• 대한한방내과학회지
• /
• 제44권2호
• /
• pp.138-145
• /
• 2023

Objective: This study identified the effects of Korean medicine treatment on a patient with metabolic dysfunction-associated fatty liver disease (MAFLD). Methods: A 43-year-old man with MAFLD was treated with Saenggangunbi-tang with regular exercise from August 13, 2022, to December 24, 2022, to reduce fatigue and dyspepsia and to improve laboratory findings, such as liver enzymes and lipid profiles. We observed changes in symptoms and laboratory findings during the approximately four-month treatment. Results: Treatment with Saenggangunbi-tang resulted in decreased serum levels of liver enzymes, triglycerides, hepatic steatosis index scores, and clinical symptoms. During the treatment, the patient performed regular exercise; however, there was no significant change in body weight until the end of the study. Conclusion: This study suggests the availability of Saenggangunbi-tang as a therapeutic option for managing MAFLD patients.

• Journal of Ginseng Research
• /
• 제48권1호
• /
• pp.89-97
• /
• 2024

Background: Ginsenoside F2 (GF2), the protopanaxadiol-type constituent in Panax ginseng, has been reported to attenuate metabolic dysfunction-associated steatotic liver disease (MASLD). However, the mechanism of action is not fully understood. Here, this study investigates the molecular mechanism by which GF2 regulates MASLD progression through liver X receptor (LXR). Methods: To demonstrate the effect of GF2 on LXR activity, computational modeling of protein-ligand binding, Time-resolved fluorescence resonance energy transfer (TR-FRET) assay for LXR cofactor recruitment, and luciferase reporter assay were performed. LXR agonist T0901317 was used for LXR activation in hepatocytes and macrophages. MASLD was induced by high-fat diet (HFD) feeding with or without GF2 administration in WT and LXRα^-/- mice. Results: Computational modeling showed that GF2 had a high affinity with LXRα. LXRE-luciferase reporter assay with amino acid substitution at the predicted ligand binding site revealed that the S264 residue of LXRα was the crucial interaction site of GF2. TR-FRET assay demonstrated that GF2 suppressed LXRα activity by favoring the binding of corepressors to LXRα while inhibiting the accessibility of coactivators. In vitro, GF2 treatments reduced T0901317-induced fat accumulation and pro-inflammatory cytokine expression in hepatocytes and macrophages, respectively. Consistently, GF2 administration ameliorated hepatic steatohepatitis and improved glucose or insulin tolerance in WT but not in LXRα^-/- mice. Conclusion: GF2 alters the binding affinities of LXRα coregulators, thereby interrupting hepatic steatosis and inflammation in macrophages. Therefore, we propose that GF2 might be a potential therapeutic agent for the intervention in patients with MASLD.

• Molecules and Cells
• /
• 제43권11호
• /
• pp.964-973
• /
• 2020

Recent studies have highlighted that early enhancement of the glycolytic pathway is a mode of maintaining the proinflammatory status of immune cells. Thiamine, a wellknown co-activator of pyruvate dehydrogenase complex, a gatekeeping enzyme, shifts energy utilization of glucose from glycolysis to oxidative phosphorylation. Thus, we hypothesized that thiamine may modulate inflammation by alleviating metabolic shifts during immune cell activation. First, using allithiamine, which showed the most potent anti-inflammatory capacity among thiamine derivatives, we confirmed the inhibitory effects of allithiamine on the lipopolysaccharide (LPS)-induced pro-inflammatory cytokine production and maturation process in dendritic cells. We applied the LPS-induced sepsis model to examine whether allithiamine has a protective role in hyper-inflammatory status. We observed that allithiamine attenuated tissue damage and organ dysfunction during endotoxemia, even when the treatment was given after the early cytokine release. We assessed the changes in glucose metabolites during LPS-induced dendritic cell activation and found that allithiamine significantly inhibited glucose-driven citrate accumulation. We then examined the clinical implication of regulating metabolites during sepsis by performing a tail bleeding assay upon allithiamine treatment, which expands its capacity to hamper the coagulation process. Finally, we confirmed that the role of allithiamine in metabolic regulation is critical in exerting anti-inflammatory action by demonstrating its inhibitory effect upon mitochondrial citrate transporter activity. In conclusion, thiamine could be used as an alternative approach for controlling the immune response in patients with sepsis.

• 대한유전성대사질환학회지
• /
• 제18권1호
• /
• pp.13-17
• /
• 2018

메틸말론산혈증은 선천성 유기산대사질환 중 하나로 증상의 발현시기 및 임상 증상이 매우 다양하며, 장기간의 합병증으로 세뇨관 간질 신염과 만성 신기능 저하, 췌장염, 기저핵 손상, 지능저하가 발생 할 수 있다. 연구자들은 이러한 메틸말론산혈증의 세뇨관 간질신염을 동반한 활동저하 환자에서 파미드로네이트 치료를 통해 고칼슘혈증과 골다공증의 호전을 경험하였기에 보고하는 바이다.

• 사상체질의학회지
• /
• 제31권2호
• /
• pp.22-30
• /
• 2019

Objectives The aim of this study is to investigate the related factors of nonalcoholic fatty liver disease (NAFLD). Methods The subjects were 187 persons diagnosed as fatty liver by abdominal ultrasonography. They were divided into three groups according to the severity of fatty liver: control, mild, moderate or severe. The three groups' general characteristics, laboratory results, liver function indexes, metabolic syndrome indexes, tumor markers, heart rate variability values and Sasang constitution distribution were compared and analyzed. Results Male ratio, height, weight, body mass index, red blood cell count, hemoglobin level and creatinine level were higher in NAFLD groups than in control group. The levels of sodium and amylase were higher in control than in NAFLD. In liver function, the levels of aspartate transaminase, alanine transaminase and gamma-glutamyl transpepsidase of NAFLD were higher. In metabolic syndrome index, systolic blood pressure, diastolic blood pressure, waist circumference, total cholesterol, triglyceride and low density lipoprotein cholesterol levels were higher in NAFLD, while high density lipoprotein cholesterol level was higher in control. The alpha-feto protein level was higher in NAFLD, and the heart rate variability was not different between NAFLD and control groups. In Sasang constitution, Taeeumin ratio of NAFLD was higher than of control. Conclusions The results suggest that nonalcoholic fatty liver is clinically related to liver dysfunction, metabolic syndrome, tumor markers, and Sasang constitution. Further studies are needed to control nonalcoholic fatty liver disease and prevent severe disease such as cirrhosis and cancer caused by fatty liver.

• 한방비만학회지
• /
• 제14권2호
• /
• pp.55-62
• /
• 2014

Objective: The prevalence of metabolic syndrome and type 2 diabetes is increasing worldwide. Mitochondrial dysfunction is known to be involved in insulin resistance and obesity, researches have been increasing highly. Astragali Radix extract (ARE) or its main components have been shown to perform comparably to insulin by significantly reducing blood glucose levels in animal models however, the influence on mitochondrial dysfunction are not well understood. Methods: ARE (0.2, 0.5 and 1.0 mg/ml) or metformin (2.5 mM) were treated in C2C12 after 6 day-differentiation. The expressions of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and phosphorylation AMPK, peroxisome proliferators-activated receptror ${\gamma}$ coactivator $1{\alpha}$ ($PGC1{\alpha}$), nuclear respiratory factors 1 (NRF1), mitochondrial transcription factor (Tfam) and myosin heavy chain were detected with western blotting or polymerase chain reaction analysis. The morphological changes were also investigated. Results: ARE dose dependently increased phosphorylation of AMPK and respectively activated mRNA expressions of $PGC1{\alpha}$, NRF1 and Tfam which are mitochondrial biogenesis regulators. Furthermore, there were some morphologic differences of differentiated cells between ARE treatment and control. Conclusions: This study suggests that ARE has the potential to increase muscle mitochondrial function by activating AMPK and $PGC1{\alpha}$.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• 제16권4호
• /
• pp.207-218
• /
• 2013

Long term outcomes after liver transplantation are major determinants of quality of life and of the value of this heroic treatment. As short term outcomes are excellent, our community is turning to take a harder look at long term outcomes. The purpose of this paper is to review these outcomes, and highlight proposed treatments, as well as pressing topics needing to be studied. A systemic review of the English literature was carried in PubMed, covering all papers addressing long term outcomes in pediatric liver transplant from 2000-2013. Late outcomes after pediatric liver transplant affect the liver graft in the form of chronic liver dysfunction. The causes include rejection particularly humoral rejection, but also de novo autoimmune hepatitis, and recurrent disease. The metabolic syndrome is a major factor in long term cardiovascular complication risk. Secondary infections, kidney dysfunction and malignancy remain a reality of those patients. There is growing evidence of late cognitive and executive function delays affecting daily life productivity as well as likely adherence. Finally, despite a good health status, quality of life measures are comparable to those of children with chronic diseases. Long term outcomes are the new frontier in pediatric liver transplantation. Much is needed to improve graft survival, but also to avoid systemic morbidities from long term immunosuppression. Quality of life is a new inclusive measure that will require interventions and innovative approaches respectful not only on the patients but also of their social circle.

• 한국의학물리학회:학술대회논문집
• /
• 한국의학물리학회 2003년도 제27회 추계학술대회
• /
• pp.73-73
• /
• 2003

Purpose: To determine the motor cortex dysfunction in hemiparetic patients due to deep intracerebral hematoma, authors performed proton magnetic resonance spectroscopy (lH MRS) for the evaluation of biochemical changes in the cortex on affected hemisphere according to axonal injury at the level of internal capsule. Methods: Ten control subjects and 14 patients with documentable hemiparesis of varying severity hemiparesis were included. All the hemiparesis was caused by deep intracerebral hematoma (putaminal and thalamic hemorrhage). In vivo 1H MRS study was performed on a 3T MRI/MRS system using STEAM sequence. As a single-voxel technique, Spectral parameters were: 20 ms TE, 2000 ms TR, 128 averages, 2500 Hz spectral width, and 2048 data points. Results: We found that the mean N-acetylaspartate (NAA)/phosphocreatine (Cr) and NAA/choline (Cho) ratios were significantly decreased in the motor cortex of the hemiparesis patients compared with control subjects. Conclusions: 1H MRS examinations of the motor cortex might help to differentiate distinct clinical entities of hemiparesis and to monitor pharmacological effects in therapeutic trials, providing a quantitative biological marker for motor neuron dysfunction. Acknowledgement: This study was supported by a grant of the Center for Functional and Metabolic Imaging Technology, Ministry of Health & Welfare, Republic of Korea. (02-PJ3-PG6-EV07-000).

• Annals of Clinical Neurophysiology
• /
• 제8권1호
• /
• pp.84-87
• /
• 2006

The MELAS (Mitochondrial Encephalomyopathy with Lactic Acidosis, and Stroke-like episodes) syndrome is one of the inherited mitochondrial disorder. We have experienced a 16-year-old girl with headaches and left hemianopsia. Diagnosis of MELAS syndrome with multiple brain parenchymal lesions was confirmed by gene study. The stroke-like lesion of MELAS syndrome showed significant improvement in radiological follow up study. Therefore, MRI findings in MELAS could be interpreted as metabolic cellular dysfunction rather than ischemic vasculopathy.

• 한국응급구조학회지
• /
• 제25권1호
• /
• pp.243-249
• /
• 2021

A decrease in coronary blood flow leads to an imbalance between the supply of oxygen to the myocardium and its demand, and reversible or irreversible damage to the myocardium could occur depending on the severity of the resultant ischemia and the duration of the imbalance. This imbalance results in a cascade of ischemic reactions in the following order: metabolic abnormalities, diastolic dysfunction, systolic dysfunction, and electrocardiogram changes. Variant angina is caused by the closure of the coronary artery due to reversible coronary artery spasm, resulting in myocardial ischemia and subsequent chest pain as a clinical symptom. Variant angina may be observed as ST segment elevation in electrocardiogram measured when present in chest pain. However, 12-lead electrocardiogram performed after the patient's chest pain resolves does not help in the diagnosis. Since the duration of chest pain appears to be <15 minutes, it is important to perform the 12-lead electrocardiogram when clinical symptoms are present. If nitroglycerin is administered without performing 12-lead electrocardiogram by 119 pre-hospital paramedics, the chest pain would be resolved, making it impossible to identify changes in the ST segment. Before administration of nitroglycerin, changes in the ST segment must be recorded by performing 12-lead electrocardiogram.