Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding

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Standard

Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding. / Hansen, Finn Mølgård; Nilsson, Poul; Sonne, Ole; Hustvedt, B E; Nilsson-Ehle, P; Løvø, A; Nielsen, Jens Høiriis.

I: Diabetologia, Bind 24, Nr. 2, 02.1983, s. 131-5.

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

Harvard

Hansen, FM, Nilsson, P, Sonne, O, Hustvedt, BE, Nilsson-Ehle, P, Løvø, A & Nielsen, JH 1983, 'Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding', Diabetologia, bind 24, nr. 2, s. 131-5.

APA

Hansen, F. M., Nilsson, P., Sonne, O., Hustvedt, B. E., Nilsson-Ehle, P., Løvø, A., & Nielsen, J. H. (1983). Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding. Diabetologia, 24(2), 131-5.

Vancouver

Hansen FM, Nilsson P, Sonne O, Hustvedt BE, Nilsson-Ehle P, Løvø A o.a. Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding. Diabetologia. 1983 feb.;24(2):131-5.

Author

Hansen, Finn Mølgård ; Nilsson, Poul ; Sonne, Ole ; Hustvedt, B E ; Nilsson-Ehle, P ; Løvø, A ; Nielsen, Jens Høiriis. / Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding. I: Diabetologia. 1983 ; Bind 24, Nr. 2. s. 131-5.

Bibtex

@article{94c1db6dfd9047d082934e1381e55a9c,
title = "Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding",
abstract = "Insulin resistance was studied by comparing insulin response and insulin binding in four groups of rats. Glucose metabolism in isolated fat cells from male Wistar rats weighing 340 g was less responsive to a supramaximal dose of insulin than glucose metabolism in fat cells from rats weighing 200 g. Induction of streptozotocin-diabetes in rats weighing 200 g resulted in a marked decrease in the insulin responsiveness of fat cells. Ventromedial hypothalamic lesions of 340 g rats had the opposite effect and restored the insulin responsiveness of fat cells. The responsiveness in the four groups was correlated to the rate of glucose conversion to fatty acids in fat cells. The binding of 125I-insulin was the same in both 340 and 200 g rats. The ventromedial hypothalamic lesioned rats and the diabetic rats showed, in spite of their great difference in insulin responsiveness, the highest binding of 125I-insulin to fat cells. Insulin binding was not correlated to the plasma insulin level which however was reflected in the lipoprotein lipase activity in the adipose tissue. In conclusion, these results indicate that variations in insulin responsiveness in fat cells are due to alterations in cellular metabolism rather than in insulin binding.",
keywords = "Adipose Tissue, Animals, Body Weight, Diabetes Mellitus, Experimental, Fatty Acids, Glucose, Hypothalamus, Middle, Insulin, Insulin Resistance, Male, Obesity, Rats, Rats, Inbred Strains",
author = "Hansen, {Finn M{\o}lg{\aa}rd} and Poul Nilsson and Ole Sonne and Hustvedt, {B E} and P Nilsson-Ehle and A L{\o}v{\o} and Nielsen, {Jens H{\o}iriis}",
year = "1983",
month = feb,
language = "English",
volume = "24",
pages = "131--5",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - Variations in insulin responsiveness in rat fat cells are due to metabolic differences rather than insulin binding

AU - Hansen, Finn Mølgård

AU - Nilsson, Poul

AU - Sonne, Ole

AU - Hustvedt, B E

AU - Nilsson-Ehle, P

AU - Løvø, A

AU - Nielsen, Jens Høiriis

PY - 1983/2

Y1 - 1983/2

N2 - Insulin resistance was studied by comparing insulin response and insulin binding in four groups of rats. Glucose metabolism in isolated fat cells from male Wistar rats weighing 340 g was less responsive to a supramaximal dose of insulin than glucose metabolism in fat cells from rats weighing 200 g. Induction of streptozotocin-diabetes in rats weighing 200 g resulted in a marked decrease in the insulin responsiveness of fat cells. Ventromedial hypothalamic lesions of 340 g rats had the opposite effect and restored the insulin responsiveness of fat cells. The responsiveness in the four groups was correlated to the rate of glucose conversion to fatty acids in fat cells. The binding of 125I-insulin was the same in both 340 and 200 g rats. The ventromedial hypothalamic lesioned rats and the diabetic rats showed, in spite of their great difference in insulin responsiveness, the highest binding of 125I-insulin to fat cells. Insulin binding was not correlated to the plasma insulin level which however was reflected in the lipoprotein lipase activity in the adipose tissue. In conclusion, these results indicate that variations in insulin responsiveness in fat cells are due to alterations in cellular metabolism rather than in insulin binding.

AB - Insulin resistance was studied by comparing insulin response and insulin binding in four groups of rats. Glucose metabolism in isolated fat cells from male Wistar rats weighing 340 g was less responsive to a supramaximal dose of insulin than glucose metabolism in fat cells from rats weighing 200 g. Induction of streptozotocin-diabetes in rats weighing 200 g resulted in a marked decrease in the insulin responsiveness of fat cells. Ventromedial hypothalamic lesions of 340 g rats had the opposite effect and restored the insulin responsiveness of fat cells. The responsiveness in the four groups was correlated to the rate of glucose conversion to fatty acids in fat cells. The binding of 125I-insulin was the same in both 340 and 200 g rats. The ventromedial hypothalamic lesioned rats and the diabetic rats showed, in spite of their great difference in insulin responsiveness, the highest binding of 125I-insulin to fat cells. Insulin binding was not correlated to the plasma insulin level which however was reflected in the lipoprotein lipase activity in the adipose tissue. In conclusion, these results indicate that variations in insulin responsiveness in fat cells are due to alterations in cellular metabolism rather than in insulin binding.

KW - Adipose Tissue

KW - Animals

KW - Body Weight

KW - Diabetes Mellitus, Experimental

KW - Fatty Acids

KW - Glucose

KW - Hypothalamus, Middle

KW - Insulin

KW - Insulin Resistance

KW - Male

KW - Obesity

KW - Rats

KW - Rats, Inbred Strains

M3 - Journal article

C2 - 6341137

VL - 24

SP - 131

EP - 135

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 2

ER -

ID: 47975300