• 한국건강관리협회지
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• 제2권1호
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• pp.71-76
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• 2004

The Metabolic syndrome is a constellation of lipid and non-lipid factors of metabolic origin. The presence of any 3 of the following factors is considered sufficient for diagnosis : hypertension(BP <130/85mmHg), low HDL-cholesterol (<40mg% in men, <50mg% in woman), high triglyceride(>150mg%) and abdominal obesity(abdominal girth >102cm in men, 88cm in woman). The major adverse consequence of the metabolic syndrome is cardiovascular disease. Several studies have shown an association between metabolic syndrome and increased cardiovascular events. In Korea, the prevalence of the factor of metabolic syndrome has been increasing since 20 years previously when the Korean economy began to grow rapidly, with a resultant change in lifestyle, toward that of western countries. Thus, the management of the metabolic syndrome is an important social and medical issue in terms of the national health problem. This review will consider each factor in turn, providing insight for health care providers in an effort to prevention of cardiovascular events and maintenance of quality of life in persons with metabolic syndrome was discussed.

• 대한유전성대사질환학회지
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• 제13권2호
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• pp.75-80
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• 2013

Specific genetic conditions may lead to sudden unexpected deaths in infancy, such as inborn errors of fatty acid oxidation and genetic disorders of cardiac ion channels. The disease may present dramatically with severe hypoketotic hypoglycemia, Reye syndrome or sudden death, typically with a peak of frequency around 3-6 month, whilst neonatal sudden death is quite rare. When undetected, approximately 20-25% of infants will die or suffer permanent neurologic impairment as a consequence of the first acute metabolic decompensation. Meanwhile, the advent of newborn screening for metabolic diseases has revealed populations of patients with disorders of fatty acid oxidation (FAO), the most frequent of which is medium chain acyl-CoA dehydrogenase (MCAD) deficiency. Without this screening, affected individuals would likely succumb to sudden infant death syndrome (SIDS). Here we describe an overview of sudden infant death syndrome and inherited metabolic disorder.

• Bulletin of the Korean Chemical Society
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• 제34권1호
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• pp.35-41
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• 2013

Metabolic analysis of CR6 interacting factor 1 (Crif1) deficient mouse embryonic fibroblasts with impaired oxidative phosphorylation has been carried out using LC-MS/MS and GC-MS methods. Metabolic profiles of the Crif1 deficient cells were comprehensively obtained for the first time. Loss of oxidative phosphorylation functions in mitochondria resulted in cancer-like metabolic reprogramming with consumption of majority of glucose carbon from up-regulated glycolysis to produce lactate, suppressed utilization of glucose carbon in the TCA cycle, increased amounts of amino acids. The changes in metabolic profile of the Crif1 deficient cells are most probably a consequence of metabolic reprogramming to meet the needs of energy balance and anabolic precursors in compensation for the loss of major oxidative phosphorylation functions.

• Genomics & Informatics
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• 제17권4호
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• pp.38.1-38.6
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• 2019

DNA methylation is a relatively stable epigenetic modification that can regulate and stabilize gene expression patterns and hence establish cell identity. Because metabolic intermediates are key factors of DNA methylation and demethylation, perturbations in metabolic homeostasis can trigger alterations in cell-specific patterns of DNA methylation and contribute to disease development, including type 2 diabetes (T2D). During the past decade, genome-wide DNA methylation studies of T2D have expanded our knowledge of the molecular mechanisms underlying T2D. This review summarizes case-control studies of the DNA methylome of T2D and discusses DNA methylation as both a cause and consequence of T2D. Therefore, DNA methylation has potential as a promising T2D biomarker that can be applied to the development of therapeutic strategies for T2D.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.214.4-215
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• 2003

In galactose metabolic pathway : there are three inborn metabolic disorders galactokinase deficiency (galactosemia type II), galactose-1-phosphate uridyl transferase(GALT) daficiency (galactosemia type I ), uridine diphosphate galactose-4-epimerase deficiency (galactosemia typeIII). Among these disorders GALT deficiency is the most severe and common. Infants with GALT deficiency fail to metabolize galactose-1-phosphate. As a consequence, galactose-1-phosphate and galactose are accumulated in blood in which GALS enzyme plays the role of a pathognomonic marker. (omitted)

• BMB Reports
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• 제47권1호
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• pp.15-20
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• 2014

Intracellular lipid-binding proteins (LBPs) impact fatty acid homeostasis in various ways, including fatty acid transport into mitochondria. However, the physiological consequences caused by mutations in genes encoding LBPs remain largely uncharacterized. Here, we explore the metabolic consequences of lbp-5 gene deficiency in terms of energy homeostasis in Caenorhabditis elegans. In addition to increased fat storage, which has previously been reported, deletion of lbp-5 attenuated mitochondrial membrane potential and increased reactive oxygen species levels. Biochemical measurement coupled to proteomic analysis of the lbp-5(tm1618) mutant revealed highly increased rates of glycolysis in this mutant. These differential expression profile data support a novel metabolic adaptation of C. elegans, in which glycolysis is activated to compensate for the energy shortage due to the insufficient mitochondrial ${\beta}$-oxidation of fatty acids in lbp-5 mutant worms. This report marks the first demonstration of a unique metabolic adaptation that is a consequence of LBP-5 deficiency in C. elegans.

• Journal of Microbiology and Biotechnology
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• 제25권1호
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• pp.81-88
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• 2015

This study describes a novel strategy to regulate the metabolic flux for lactic acid production in Lactobacillus casei. The ldhL gene encoding _L-lactate dehydrogenase (L-LDH) was overexpressed in L. casei, and a two-stage oxygen supply strategy (TOS) that maintained a medium oxygen supply level during the early fermentation phase, and a low oxygen supply level in the later phase was carried out. As a consequence, a maximum L-LDH activity of 95.6 U/ml was obtained in the recombinant strain, which was over 4-fold higher than that of the initial strain. Under the TOS for L. casei (pMG-ldhL), the maximum lactic acid concentration of 159.6 g/l was obtained in 36 h, corresponding to a 62.8% increase. The results presented here provide a novel way to regulate the metabolic flux of L. casei for lactic acid production in different fermentation stages, which is available to enhance organic acid production in other strains.

• Clinical and Experimental Pediatrics
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• 제64권1호
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• pp.12-20
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• 2021

The mean age at menarche (AAM) of Korean females has been rapidly decreasing over the last 50 years; currently, the prevalence of early menarche (<12 years) is 22.3%. Female adolescents who experience early menarche are known to be at greater risk of psychosocial and behavioral problems along with several physical health problems such as menstrual problems. They also tend to achieve a shorter final height and develop obesity. Population-based Korean studies have shown a strong association between early menarche and the risk of obesity, insulin resistance, metabolic syndrome, nonalcoholic fatty liver disease, diabetes, breast cancer, and cardiovascular disease in adulthood. Although the exact mechanism of how early menarche causes cardiometabolic derangement in later adulthood is unknown, childhood obesity and insulin resistance might be major contributors. Recent studies demonstrated that an excessive consumption of fructose might underlie the development of obesity and insulin resistance along with an earlier AAM. A positive association was observed between sugar-sweetened beverages (a major source of fructose) intake and obesity, metabolic syndrome, insulin resistance, and cardiometabolic risk in Korean females. In pediatrics, establishing risk factors is important in preventing disease in later life. In this regard, early menarche is a simple and good marker for the management of cardiometabolic diseases in adulthood. Decreasing one's fructose intake might prevent early menarche as well as the development of obesity, insulin resistance, and cardiometabolic diseases.

• Archives of Plastic Surgery
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• 제35권1호
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• pp.42-47
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• 2008

Purpose: Advanced techniques now make it possible to remove considerable amounts of subcutaneous adipose tissue more safely with minimum blood loss. However, few have analyzed the metabolic consequences of liposuction. The purpose of this study was to identify the early effects of the surgical removal of subcutaneous fat on metabolic changes in patients who have undergone liposuction. Methods: Nineteen patients were evaluated from June 2005 to December 2005. Preoperative body weight, serums levels of lipids, apolipoprotein A1, dehydroepiandrosterone(DHEA), uric acid, insulin, and glucose were evaluated. Insulin resistance was determined using the homeostasis model assessment of insulin resistance (HOMA-IR), which is based on fasting glucose and insulin concentrations. All of these data were remeasured in 1 and 4 weeks postoperatively. Tumescent fluid was infiltrated using the superwet technique. The liposuction device used was a $Liposlim^{(R)}$ power-assisted unit. Results: Average volumes of infiltrate and aspirate were 3,268mL and 2,892mL, respectively. Results in 1 week postoperatively demonstrated a significant difference in high-density lipoprotein(HDL) cholesterol, apolipoprotein A1, insulin, and HOMA-IR levels. However, all values were within normal limits and returned to baseline in 4 weeks postoperatively.Conclusion: This study provides little to support the presumed therapeutic effect of liposuction. And, it is unclear whether liposuction can prevent or be used to treat the metabolic complications of obesity. However, the results of the present study lead us to believe that liposuction is a metabolically safe procedure.

• Toxicological Research
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• 제32권3호
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• pp.177-193
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• 2016

After more than half of century since the Warburg effect was described, this atypical metabolism has been standing true for almost every type of cancer, exhibiting higher glycolysis and lactate metabolism and defective mitochondrial ATP production. This phenomenon had attracted many scientists to the problem of elucidating the mechanism of, and reason for, this effect. Several models based on oncogenic studies have been proposed, such as the accumulation of mitochondrial gene mutations, the switch from oxidative phosphorylation respiration to glycolysis, the enhancement of lactate metabolism, and the alteration of glycolytic genes. Whether the Warburg phenomenon is the consequence of genetic dysregulation in cancer or the cause of cancer remains unknown. Moreover, the exact reasons and physiological values of this peculiar metabolism in cancer remain unclear. Although there are some pharmacological compounds, such as 2-deoxy-D-glucose, dichloroacetic acid, and 3-bromopyruvate, therapeutic strategies, including diet, have been developed based on targeting the Warburg effect. In this review, we will revisit the Warburg effect to determine how much scientists currently understand about this phenomenon and how we can treat the cancer based on targeting metabolism.