACR > or = 2 mg/mmol) groups. A total of 61 (12.2%) out of 497 subjects were found to have microalbuminuria. Subjects with microalbuminuria had significantly higher values in age, body mass index (BMI), waist-to-hip ratio in women, systolic and diastolic blood pressure, prevalence of hypertension, plasma cholesterol and triglyceride, and fasting plasma insulin. When subjects with microalbuminuria were compared with age-, sex-, and BMI-matched controls without microalbuminuria, systolic and diastolic blood pressure, and fasting plasma insulin concentrations were higher in microalbuminuric subjects. Multiple logistic regression analysis showed that fasting plasma insulin level and systolic blood pressure were independently associated with microalbuminuria. These results indicate that the prevalence of microalbuminuria in Korean non-diabetic subjects is lower than that in Mexico and Finland, but similar to that in Caucasians from the UK and USA, or in Pima Indians. Also, microalbuminuria in Korean non-diabetic subjects is associated with atherosclerotic risk factors such as hyperinsulinemia and hypertension, suggesting that microalbuminuria in these subjects may be a feature of insulin resistance syndrome.

Albuminuria↗