• Title/Summary/Keyword: glucose homeostasis

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Regulation of Blood Glucose Homeostasis during Prolonged Exercise

  • Suh, Sang-Hoon;Paik, Il-Young;Jacobs, Kevin A.
    • Molecules and Cells
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    • v.23 no.3
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    • pp.272-279
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    • 2007
  • The maintenance of normal blood glucose levels at rest and during exercise is critical. The maintenance of blood glucose homeostasis depends on the coordination and integration of several physiological systems, including the sympathetic nervous system and the endocrine system. During prolonged exercise increased demand for glucose by contracting muscle causes to increase glucose uptake to working skeletal muscle. Increase in glucose uptake by working skeletal muscle during prolonged exercise is due to an increase in the translocation of insulin and contraction sensitive glucose transporter-4 (GLUT4) proteins to the plasma membrane. However, normal blood glucose level can be maintained by the augmentation of glucose production and release through the stimulation of liver glycogen breakdown, and the stimulation of the synthesis of glucose from other substances, and by the mobilization of other fuels that may serve as alternatives. Both feedback and feedforward mechanisms allow glycemia to be controlled during exercise. This review focuses on factors that control blood glucose homeostasis during prolonged exercise.

Glucose metabolism and evaluation of hypoglycemia in neonates (신생아에서의 포도당 대사와 저혈당증의 평가)

  • Kim, Eun Young
    • Clinical and Experimental Pediatrics
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    • v.50 no.3
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    • pp.223-229
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    • 2007
  • The fetus is completely dependent on mother for glucose and other nutrient transfer across the placenta. At birth, when the maternal supply is discontinued, the neonate must adjust to an independent existence. The changes in the neonate's glucose homeostasis during this transition to the extrauterine environment are influenced by the mother's metabolism and intrinsic fetal and placental problems. Maturation of carbohydrate homeostasis results from a balance between substrate availability and coordination of developing hormonal, enzymatic, and neural systems. These mechanisms may not be fully developed in neonates, so the neonate is vulnerable to carbohydrate disequilibrium resulting in damage to the central nervous system. Hypoglycemia is a relatively common metabolic problem seen during newborn care. However its definition, management and long term sequalae remain controversial. Hyporglycemia occurs frequently as a transient disorder with excellent prognosis. It also may persist and recur and cause permanent neurological complications. Although the key to effective treatment of hypoglycemia is diagnostic specific, the maintenance of euglycemia is critical to the preservation of central nervous system function. This article discusses physiology of perinatal glucose homeostasis, focusing on evaluation and treatment of hypoglycemia.

A Journey to Understand Glucose Homeostasis: Starting from Rat Glucose Transporter Type 2 Promoter Cloning to Hyperglycemia

  • Ahn, Yong Ho
    • Diabetes and Metabolism Journal
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    • v.42 no.6
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    • pp.465-471
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    • 2018
  • My professional journey to understand the glucose homeostasis began in the 1990s, starting from cloning of the promoter region of glucose transporter type 2 (GLUT2) gene that led us to establish research foundation of my group. When I was a graduate student, I simply thought that hyperglycemia, a typical clinical manifestation of type 2 diabetes mellitus (T2DM), could be caused by a defect in the glucose transport system in the body. Thus, if a molecular mechanism controlling glucose transport system could be understood, treatment of T2DM could be possible. In the early 70s, hyperglycemia was thought to develop primarily due to a defect in the muscle and adipose tissue; thus, muscle/adipose tissue type glucose transporter (GLUT4) became a major research interest in the diabetology. However, glucose utilization occurs not only in muscle/adipose tissue but also in liver and brain. Thus, I was interested in the hepatic glucose transport system, where glucose storage and release are the most actively occurring.

Blood glucose levels, insulin concentrations, and insulin resistance in healthy women and women with premenstrual syndrome: a comparative study

  • Zarei, Safar;Mosalanejad, Leili;Ghobadifar, Mohamed Amin
    • Clinical and Experimental Reproductive Medicine
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    • v.40 no.2
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    • pp.76-82
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    • 2013
  • Objective: To compare the blood glucose levels, insulin concentrations, and insulin resistance during the two phases of the menstrual cycle between healthy women and patients with premenstrual syndrome (PMS). Methods: From January of 2011 to the August of 2012, a descriptive cross-sectional study was performed among students in the School of Medicine of Jahrom University of Medical Sciences. We included 30 students with the most severe symptoms of PMS and 30 age frequency-matched healthy controls. We analyzed the serum concentrations of glucose, insulin, and insulin resistance by using the glucose oxidase method, radioimmunometric assay, and homeostasis model assessment of insulin resistance equation, respectively. Results: No significant differences between the demographic data of the control and PMS groups were observed. The mean concentrations of glucose of the two study groups were significantly different during the follicular and luteal phases (p=0.011 vs. p<0.0001, respectively). The amounts of homeostasis model assessment of insulin resistance of the two study groups were significantly different in the luteal phase (p=0.0005). Conclusion: The level of blood glucose and insulin resistance was lower during the two phases of the menstrual cycle of the PMS group than that of the controls.

Aryl Hydrocarbon Receptor Nuclear Translocator is Involved in ATP Homeostasis in Both Normoxic and Hypoxic Monolayer Mouse Hepatoma Cells

  • Choi, Su-Mi;Park, Hyun-Sung
    • Biomolecules & Therapeutics
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    • v.14 no.3
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    • pp.132-136
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    • 2006
  • Aryl hydrocarbon receptor nuclear translocator (Arnt) belongs to bHLH-PAS protein family. Here, we study the role of Arnt in both cell growth and glucose metabolism. Our results demonstrated that the absence of Arnt does affect ATP homeostasis but not cell growth in monolayer-cultured mouse hepatoma cells. ATP level of Arnt defective BpRc1 hepatoma cells is less than that of wild type hepatoma cells in both normoxia and hypoxia. BpRc1 cells also fail to increase the expression of glycolytic enzymes in response to hypoxia. Our results suggest that Arnt is essential for glucose metabolism and ATP production but not for cell growth.

Improvement of blood glucose homeostasis in mice fed with Capsosiphon fulvescens extract-added whole wheat cookie (매생이 추출물 첨가 통밀 쿠키의 마우스 혈당 항상성 개선 효과)

  • Lim, Jae-Min;Chun, Su-Hyun;Jeong, Yu-Jin;Lee, Kwang-Won
    • Korean Journal of Food Science and Technology
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    • v.53 no.3
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    • pp.313-320
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    • 2021
  • The present study aimed to investigate the effect of whole wheat cookie supplemented with Capsosiphon fulvescens (CF) extract on serum glucose homeostasis in C57BL/6 mice. This study examined whether the same effect was demonstrated for whole wheat cookie in comparison to previous research documenting the glucose-lowering effect of food products combined with CF extract. Mice were divided into three groups depending on the diet administered: normal cookie (NC), whole wheat cookie (WC), and WC blended with CF extract (WCFE). After 4 weeks of administering the experimental diet, the blood glucose level, serum insulin level, and homeostatic model assessment for insulin resistance index were found to be significantly lower in the WCFE group than in the NC and WC groups. These results suggest that whole wheat cookie containing CF extract is effective in preventing insulin resistance and maintaining blood glucose homeostasis.

Diabetes, Glucose Transport and Hypoglycaemic Agents

  • Khil, Lee-Yong
    • Biomolecules & Therapeutics
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    • v.12 no.4
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    • pp.202-208
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    • 2004
  • Diabetes mellitus is a complex metabolic derangement with hyperglycaemia being the most characteristic symptom of diabetes. Hyperglycaemia can be caused by an increase in the rate of glucose production by the liver or by a decrease in the rate of glucose use by peripheral tissues. Impaired glucose transport is one of the major factors contributing to insulin resistance in type 2 diabetic patients. The ability of insulin to mediate tissue glucose uptake is a critical step in maintaining glucose homeostasis and in clearing the post-prandial glucose load. Glucose transport is mediated by specific carriers called glucose transporters (GLUTs). In this article, the functional importance and molecular mechanisms of insulin-induced glucose transport and development of hypoglycaemic agents which increase glucose transport are reviewed.

Effects of Fructus Piperis Longi Extracts on Glucose Uptake in Adipocyte (필발 추출물의 포도당 흡수능에 대한 효과)

  • Kim, Mi Seong;Kwon, Kang Beom;Song, Je Ho
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.28 no.1
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    • pp.59-62
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    • 2014
  • Glucose uptake plays a pivotal role in maintaining whole body glucose homeostasis in adipocytes and skeletal muscles. In the present study we have shown that Fructus Piperis Longi Extracts (FPLE) can stimulate glucose uptake in OP9 adipocytes. The increasing effects of FPLE on glucose uptake were inhibited by compound C pretreatment, which means that the glucose uptake effects by FPLE were carried out by AMP-activated protein kinase (AMPK) activation. Further studies revealed that FPLE stimulated glucose transport occurs through a mechanism involving extracellular signal-regulated kinase (ERK1/2) activation.

Cell Death and Stress Signaling in Glycogen Storage Disease Type I

  • Kim, So Youn;Bae, Yun Soo
    • Molecules and Cells
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    • v.28 no.3
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    • pp.139-148
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    • 2009
  • Cell death has been traditionally classified in apoptosis and necrosis. Apoptosis, known as programmed cell death, is an active form of cell death mechanism that is tightly regulated by multiple cellular signaling pathways and requires ATP for its appropriate process. Apoptotic death plays essential roles for successful development and maintenance of normal cellular homeostasis in mammalian. In contrast to apoptosis, necrosis is classically considered as a passive cell death process that occurs rather by accident in disastrous conditions, is not required for energy and eventually induces inflammation. Regardless of different characteristics between apoptosis and necrosis, it has been well defined that both are responsible for a wide range of human diseases. Glycogen storage disease type I (GSD-I) is a kind of human genetic disorders and is caused by the deficiency of a microsomal protein, glucose-6-phosphatase-${\alpha}$ ($G6Pase-{\alpha}$) or glucose-6-phosphate transporter (G6PT) responsible for glucose homeostasis, leading to GSD-Ia or GSD-Ib, respectively. This review summarizes cell deaths in GSD-I and mostly focuses on current knowledge of the neutrophil apoptosis in GSD-Ib based upon ER stress and redox signaling.