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Beta cell function: difference between revisions

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Revision 2 — 06:49, 31 Aug 2024
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Revision 3 — 22:22, 1 Sep 2024
Chromatokid (talk)
add the species in which the knockout work was done
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10The central methodological difficulty is that secretion and sensitivity are not independent. A healthy beta cell compensates for insulin resistance by secreting more, so an absolute secretion figure that looks normal may represent substantial dysfunction in a very insulin-resistant person. Measures that do not adjust for sensitivity — including fasting insulin and HOMA-B — are therefore weak, and the disposition index, the product of a secretion measure and a sensitivity measure, was devised to address exactly this.{{r|bergman2002}}10The central methodological difficulty is that secretion and sensitivity are not independent. A healthy beta cell compensates for insulin resistance by secreting more, so an absolute secretion figure that looks normal may represent substantial dysfunction in a very insulin-resistant person. Measures that do not adjust for sensitivity — including fasting insulin and HOMA-B — are therefore weak, and the disposition index, the product of a secretion measure and a sensitivity measure, was devised to address exactly this.{{r|bergman2002}}
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+12== What is being measured ==
+13Insulin secretion cannot be sampled at source. Peripheral venous insulin has already passed the liver, which extracts a variable 40–80% at first pass, so peripheral concentration understates secretion by an amount that itself varies between people and with pulsatility.{{r|rorsman2013}}
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+15[[C-peptide]] avoids this. It is co-secreted with insulin in equimolar amounts, is not extracted by the liver, and has predictable kinetics, so a peripheral C-peptide profile can be deconvolved into a secretion rate. This is the basis of every rigorous measure of beta-cell function.
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12== References ==17== References ==
13{{reflist}}18{{reflist}}