Insulin is the signal telling tissues to take up glucose and store it. When those tissues respond less well, the pancreas compensates by releasing more insulin. For a while glucose stays normal at the cost of high insulin levels; if compensation fails, glucose rises and type 2 diabetes appears.
It is associated mainly with excess visceral fat and fat build-up in the liver and muscle, with physical inactivity and with genetic factors. It is the common background of obesity, type 2 diabetes and metabolic fatty liver disease.
In studies of incretin agonists and multi-agonists, measures of insulin sensitivity (such as the HOMA-IR index or euglycaemic clamps) are standard markers, because part of these molecules' effect comes through fat loss and part more directly.
Understanding insulin resistance helps explain why metabolic compounds are assessed with several markers (glucose, insulin, liver fat, weight) rather than just one.
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Learn it in depth at the Peptide University
- Incretin physiology · Module 3
- Amylin, the oral route and the next generation · Module 3
- IGF-1, its binding proteins and its variants · Module 5
- Safety profiles by class · Module 10
- Metabolic and repair (1–5) · Module 14
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