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NBME 22 Answers

nbme22/Block 4/Question#25

A healthy 25-year-old man eats a meal consisting of ...

Fusion of an intracellular vesicle with the plasma membrane

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 +2  upvote downvote
submitted by trichotillomaniac(17),

basically glucose stimulates Beta cells to exocytose insulin. Any process involving exocytosis involves fusion of an intracellular vesicle with the plasma membrane.





 +1  upvote downvote
submitted by humble_station(6),

In a pancreatic B cell glucose enters via GLUT 2 and enters glycolysis. This causes the increased concentration of ATP in the cell causes the closure of ATP sensitive K+ channels. When this happens the cells becomes depolarized allowing Voltage gated Ca2+ channels to be open. The Ca2+ allows for exocytosis of insulin into the blood vessel.

Hence the answer here... Fusion of an intracellular vesicle with the plasma membrane.

pg 324 FA 2019 has the image





 -1  upvote downvote
submitted by trichotillomaniac(17),

basically glucose stimulates Beta cells to exocytos insulin. An process involving exocytosis involves fusion od an intracellular vesicle with the plasma membrane.





 -3  upvote downvote
submitted by dr.xx(42),

The β-cells have evolved a mechanism to detect the amount of insulin stored and secreted and adjust insulin synthesis accordingly. A granule transmembrane protein called islet cell autoantigen 512 (ICA512), is a crucial part of this feedback control. Insulin granules travel a long distance on tubulin tracks before arriving at the peripheral actin network [125]. Before becoming linked to the cytoskeleton, insulin granules are anchored to actin cortex via ICA512 and β2-synthrophin. Upon activation, the granule membrane fuses transiently to the cell membrane to release insulin. Elevated Ca2+ levels in the meantime activate the protease μ-calpain to cleave away a cytosolic fragment from ICA512. The free ICA512 cytosolic fragment then moves to the nucleus and binds to the tyrosine-phosphorylated transcriptional factor STAT5 to prevent STAT 5 from dephosphorylation, which in turn upregulates insulin transcription [127]. Nuclear free ICA512 cytosolic fragments also bind to sumoylating enzyme PIASγ. The sumoylation of ICA512 by PIAS γ reverses the binding of ICA512 to STAT5 [127]. Hence, the release of insulin from secretory granules is communicated to the nucleus, which serves as a positive feedback mechanism to initiate insulin translation for maintaining an adequate amount of stored insulin.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3934755/