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#glucose uptake

5 public questions tagged with this topic.

Membrane Transportation

Which transporter is primarily responsible for glucose uptake in the small intestine?

Dietary carbohydrate absorption predominantly occurs in duodenum and jejunum where luminal concentrations fluctuate from millimolar after meal to micromolar between meals, requiring active accumulation. Enterocytes polarized with brush border apical membrane expressing SGLT1 coded by SLC5A1 high affinity sodium glucose cotransporter belonging to sodium substrate symporter family LeuT fold with 14 transmembrane helices, sodium binding sites Na1 Na2 coordinating carbonyls and glucose vestibule lined by aromatic residues conferring D-glucose galactose specificity. Stoichiometry two sodium per one glucose harnessing electrochemical sodium gradient established by basolateral Na+/K+ ATPase exporting three sodium importing two potassium per ATP maintaining low intracellular sodium about 12 millimolar and negative potential minus 60 millivolts, giving driving force about 10 kilojoules per mol. Concentrative uptake raises intracellular glucose to millimolar enabling exit via basolateral GLUT2 low affinity high Km about 17 millimolar facilitating diffusion into bloodstream. GLUT1 restricted to erythrocytes blood brain barrier basal, GLUT4 insulin dependent in muscle adipose, but intestinal apical uptake relies on SGLT1. Phlorizin competitive inhibitor blocks it, causing glucosuria and used therapeutically.

Ref: Wright et al., Physiol Rev, SGLT1 Sodium Glucose Cotransporter Intestinal Glucose Absorption Mechanism.

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Membrane Transportation

Which GLUT transporter is insulin-dependent?

GLUT family encoded by SLC2A genes includes fourteen isoforms differing in distribution, affinity and regulation. GLUT4 product of SLC2A4 stands out as only major isoform acutely dependent on insulin via regulated exocytosis. It contains twelve transmembrane helices forming MFS fold with central glucose cavity. Basally most protein sequestered in perinuclear storage vesicles associated with TUG and VAMP2 retained by AS160 GAP keeping Rab proteins GDP-bound. Insulin activates receptor tyrosine kinase, IRS1 phosphorylation, PI3K producing PIP3, recruiting Akt2 which phosphorylates TBC1D1 and TBC1D4 relieving Rab8A, Rab10, Rab14 to GTP driving vesicle translocation, docking via exocyst and fusion via syntaxin4 SNAP23. Exercise also triggers translocation via AMPK and calcium CaMKK independent of insulin. Once inserted, GLUT4 transports glucose by facilitated diffusion Km around 5 mM matching plasma glucose, enabling rapid postprandial uptake into muscle and adipose for glycogen and triglyceride formation, crucial for glucose homeostasis and postmeal glycemic control impaired in diabetes.

Ref: Huang & Czech, Cell Metabolism 2007: GLUT4 – Insulin-Dependent Glucose Transporter.

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Cell Signaling ELR Pathways - I

Which glucose transporter is insulin responsive?

GLUT4, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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Cell Signaling ELR Pathways - I

Which pathway mainly regulates glucose uptake downstream of insulin?

PI3K–Akt, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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