Abstract
Plasma insulin clearance is an important determinant of plasma insulin concentration. In this review, we provide an overview of the factors that regulate insulin removal from plasma and discuss the interrelationships among plasma insulin clearance, excess adiposity, insulin sensitivity, and type 2 diabetes (T2D). We conclude with the perspective that the commonly observed lower insulin clearance rate in people with obesity, compared with lean people, is not a compensatory response to insulin resistance but occurs because insulin sensitivity and insulin clearance are mechanistically, directly linked. Furthermore, insulin clearance decreases postprandially because of the marked increase in insulin delivery to tissues that clear insulin. The commonly observed high postprandial insulin clearance in people with obesity and T2D likely results from the relatively low insulin secretion rate, not an impaired adaptation of tissues that clear insulin.
Highlights
Compared with healthy lean people, people with obesity have increased basal and postprandial plasma insulin concentrations [1–3]
Results from studies that evaluated the relationships among adiposity, insulin sensitivity and plasma insulin clearance by using intravenous glucose infusion protocols suggest that reduced insulin clearance in people with obesity is related to insulin resistance, and is not due to increased body fat per se
Provided a comprehensive analysis the insulin relationships among insulin secretion in response to glucose ingestion and hepatic, extrahepatic, and whole-body insulin plasma clearance and tissue extraction rates suggest that Non-alcoholic fatty liverextraction diseaserates (NAFLD) does not impair hepatic insulin extraction per se, but rather the lower hepatic and whole-body insulin clearance in people with NAFLD are due to insulin resistance and insulin hypersecretion [84,95]
Summary
Compared with healthy lean people, people with obesity have increased basal and postprandial plasma insulin concentrations [1–3]. The higher postprandial insulin clearance in people with T2D, compared to those without, is not a maladaptation in tissues that clear insulin, but a consequence of β-cell dysfunction and reduced postprandial insulin secretion, which blunts insulin delivery to tissues that clear insulin This has important clinical implications because it suggests that pancreatic β cells, not tissues that clear insulin, are responsible for the higher postprandial plasma insulin clearance in people with T2D. Assuming average basal insulin secretion and secretion clearance rates in people obesity [8,27], a 10%in decrease plasmaclearance insulin clearanceand rates in people with obesitywith [8,27], a 10%.
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