Metabolic effects of IGF-I and insulin in spontaneously diabetic BB/w rats

Jacob, Ralph; Sherwin, Robert S.; Bowen, Lorrie; Fryburg, David A.; Fagin, Katherine D.; Tamborlane, William V.; Shulman, Gerald I.

doi:10.1152/ajpendo.1991.260.2.e262

Cited by 38 publications

(33 citation statements)

References 31 publications

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“…In the normal rats, the ratio of ED85 of potency of insulin to IGF-I on a molar basis was 1/79. In contrast, the ratio was increased to 1/24 in streptozotocin-diabetic rats, in agreement with the earlier study by Jacob et al [18] that in BB/w rats IGF-I infusion showed more suppression of hepatic glucose production than non-diabetic rats. The reason for the rather increased sensitivity of hepatic glucose output to IGF-I is not clearly explained.…”

Section: Suppressive Effect Of Igf-i and Insulin On Hepatic Glucose Osupporting

confidence: 92%

“…The maximum effects of insulin and IGF-I were identically decreased to about 70% of that of normal rats. This result was in accord with an earlier report by Jacob et al [18] on spontaneously diabetic BB/w rats, although controversial results of no IGF-I resistance in partially pancreatectomized rats were reported by Rosetti et al [19]. Sowell et al [20] reported the interesting observation that rat skeletal muscle treated with phenylarsine oxide (PAO), an agent believed to block insulin stimulated glucose transport at a postreceptor level, was resistant also to IGF-I.…”

Section: Suppressive Effect Of Igf-i and Insulin On Hepatic Glucose Osupporting

confidence: 88%

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Insulin-Like Growth Factor I Resistance in Peripheral Tissue but not in Liver in Streptozotocin-Induced Diabetic Rats.

et al. 1995

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Abstract.The metabolic effect of recombinant human insulin-like growth factor I (IGF-I) was investigated by the glucose clamp technique in normal rats and streptozotocin-induced diabetic rats, a model of insulin-dependent diabetes mellitus (IDDM), and compared with that of insulin. Glucose uptake by peripheral tissues was stimulated by intravenous administration of IGF-I at rates of from 0.369 to 3.690 nmol/kg/min in a dose dependent manner, with a potency of 1/52 that of insulin estimated on the basis of the ED50 molar ratio in normal rats. In streptozotocin-induced diabetic rats, the maximum effects of IGF-I and insulin were reduced to 72% and 70% of those in normal rats, respectively, indicating the presence of both IGF-I and insulin resistance.Hepatic glucose output in normal rats was suppressed by IGF-I in a dose dependent manner with a weaker potency of 1/99 that of insulin assessed on the basis of the ED50 values.In streptozotocin-induced diabetic rats, a dose-response curve of the suppressive effect of insulin on hepatic glucose output shifted to the right, indicating the presence of hepatic insulin resistance, but a leftward shifting of the suppressive effect of IGF-I on hepatic glucose output was observed.We concluded that the IGF-I effect on peripheral tissue was decreased but that on the liver was rather increased in streptozotocin-induced diabetic rats, in contrast to the resistance of both peripheral tissues and liver to insulin.

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Section: Suppressive Effect Of Igf-i and Insulin On Hepatic Glucose Osupporting

confidence: 92%

Section: Suppressive Effect Of Igf-i and Insulin On Hepatic Glucose Osupporting

confidence: 88%

Insulin-Like Growth Factor I Resistance in Peripheral Tissue but not in Liver in Streptozotocin-Induced Diabetic Rats.

et al. 1995

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“…In a previous study, lipid metabolism was investigated in mouse monocytes after incubation with [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]oleate (33). Of the radioactivity associated with lipid, 80% of oleate was shown to be incorporated into triglycerides, 18% was incorporated into phospholipids, and 2% was recovered as non-esterified fatty acids.…”

Section: Effects Of Igf-i On Glut Isoformsmentioning

confidence: 99%

“…However, in contrast to insulin, IGF-I is ineffective in suppressing hepatic glucose production (6)(7)(8) and has a preferential effect to increase the rates of glycolysis in tissues such as muscle (5). The effects of IGF-I on glucose disposal in hyperthyroidism have never been investigated.…”

Section: Introductionmentioning

confidence: 99%

IGF-I increases the recruitment of GLUT4 and GLUT3 glucose transporters on cell surface in hyperthyroidism

Dimitriadis

Maratou²,

Boutati³

et al. 2008

European Journal of Endocrinology

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Objective: In hyperthyroidism, tissue glucose disposal is increased to adapt to high energy demand. Our aim was to examine the regulation of glucose transporter (GLUT) isoforms by IGF-I in monocytes from patients with hyperthyroidism. Design and methods: Blood (20 ml) was drawn from 21 healthy and 10 hyperthyroid subjects. The abundance of GLUT isoforms on the monocyte plasma membrane was determined in the absence and presence of IGF-I (0.07, 0.14, and 0.7 nM) using flow cytometry. Anti-CD14-phycoerythrin monocional antibody was used for monocyte gating. GLUT isoforms were determined after staining the cells with specific antisera to GLUT3 and GLUT4. Results: In monocytes from the euthyroid subjects, IGF-I increased the abundance of GLUT3 and GLUT4 on the monocyte surface by 25 and 21% respectively (P!0.0005 with repeated measures ANOVA). Hyperthyroidism increased the basal monocyte surface GLUT3 and GLUT4; in these cells, IGF-I had a marginal but highly significant effect (PZ0.003, with repeated measures ANOVA) on GLUT3 (11%) and GLUT4 (10%) translocation on the plasma membrane. Conclusions: In hyperthyroidism: 1) basal abundance of GLUT3 and GLUT4 on the plasma membrane is increased and 2) the sensitivity of the recruitment of GLUT3 and GLUT4 transporters on the plasma membrane in response to IGF-I is increased. These findings may contribute to the understanding of the mechanism by which hyperthyroidism increases glucose disposal in peripheral tissues.

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“…This effect was associated with enhanced glucose utilization by skeletal muscle [4] and indeed was reflected in increased hexose uptake by muscles in vivo [5]. This metabolic effect of IGF-I is specific and independent of actions on the insulin receptor, and it has been proposed that IGF-I stimulation of glucose uptake can bypass insulin resistance in certain animal models of diabetes [3,6]. The molecular mechanism underlying such stimulation of glucose influx into muscle is unknown.…”

mentioning

confidence: 99%

Acute and long‐term effects of insulin‐like growth factor I on glucose transporters in muscle cells Translocation and biosynthesis

et al. 1992

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Insulin-like growth factor I (IGF-I) rapidly (cl0 min) stimulated glucose uptake into myotubes of the L6 muscle cell line, al concemrdtions that act specifically on IGF-I receptors. Uptake remained stimulated at a steady level for l-2 h, after which a second stimulation occurred. The first phase was insensitive to inhibition of protein synthesis, Subcellular fractionation demonstrated that it was accompanied by lranslocalion ofgluwse transporters (both GLUTI and GLUM) to the plasma membrane from intracellular membranes. Trdnslocation sufficed lo explain the first phase increase in glucose transport, and there was no change in the total cellular content of GLUT1 or GLUT4 glucose transporters. The second phase of stimulation was inhibitable by cyclohcximidc, and involved a net increase in either GLUTI or GLUT4 transporter conlcnt, which was reflected in an increase in transporter number in plasma membranes. These results define a cellular mechanism of metabolic action of IGF-I in muscle cells; furthermore, they suggest that IGF-I has acute metabolic effects that mimic those of insulin, bypassing action on the insulin receptor.Sugar transport; Glucose transporter; Insulin-like growth factor; L6 muscle cell 1 a INTRODUCTION Insulin-like growth factor I (IGF-I) is a potent growth factor [I] inducing both muscle growth and differentiation [2]. These effects are extremely important during fetal maturation, but also during post-natal growth and for muscle regeneration. Recently, effects of IGF-I other than its growth and differentiation promoting actions were recognized, specifically the ability to lower glycemia when perfused in rats [3] or dogs [4]. This effect was associated with enhanced glucose utilization by skeletal muscle [4] and indeed was reflected in increased hexose uptake by muscles in vivo [5]. This metabolic effect of IGF-I is specific and independent of actions on the insulin receptor, and it has been proposed that IGF-I stimulation of glucose uptake can bypass insulin resistance in certain animal models of diabetes [3,6]. The molecular mechanism underlying such stimulation of glucose influx into muscle is unknown. In the present study we examined the effect of acute (5-45 min) and prolonged (2-8 h) effects of IGF-I Abbreviurimu: aMEM, a Minimal Essential Medium; TM, Lola1 membranes; IM. intracellular light microsomes; PM, isolated plasma membranes; WGA, wheat germ agglutinin; GLUTI. brain/HEP-G2 glucose trnnsportrr; GLUT4, muscle/fat glucose transporter. EXPERIMENTAL Celi cdtrrrcs, ifwubariorrs and h~tw5e uprukkc assu_ssA clonally selected line of L6 muscle cells (selected for high fusion potential into myotubes) was grown in culture and allowed to fuse and diffcrcniiate, essentially as reported earlier [ql. Cells were studied at the myotubc stage, when r90% fusion was attained. Monolayer cultures of myotubes in 3.5 cm diameter wells wcrc incubated for 5 h in aMEM containing 25 mM D-glucose in the abgnce of serum. This results in low and steady basal glucose uptake ralcs [S]. Human recombinant IGF-I wa...

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Metabolic effects of IGF-I and insulin in spontaneously diabetic BB/w rats

Cited by 38 publications

References 31 publications

Insulin-Like Growth Factor I Resistance in Peripheral Tissue but not in Liver in Streptozotocin-Induced Diabetic Rats.

Insulin-Like Growth Factor I Resistance in Peripheral Tissue but not in Liver in Streptozotocin-Induced Diabetic Rats.

IGF-I increases the recruitment of GLUT4 and GLUT3 glucose transporters on cell surface in hyperthyroidism

Acute and long‐term effects of insulin‐like growth factor I on glucose transporters in muscle cells Translocation and biosynthesis

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