• 제목/요약/키워드: metabolic dysfunction

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Heart Rate Variability and Metabolic Syndrome in Hospitalized Patients with Schizophrenia

  • Lee, Kyung-Hee;Park, Jeong-Eon;Choi, Jeong-Im;Park, Chang-Gi
    • 대한간호학회지
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    • 제41권6호
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    • pp.788-794
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    • 2011
  • Purpose: Reduced heart rate variability significantly increases cardiovascular mortality. Metabolic syndrome increases the cardiac autonomic dysfunction. Recently, increasing cardiovascular mortality has been reported in patients with schizophrenia. This study was done to compare heart rate variability between adults with and without schizophrenia and to compare the relationship of heart rate variability to metabolic syndrome in hospitalized patients with schizophrenia. Methods: This was a descriptive and correlational study in which 719 adults without schizophrenia and 308 adults with schizophrenia took part between May and June 2008. We measured the following: five-minute heart rate variability; high-frequency, low-frequency, the ratio of low-frequency to high-frequency, and the Standard Deviation of all the normal RR intervals. Data was also collected on metabolic syndrome, abdominal obesity, triglycerides, HDL cholesterol, blood pressure and fasting glucose. Results: The Standard Deviation of all the normal RR intervals values of heart rate variability indices were $1.53{\pm}0.18$. The low-frequency and high-frequency values of heart rate variability indices were significantly higher in hospitalized patients with schizophrenia ($3.89{\pm}1.36$; $3.80{\pm}1.20$) than those in the healthy participants ($2.20{\pm}0.46$; $2.10{\pm}0.46$). There were no significant differences between the schizophrenic patients with and without metabolic syndrome. Conclusion: The results of this study indicate that schizophrenia patients have significantly lower cardiac autonomic control, but they have significantly higher low-frequency and high-frequency values than those of healthy adults. Use of antipsychotic drug may affect the autonomic nervous system in schizophrenic patients. Metabolic syndrome was not associated with cardiac autonomic control in schizophrenia patients.

비만에서 adipose tissue 호르몬에 의한 metabolic signaling (Metabolic Signaling by Adipose Tissue Hormones in Obesity)

  • 장영훈
    • 생명과학회지
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    • 제33권3호
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    • pp.287-294
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    • 2023
  • 건강한 adipose tissue는 대사 항상성 통해 비만을 막는데 중요하다고 할 수 있다. Adipose tissue는 포도당과 지질 대사를 통해 에너지 균형에 중요한 역할을 한다. 영양분 상태에 따라, adipose tissue는 지질을 저장하여 커지기도 하고, 지질 분해를 통해 에너지를 소비하기도 한다. 게다가, adipose tissue는 호르몬 분비기관으로 작용이 부각되고 있다. 다양한 adipose tissue 호르몬이 존재하며, metabolic signaling을 통해 다른장기와 조직에 영향을 준다. 예를 들면, adipose tissue에서 분비하는 대표적인 펩타이드 호르몬(adipokine)은 섭식조절을 위해 뇌의 중추신경을 자극한다. 또한 adipocytes도 염증성 cytokines을 분비하여 adipose tissue의 immune cells을 표적으로 한다. 당연하게도, adipocytes는 지질에서 만들어지는 호르몬(lipokine)이 분비되어 특정 수용체와 결합하여 paracrine 및 endocrine으로 영향을 준다. 이러한 adipose tissue 호르몬에 의한 장기 조직 간의 상호작용을 이해하기 위해서는, 세부적인 adipocytes 및 다른 표적 세포에서 metabolic sig- naling이 규명되어야 한다. 그러므로, 과체중이나 비만의 건강하지 못한 adipose tissue에서는 metabolic sig- naling의 비정상적인 조절이 일어난다고 할 수 있다. 새로운 adipose metabolic signaling을 표적으로 하는 치료제는 항 비만 약물개발을 이끌어 낼 수 있다. 본 총설논문은 비만과 대사질환 관점에서 adipose tissue 호르몬과 metabolic signaling의 최신 연구결과를 요약 정리한다.

The pathophysiology of diabetic foot: a narrative review

  • Jiyoun Kim
    • Journal of Yeungnam Medical Science
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    • 제40권4호
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    • pp.328-334
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    • 2023
  • An aging population and changes in dietary habits have increased the incidence of diabetes, resulting in complications such as diabetic foot ulcers (DFUs). DFUs can lead to serious disabilities, substantial reductions in patient quality of life, and high financial costs for society. By understanding the etiology and pathophysiology of DFUs, their occurrence can be prevented and managed more effectively. The pathophysiology of DFUs involves metabolic dysfunction, diabetic immunopathy, diabetic neuropathy, and angiopathy. The processes by which hyperglycemia causes peripheral nerve damage are related to adenosine triphosphate deficiency, the polyol pathway, oxidative stress, protein kinase C activity, and proinflammatory processes. In the context of hyperglycemia, the suppression of endothelial nitric oxide production leads to microcirculation atherosclerosis, heightened inflammation, and abnormal intimal growth. Diabetic neuropathy involves sensory, motor, and autonomic neuropathies. The interaction between these neuropathies forms a callus that leads to subcutaneous hemorrhage and skin ulcers. Hyperglycemia causes peripheral vascular changes that result in endothelial cell dysfunction and decreased vasodilator secretion, leading to ischemia. The interplay among these four preceding pathophysiological factors fosters the development and progression of infections in individuals with diabetes. Charcot neuroarthropathy is a chronic and progressive degenerative arthropathy characterized by heightened blood flow, increased calcium dissolution, and repeated minor trauma to insensate joints. Directly and comprehensively addressing the pathogenesis of DFUs could pave the way for the development of innovative treatment approaches with the potential to avoid the most serious complications, including major amputations.

Review of ginsenosides targeting mitochondrial function to treat multiple disorders: Current status and perspectives

  • Huang, Qingxia;Gao, Song;Zhao, Daqing;Li, Xiangyan
    • Journal of Ginseng Research
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    • 제45권3호
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    • pp.371-379
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    • 2021
  • Mitochondrial dysfunction contributes to the pathogenesis and prognosis of many common disorders, including neurodegeneration, stroke, myocardial infarction, tumor, and metabolic diseases. Ginsenosides, the major bioactive constituents of Panax ginseng (P. ginseng), have been reported to play beneficial roles in the molecular pathophysiology of these diseases by targeting mitochondrial dysfunction. In this review, we first introduce the types of ginsenosides and basic mitochondrial functions. Then, recent findings are summarized on different ginsenosides targeting mitochondria and their key signaling pathways for the treatment of multiple diseases, including neurological disorders, cancer, heart disease, hyperglycemia, and inflammation are summarized. This review may explain the common targets of ginsenosides against multiple diseases and provide new insights into the underlying mechanisms, facilitating research on the clinical application of P. ginseng.

정신지체 및 발달지연으로 수용된 인구의 임상, 내분비 및 대사 질환 평가 (Clinical and Biochemical Evaluation of Institutionalized Population with Mental Retardation or Developmental Delay)

  • 김숙자;전영미;송웅주;김학성;조화연;길홍량;김승환
    • 대한유전성대사질환학회지
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    • 제12권2호
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    • pp.94-98
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    • 2012
  • Purpose: Developmental delay and mental retardation are frequently occurring disorders that present major socio-economic burden on the affected individual's family and society. Both can be congenital or acquired. However, a large number of people are institutionalized without exact diagnosis and, as a result, have not received proper care. Methods: 508 subjects with mental retardation or developmental delay from six institutions in Chung Buk Province were clinically evaluated and screened for metabolic and endocrinologic problems between 2000 and 2012. Results: Clinical genetic disorders were observed in 52 (10.2%) subjects. Cerebral palsy attributed to 21% of the institutionalized. 18 (3.5%) were diagnosed with metabolic disorders and 13 (2.6%) exhibited secondary endocrinologic dysfunction. Over 16% showed metabolic evidence of malnutrition. Conclusion: 21% and 3.5% of the population institutionalized due to mental retardation or developmental delay were afflicted by preventable cerebral palsy and metabolic disorders, respectively. Through early identification of the causes and early treatment, it may be possible to prevent, reduce, or alleviate the disability of many institutionalized individuals. Further research is imperative for establishing guidelines for diagnostic investigation for mental retardation.

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Association between metabolic syndrome components and cardiac autonomic modulation in southern Indian adults with pre-metabolic syndrome: hyperglycemia is the major contributing factor

  • Endukuru Chiranjeevi Kumar;Girwar Singh Gaur;Dhanalakshmi Yerrabelli;Jayaprakash Sahoo;Balasubramaniyan Vairappan;Alladi Charanraj Goud
    • The Korean Journal of Physiology and Pharmacology
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    • 제27권1호
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    • pp.49-59
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    • 2023
  • Metabolic syndrome (MetS) involves multi-factorial conditions linked to an elevated risk of type 2 diabetes mellitus and cardiovascular disease. Pre-metabolic syndrome (pre-MetS) possesses two MetS components but does not meet the MetS diagnostic criteria. Although cardiac autonomic derangements are evident in MetS, there is little information on their status in pre-MetS subjects. In this study, we sought to examine cardiac autonomic functions in pre-MetS and to determine which MetS component is more responsible for impaired cardiac autonomic functions. A total of 182 subjects were recruited and divided into healthy controls (n=89) and pre-MetS subjects (n=93) based on inclusion and exclusion criteria. We performed biochemical profiles on fasting blood samples to detect pre-MetS. Using standardized protocols, we evaluated anthropometric data, body composition, baroreflex sensitivity (BRS), heart rate variability (HRV), and autonomic function tests (AFTs). We further examined these parameters in pre-MetS subjects for each MetS component. Compared to healthy controls, we observed a significant cardiac autonomic dysfunction (CAD) through reduced BRS, lower overall HRV, and altered AFT parameters in pre-MetS subjects, accompanied by markedly varied anthropometric, clinical and biochemical parameters. Furthermore, all examined BRS, HRV, and AFT parameters exhibited an abnormal trend and significant correlation toward hyperglycemia. This study demonstrates CAD in pre-MetS subjects with reduced BRS, lower overall HRV, and altered AFT parameters. Hyperglycemia was considered an independent determinant of alterations in all the examined BRS, HRV, and AFT parameters. Thus, hyperglycemia may contribute to CAD in pre-MetS subjects before progressing to MetS.

The use of ketogenic diet in special situations: expanding use in intractable epilepsy and other neurologic disorders

  • Lee, Mun-Hyang
    • Clinical and Experimental Pediatrics
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    • 제55권9호
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    • pp.316-321
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    • 2012
  • The ketogenic diet has been widely used and proved to be effective for intractable epilepsy. Although the mechanisms underlying its antiepileptic effects remain to be proven, there are increasing experimental evidences for its neuroprotective effects along with many researches about expanding use of the diet in other neurologic disorders. The first success was reported in glucose transporter type 1 deficiency syndrome, in which the diet served as an alternative metabolic source. Many neurologic disorders share some of the common pathologic mechanisms such as mitochondrial dysfunction, altered neurotransmitter function and synaptic transmission, or abnormal regulation of reactive oxygen species, and the role of the ketogenic diet has been postulated in these mechanisms. In this article, we introduce an overview about the expanding use and emerging trials of the ketogenic diet in various neurologic disorders excluding intractable epilepsy and provide explanations of the mechanisms in that usage.

Lipophagy: Molecular Mechanisms and Implications in Metabolic Disorders

  • Shin, Dong Wook
    • Molecules and Cells
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    • 제43권8호
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    • pp.686-693
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    • 2020
  • Autophagy is an intracellular degradation system that breaks down damaged organelles or damaged proteins using intracellular lysosomes. Recent studies have also revealed that various forms of selective autophagy play specific physiological roles under different cellular conditions. Lipid droplets, which are mainly found in adipocytes and hepatocytes, are dynamic organelles that store triglycerides and are critical to health. Lipophagy is a type of selective autophagy that targets lipid droplets and is an essential mechanism for maintaining homeostasis of lipid droplets. However, while processes that regulate lipid droplets such as lipolysis and lipogenesis are relatively well known, the major factors that control lipophagy remain largely unknown. This review introduces the underlying mechanism by which lipophagy is induced and regulated, and the current findings on the major roles of lipophagy in physiological and pathological status. These studies will provide basic insights into the function of lipophagy and may be useful for the development of new therapies for lipophagy dysfunction-related diseases.

장쇄 수산화 아세틸코에이 탈수소효소 결핍증에 대한 고찰 (Very Long Chain Acyl-coenzyme A Dehydrogenase Deficiency: A Review of Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment)

  • 강석진
    • 대한유전성대사질환학회지
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    • 제22권1호
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    • pp.21-27
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    • 2022
  • Very long-chain acyl-coenzyme A dehydrogenase (VLCAD) deficiency (VLCADD) leads to a defective 𝛽-oxidation, specifically during prolonged fasting, infection, or exercise. Patients with VLCADD usually suffer from cardiomyopathy, hypoketotic hypoglycemia, hepatic dysfunction, exercise intolerance, muscle pain, and rhabdomyolysis, and sometimes succumb to sudden death. VLCADD is generally classified into three phenotypes: severe early-onset cardiac and multiorgan failure, hypoketotic hypoglycemia, and later-onset episodic myopathy. Diagnostic evaluation comprises acylcarnitine analysis, genetic analysis, and VLCAD activity assay. In the acylcarnitine analysis, the key metabolites are C14:1, C14:2, C14, and C12:1. A C14:1 level >1 mmol/L strongly suggests VLCADD. Various treatment recommendations are available for this condition. Dietary management includes decreasing fat content, increasing medium-chain triglyceride levels, and decreasing fasting periods. Supplementation with L-carnitine is controversial. Triheptanoin (a seven-carbon fatty acid triglyceride) treatment demonstrates improvement of cardiac functions. Bezafibrate may improve the quality of life of patients with VLCAD.

Potent HAT Inhibitory Effect of Aqueous Extract from Bellflower (Platycodon grandiflorum) Roots on Androgen Receptor-mediated Transcriptional Regulation

  • Lee, Yoo-Hyun;Kim, Yong-Jun;Kim, Ha-Il;Cho, Hong-Yon;Yoon, Ho-Geun
    • Food Science and Biotechnology
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    • 제16권3호
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    • pp.457-462
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    • 2007
  • Histone acetyltransferase (HAT) is a family of enzymes that regulate histone acetylation. Dysfunction of HAT plays a critical role in the development of cancer. Here we have screened the various plant extracts to find out the potent HAT inhibitors. The bellflower (Platycodon grandiflorum) root have exhibited approximately 30% of the inhibitory effects on HAT activity, especially p300 and CBP (CREB-binding protein) at the concentration of $100\;{\mu}g/mL$. The cell viability was decreased approximately 52% in LNCaP cell for 48 hr incubation. Furthermore, mRNA level of 3 androgen receptor target genes, PSA, NKX3.1, and TSC22 were decreased with bellflower root extract treatment ($100\;{\mu}g/mL$) in the presence of androgen. In ChIP assay, the acetylation of histone H3 and H4 in PSA promoter region was dramatically repressed by bellflower root treatment, but not TR target gene, Dl. Therefore, the potent HAT inhibitory effect of bellflower root led to the decreased transcription of AR target genes and prostate cancer cell growth with the repression of histone hyperacetylation.