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Effect of hemipancreatectomy and of pancreatic diversion on the tolerance to a glucose load in humans
Author(s) -
Alberto Battezzati,
Alessandro Zerbi,
Gianluca Perseghin,
Andrea Caumo,
Ileana Terruzzi,
V. Di Carlo,
Livio Luzi
Publication year - 2000
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2000.00648.x
Subject(s) - insulin , medicine , endocrinology , peripheral , pancreatic hormone , pancreas , insulin resistance
Background The role of the pattern, quantity and site of insulin secretion in the tolerance to a glucose challenge is not fully evaluated in humans because it is difficult to obtain appropriate clinical models. Design To address this issue, we studied subjects with reduced pancreatic mass (hemipancreatectomized, HEMI), systemic insulin delivery (pancreas transplant recipients, PTX), and two control groups (healthy, CON; and with uveitis on the same immunosuppression as PTX, UVE), with an hyperglycaemic clamp (study 1, + 4.2 mmol L −1 ), using a repeat experiment (study 2) with a fixed glucose infusion, calculated to increase by 35% that in study 1. Results In study 1, CON increased glucose uptake to 20 ± 3 μmol kg −1 min −1 after a biphasic insulin response. In study 2, CON further increased the glucose uptake via an increment in prehepatic insulin secretion that stimulated insulin sensitivity without changes in peripheral insulin and glucose concentrations. HEMI and PTX had 35% less glucose uptake in study 1, compared to CON, and increased glucose concentrations (+ 1.6 mmol L −1 ) in study 2. UVE had an intermediate defect. The causes of intolerance were different: HEMI had a defective first‐phase insulin secretion (50% peripheral insulin concentrations) but maintained insulin sensitivity; PTX had normal peripheral insulin but only one‐third of the insulin sensitivity of CON. Conclusions Hemipancreatectomy and systemic insulin delivery impair first‐phase insulin secretion; second‐phase peripheral insulinization (HEMI); insulin sensitivity (PTX); and a mechanism evidentiated in study 2 of CON that increases insulin sensitivity in response to prehepatic insulin secretion (both groups). Failure of these mechanisms is largely compensated by hyperglycaemia.