Effect of Fasting and Streptozotocin Diabetes on Insulin Binding and Action in the Isolated Mouse Soleus Muscle

Marchand-Brustel, Y. Le; Freychet, P

doi:10.1172/jci109609

Cited by 113 publications

(76 citation statements)

References 39 publications

(55 reference statements)

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“…Supporting this view, we have observed that, in heart and skeletal muscle from diabetic rats, a fall in GLUT-4 protein content coincides with a decreased effect of insulin stimulating glucose transport [4,[6][7][8]. However, our study also reveals that this is not a general finding, and, whereas the effect of insulin on glucose utilization is increased in skeletal muscle during fasting [12][13][14][15], this is concomitant with either unaltered or even decreased GLUT-4 protein levels. In this regard, it should be kept in mind that insulin action relies not only on the content of cellular GLUT-4 but also on the biological activities of the insulin receptor, as well as on several post-receptor events distal to the glucose carrier itself.…”

Section: Discussionsupporting

confidence: 72%

“…In this regard, it should be kept in mind that insulin action relies not only on the content of cellular GLUT-4 but also on the biological activities of the insulin receptor, as well as on several post-receptor events distal to the glucose carrier itself. In this regard, it should be mentioned that streptozotocininduced diabetes leads to a marked impairment of tyrosine receptor kinase activity in skeletal muscle [51], and that fasting enhances insulin binding as assessed in the incubated muscle preparation [13,14].…”

Section: Discussionmentioning

confidence: 99%

“…In fasting, there is also an impaired stimulation of glucose transport in response to insulin in adipocytes [9][10][11] and heart [4]. However, an increased sensitivity and responsiveness to insulin has been reported in perfused and incubated preparations of skeletal muscle from fasted rodents [12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Effect of diabetes and fasting on GLUT-4 (muscle/fat) glucose-transporter expression in insulin-sensitive tissues. Heterogeneous response in heart, red and white muscle

Camps

Castelló

Muñoz

et al. 1992

Biochemical Journal

146

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1. GLUT-4 glucose-transporter protein and mRNA levels were assessed in heart, red muscle and white muscle, as well as in brown and white adipose tissue from 7-day streptozotocin-induced diabetic and 48 h-fasted rats. 2. In agreement with previous data, white adipose tissue showed a substantial decrease in GLUT-4 mRNA and protein levels in response to both diabetes and fasting. Similarly, GLUT-4 mRNA and protein markedly decreased in brown adipose tissue in both insulinopenic conditions. 3. Under control conditions, the level of expression of GLUT-4 protein content differed substantially in heart, red and white skeletal muscle. Thus GLUT-4 protein was maximal in heart, and red muscle had a greater GLUT-4 content compared with white muscle. In spite of the large differences in GLUT-4 protein content, GLUT-4 mRNA levels were equivalent in heart and red skeletal muscle. 4. In heart, GLUT-4 mRNA decreased to a greater extent than GLUT-4 protein in response to diabetes and fasting. In contrast, red muscle showed a greater decrease in GLUT-4 protein than in mRNA in response to diabetes or fasting, and in fact no decrease in GLUT-4 mRNA content was detectable in fasting. On the other hand, preparations of white skeletal muscle showed a substantial increase in GLUT-4 mRNA under both insulinopenic conditions, and that was concomitant to either a modest decrease in GLUT-4 protein in diabetes or to no change in fasting. 5. These results indicate that (a) the effects of diabetes and fasting are almost identical and lead to changes in GLUT-4 expression that are tissue-specific, (b) white adipose tissue, brown adipose tissue and heart respond similarly to insulin deficiency by decreasing GLUT-4 mRNA to a larger extent than GLUT-4 protein, and (c) red and white skeletal muscle respond to insulinopenic conditions in a heterogeneous manner which is characterized by enhanced GLUT-4 mRNA/protein ratios.

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Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 99%

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Effect of diabetes and fasting on GLUT-4 (muscle/fat) glucose-transporter expression in insulin-sensitive tissues. Heterogeneous response in heart, red and white muscle

Camps

Castelló

Muñoz

et al. 1992

Biochemical Journal

146

View full text Add to dashboard Cite

show abstract

“…In vitro, insulin responsiveness was also impaired in liver (Cech et al, 1980), but not in muscle (Brady et al, 1981 Thus, in Reddy, 1979;Herrera et al, 1981;Brady et al, 1981;Le Marchand-Brustel & Freychet, 1979). These increases correlated with the decrease in plasma insulin generally observed in fasted rats (Penicaud et al, 1985).…”

Section: Introductionmentioning

confidence: 95%

Insulin receptor binding and tyrosine kinase activity in liver and skeletal muscle from fasted rats

Balage¹,

Sornet²,

Manin³

et al. 1989

Reprod. Nutr. Dévelop.

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“…PDK activity or PDK4 protein expression was shown to be increased in skeletal muscle of high-fatfed rats (11,(13)(14)(15), a well-established model of insulin resistance. PDK activity was also elevated in skeletal muscle of streptozotocin-induced diabetic animals (1-3), which are insulin resistant (16,17). On the other hand, increased insulin sensitivity in obese patients after malabsorptive bariatric surgery was associated with reduced muscle PDK4 expression (18).…”

mentioning

confidence: 99%

Insulin Regulation of Skeletal Muscle PDK4 mRNA Expression Is Impaired in Acute Insulin-Resistant States

et al. 2006

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We previously showed that insulin has a profound effect to suppress pyruvate dehydrogenase kinase (PDK) 4 expression in rat skeletal muscle. In the present study, we examined whether insulin's effect on PDK4 expression is impaired in acute insulin-resistant states and, if so, whether this change is accompanied by decreased insulin's effects to stimulate Akt and forkhead box class O (FOXO) 1 phosphorylation. To induce insulin resistance, conscious overnight-fasted rats received a constant infusion of Intralipid or lactate for 5 h, while a control group received saline infusion. Following the initial infusions, each group received saline or insulin infusion (n ‫؍‬ 6 or 7 each) for an additional 5 h, while saline, Intralipid, or lactate infusion was continued. Plasma glucose was clamped at basal levels during the insulin infusion. Compared with the control group, Intralipid and lactate infusions decreased glucose infusion rates required to clamp plasma glucose by ϳ60% (P < 0.01), confirming the induction of insulin resistance. Insulin's ability to suppress PDK4 mRNA level was impaired in skeletal muscle with Intralipid and lactate infusions, resulting in two-to threefold higher PDK4 mRNA levels with insulin (P < 0.05). Insulin stimulation of Akt and FOXO1 phosphorylation was also significantly decreased with Intralipid and lactate infusions. These data suggest that insulin's effect to suppress PDK4 gene expression in skeletal muscle is impaired in insulin-resistant states, and this may be due to impaired insulin signaling for stimulation of Akt and FOXO1 phosphorylation. Impaired insulin's effect to suppress PDK4 expression may explain the association between PDK4 overexpression and insulin resistance in skeletal muscle. Diabetes

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Effect of Fasting and Streptozotocin Diabetes on Insulin Binding and Action in the Isolated Mouse Soleus Muscle

Cited by 113 publications

References 39 publications

Effect of diabetes and fasting on GLUT-4 (muscle/fat) glucose-transporter expression in insulin-sensitive tissues. Heterogeneous response in heart, red and white muscle

Effect of diabetes and fasting on GLUT-4 (muscle/fat) glucose-transporter expression in insulin-sensitive tissues. Heterogeneous response in heart, red and white muscle

Insulin receptor binding and tyrosine kinase activity in liver and skeletal muscle from fasted rats

Insulin Regulation of Skeletal Muscle PDK4 mRNA Expression Is Impaired in Acute Insulin-Resistant States

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