Dynamic regulation of glucose concentration in blood, muscle and adipose tissues After each meal, glucose level increases beyond 5 mM triggering the production of insulin, which will stimulate the uptake of glucose into muscles for storage in the form of glycogen, or adipocyte(triacylglycerols) Mechanism: insulin stimulate the cell surface expression of GluT4
Dynamic regulation of glucose concentration in blood, muscle and adipose tissues After each meal, glucose level increases beyond 5 mM, triggering the production of insulin, which will stimulate the uptake of glucose into muscles for storage in the form of glycogen, or adipocyte (triacylglycerols); Mechanism: insulin stimulate the cell surface expression of GluT4
When insulin interacts with its receptor, vesicles move to surface and fuse with the plasma membrane, increasing the number of glucose transporters in the plasma membrane Insulin 0 When insulin level drops glucose transporters are removed from the plasma membrane by endocytosis, forming small vesicles Insulin receptor Glucose Plasma transporter membrane Glucose transporters "stored" within cell in membrane vesicles Patches of the endosome enriched for The smaller glucose transporters bud off to become vesicles fuse with small vesicles, ready to return to the larger endosome surface when insulin levels rise again
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Type I diabetes mellitus: juvenile onset diabetes no insulin due to the lack of beta cells in pancreas therefore, low rate of glucose uptake into muscle and adipose tissue--high glucose level >>5mM Diabetics are defective in glucose uptake
Type I diabetes mellitus: juvenile onset diabetes no insulin due to the lack of beta cells in pancreas therefore, low rate of glucose uptake into muscle and adipose tissue—high glucose level >>5mM Diabetics are defective in glucose uptake
Aquaporin-2(AQP-2), Insulin and Water retention In kidney, water is reabsorbed from the renel collecting duct via AoP-2 and returned to the blood for circulation Mechanism: ADH(antidiuretic hormone)regulates this process Dy mobilizing aQp-2 from intracellular vesicles to the apical surface, enhanced the uptake of water In a rare form of genetic disorder diabetes insipidus, a genetic defect in AQP-2 is responsible, with impaired water reabsorption by the kidney--excretion of copious volumes of very diluted urine
Aquaporin-2 (AQP-2), Insulin and Water retention In kidney, water is reabsorbed from the renel collecting duct via AQP-2 and returned to the blood for circulation. Mechanism: ADH (antidiuretic hormone) regulates this process by mobilizing AQP-2 from intracellular vesicles to the apical surface, enhanced the uptake of water. In a rare form of genetic disorder, diabetes insipidus, a genetic defect in AQP-2 is responsible, with impaired water reabsorption by the kidney—excretion of copious volumes of very diluted urine
Carbon dioxide produced Bicarbonate by catabolism enters dissolves in erythrocyte blood plasma Co-transport CO2 Chloride-bicarbonate\ HCO3 CI exchange protein Chloride and In respiring tissues Bicarbonate are co transported across the carbonic anhydrase erythrocyte membrane CO+ HoO HCO3 +H CI Anion exchanger CO2+H2O← HCO3 +H CI carbonic anhydrase HCO3- for Cl- 12TM In lungs -one million fold! HCO3 CI Carbon dioxide leaves Bicarbonate enters erythrocyte and is erythrocyte from exhaled blood plasma
Chloride and Bicarbonate are cotransported across the erythrocyte membrane: Anion exchanger --HCO3- for Cl- --12TM --one million fold!!! Co-transport