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Related Concept Videos

Glucose Transporters01:27

Glucose Transporters

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Glucose transporters facilitate the transport of glucose across the cell membrane. In addition to glucose, some glucose transporters can also aid the movement of other hexoses such as fructose, mannose, and galactose.
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
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Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

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Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
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Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

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Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1...
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Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
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Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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Isolation and characterization of an Escherichia coli mutant lacking the major serine transporter, and cloning of a serine transporter gene.

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Region-specific changes in [3H]dizocilpine binding in diazepam-withdrawn rats.

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In vivo gene transfer into the adult mammalian central nervous system by continuous injection of plasmid DNA-cationic liposome complex.

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Age-related decrease in the antiseizure effect of ifenprodil against pentylenetetrazole in mice.

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A novel monoantennary complex-type sugar chain found in octopus rhodopsin: occurrence of the Gal beta1-->4Fuc group linked to the proximal N-acetylglucosamine residue of the trimannosyl core.

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[Substance-related mental disorders and expert testimony].

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[Nicotine-related mental disorders].

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[Glutaric acidemia type II]

M Tsuda1

  • 1Department of Pediatrics, Nihon University School of Medicine.

Ryoikibetsu Shokogun Shirizu
|January 1, 1997
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Summary

No abstract available in PubMed .

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