scholarly journals Comparison of the effects of sucrose and fructose on insulin action and glucose tolerance

2000 ◽  
Vol 279 (4) ◽  
pp. R1334-R1340 ◽  
Author(s):  
Jeffrey S. Thresher ◽  
Deborah A. Podolin ◽  
Yuren Wei ◽  
Robert S. Mazzeo ◽  
Michael J. Pagliassotti

The purpose of the present study was to determine whether fructose is the nutrient mediator of sucrose-induced insulin resistance and glucose intolerance. Toward this end, male rats were fed a purified starch diet (68% of total calories) for a 2-wk baseline period. After this, rats either remained on the starch (ST) diet or were switched to a sucrose (SU, 68% of total calories), fructose/glucose (F/G, 34/34% of total calories), or fructose/starch (F/ST, 34/34% of total calories) diet for 5 wk. Rats then underwent either an intravenous glucose tolerance test ( n = 10/diet) or a euglycemic, hyperinsulinemic clamp ( n = 8 or 9/diet). Incremental glucose and insulin areas under the curve in SU, F/G, and F/ST were on average 61 and 29% greater than ST, respectively, but not significantly different from one another. During clamps, glucose infusion rates (mg · kg−1 · min−1) required to maintain euglycemia were significantly lower ( P< 0.05) in SU, F/G, and F/ST (13.4 ± 0.9, 9.5 ± 1.7, 11.3 ± 1.3, respectively) compared with ST (22.8 ± 1.1). Insulin suppression of glucose appearance (mg · kg−1 · min−1) was significantly lower ( P < 0.05) in SU, F/G, and F/ST (5.6 ± 0.5, 2.2 ± 1.2, and 6.6 ± 0.7, respectively) compared with ST (9.6 ± 0.4). Insulin-stimulated glucose disappearance (mg · kg−1 · min−1) was significantly lower ( P < 0.05) in SU, F/G, and F/ST (17.9 ± 0.6, 16.2 ± 1.3, 15.3 ± 1.8, respectively) compared with ST (24.7 ± 1.2). These data suggest that fructose is the primary nutrient mediator of sucrose-induced insulin resistance and glucose intolerance.

1993 ◽  
Vol 129 (4) ◽  
pp. 360-365 ◽  
Author(s):  
Clemens Fürnsinn ◽  
Peter Nowotny ◽  
Michael Roden ◽  
Madeleine Rohac ◽  
Thomas Pieber ◽  
...  

To compare the effect of short- vs long-term amylin infusion on insulin sensitivity, glucose tolerance and serum calcemia, euglycemic-hyperinsulinemic clamp (26 pmol·kg−1·min−1) and glucose tolerance tests (2.4 mmol/kg over 30 min) were performed in lean Zucker rats. Three infusion protocols were employed: control group: 24 h of iv saline; short-term amylin exposure: 22 h of iv saline followed by 2 h of iv amylin (20 μg/h); long-term amylin exposure: 24 h of iv amylin (20 μg/h). Insulin resistance was induced by short-term amylin infusion during euglycemic clamping, as shown by a 41% decrease in space-corrected glucose infusion rates (μmol·kg−1·min−1; control group, 106.0±15.0; short-term iv amylin, 62.7±15.0; p<0.00 5). After long-term amylin exposure, insulin sensitivity was identical to control values (109.9±6.7). This fading action of amylin was confirmed by data from the glucose tolerance test, demonstrating glucose intolerance after short- but not after long-term amylin exposure. Serum calcium concentration decreased during short-term (2 h) amylin infusion (from 2.52±0.15 to 2.09±0.12 mmol/l; p<0.01) and hypocalcemia of a similar extent also was present after 22 h and 24 h of amylin exposure (2.10±0.09 and 2.04±0.14 mmol/l, respectively). The data demonstrate that short-term amylin infusion induces insulin resistance and glucose intolerance, both of which vanish during long-term (>22 h) amylin exposure, being apparently independent of induced hypocalcemia.


2009 ◽  
Vol 6 (4) ◽  
pp. 23-27
Author(s):  
A V Dreval' ◽  
I V Misnikova ◽  
I V Trigolosova ◽  
I A Barsukov

We have performed an estimation of metabolic disorders in 70 persons with various early glucose metabolism abnormalities (IFG and IGT). Oral glucose tolerance test (ОGTT) and intravenous glucose tolerance test (IVGTT) were done in all subjects. HbA1с, insulin and C-peptide levels were also determined. Further НОМА-R, QUICKI, MATSUDA indexes, speed of glucose elimination from the blood (k), production of glucose (H) and a degree of glucose metabolism disorders (pN) were estimated. Glucose hyperproduction and liver insulin resistance is more typical for IFG, than for isolated IGT. It was confirmed by higher parameter of liver glucose production (H) and HOMA-R index in patients with IFG. On the contrary peripheral insulin resistance is more typical for isolated IGT. Index of insulin sensitivity MATSUDA and speed of glucose elimination from the blood (k) were lower in IGT than in IFG patients. First phase of insulin secretion was broken in patients with combination IGT and IFG, which can explain the high incidence of transformation in 2 type diabetes mellitus in patients with combination IGT and IFG. The lowest HbA1c levels was found among persons with IGT. It is likely that ordinary life food intake (not glucose loading) in this group of patients does not result in chronic hyperglycemia and excessive hemoglobin glycation.


1960 ◽  
Vol XXXIII (II) ◽  
pp. 157-167
Author(s):  
T. Rodari ◽  
G. Specchia

ABSTRACT The double intravenous glucose tolerance test does not modify the assimilation coefficient in normal and thin diabetic subjects. On the contrary, in fat diabetic subjects the second coefficient of assimilation increases significantly, but not the first one. From these researches it is evident that the valuation of glucose assimilation by double venous hyperglycaemic test indicates the functional behaviour of the pancreas in different diabetic states. The interpretation of this behaviour of pancreatic islet response to the double venous hyperglycaemic test is discussed.


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