Dexamethasone-induced changes in glucose transporter 4 in rat heart muscle, skeletal muscle and adipocytes

Oda, Naohisa; Nakai, Asami; Mokuno, T; Sawai, Yoshikuni; Nishida, Yoko; Mano, Takamitsu; Asano, Kiyoshi; Itoh, Yasuto; Kotake, Motoko; Kato, S; Masunaga, Rumi; Iwase, Katsumi; Tsujimura, Tohru; Itoh, Mitsuyasu; Kawabe, Takao; Nagasaka, Akio

doi:10.1530/eje.0.1330121

Cited by 27 publications

(23 citation statements)

References 22 publications

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“…In muscle, LC-n-3 PUFA also inhibited PI 3Ј-kinase activity without alteration of upstream insulin signaling and amplified dexamethasone-induced inhibition of PI 3Ј-kinase activity, whereas GLUT4 content was affected neither by dexamethasone treatment as previously reported (12,23) nor by LC-n-3 PUFA. This does not exclude that GLUT4 content into plasma membranes was decreased secondarily to decreased translocation of GLUT4, itself being the consequence of decreased PI 3Ј-kinase activity.…”

Section: Discussionsupporting

confidence: 58%

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Corporeau¹,

Foll²,

Taouis³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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The present work aimed to study in rats whether substitution of a low level of fish oil (FO; 2.2% of calories) into a low-fat diet (6.6% of calories from fat as peanut-rape oil or control diet) 1) has a tissue-specific effect on insulin signaling pathway and 2) prevents dexamethasone-induced alteration of insulin signaling in liver, muscle, and adipose tissue. Sixteen rats were used for study of insulin signaling, and sixteen rats received an oral glucose load (3 g/kg). Eight rats/group consumed control diet or diet containing FO over 5 wk. Four rats from each group received a daily intraperitoneal injection of saline or dexamethasone (1 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) for the last 5 days of feeding. In liver, FO decreased phosphatidylinositol 3Ј-kinase (PI 3Ј-kinase) activity by 54% compared with control diet. A similar result was obtained in muscle. In both liver and muscle, FO clearly amplified the effect of dexamethasone. FO did not alter early steps of insulin signaling, and in muscle GLUT4 protein content remained unaltered. In adipose tissue, FO increased PI 3Ј-kinase activity by 74%, whereas dexamethasone decreased it by 65%; inhibition of PI 3Ј-kinase activity by dexamethasone was similar in rats fed FO or control diet, and GLUT4 protein content was increased by 61% by FO. Glycemic and insulinemic responses to oral glucose were not modified by FO. In conclusion, FO increased PI 3Ј-kinase activity in adipose tissue while inhibiting it in liver and muscle. The maintenance of whole body glucose homeostasis suggests an important role of adipose tissue for control of glucose homeostasis. eicosapentaenoic acid; docosahexaenoic acid; insulin resistance; polyunsaturated fatty acids INSULIN RESISTANCE is a common characteristic of type 2 diabetes, obesity, and metabolic syndrome (31), which results from genetic background and/or environmental factors (39). In patients with type 2 diabetes, liver, skeletal muscle, and adipose tissue are resistant to insulin action (8). In skeletal muscle of patients with type 2 diabetes, tyrosine phosphorylation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1) and phosphatidylinositol (PI) 3Ј-kinase activity are markedly impaired (5), whereas expressions of IR, IRS-1, or the p85␣ subunit of PI 3Ј-kinase remain unaltered (17). Muscle GLUT4 protein is decreased and GLUT4 translocation is reduced by 90% during hyperinsulinemia (27). These alterations of insulin signaling in muscle participate in the decrease in muscle glucose transport, one of the main features of type 2 diabetes (7). In adipose tissue, basal expression of GLUT4 and IRS-1 are reduced, and upregulation of p85␣ by insulin is completely blunted (11).In rats, a high-fat diet (60% of calories from fat as safflower oil) inhibits liver and muscle PI 3Ј-kinase activity (35). In addition, muscle GLUT4 content and adipose tissue GLUT4 gene expression are reduced (35). These alterations likely explain the impairment of glucose transport in these tissues and at whole body level (33). When fish oil (FO), rich in long-chai...

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Section: Discussionsupporting

confidence: 58%

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Corporeau¹,

Foll²,

Taouis³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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“…In fact, dexamethasone did not change GLUT-4 expression levels while decreasing GLUT-4 translocation and glucose uptake in 3T3-L1 cells. 30 Dexamethasone also led to decreased GLUT-4 expression in adipocytes in one study, 31 …”

Section: Discussionmentioning

confidence: 99%

Lactoferrin increases 172ThrAMPK phosphorylation and insulin-induced p473SerAKT while impairing adipocyte differentiation

et al. 2009

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Objective: Lactoferrin is a pleiotropic glycoprotein of the innate immune system with known effects on immunomodulation and cell differentiation. To gain an insight into the interaction among obesity, inflammation and insulin action, we aimed to examine the effects of lactoferrin on adipogenesis and the response to insulin in human hepatocarcinoma (HepG2) and 3T3-L1 cell lines. Design: The cells were cultured with increasing lactoferrin concentration under non-inflammatory, inflammatory and standard conditions. The response to insulin was evaluated through 473Ser AKT phosphorylation. The effects of lactoferrin on adipogenesis were studied through the expression of different lipogenic markers, AMP-activated protein kinase (AMPK) activation, retinoblastoma (Rb) activity and Oil Red O staining in 3T3-L1 cells. Results: Lactoferrin increased dose-dependent insulin-induced 473Ser AKT phosphorylation in both cell lines. Inflammationinduced decreased 473Ser AKT phosphorylation was also rescued by lactoferrin. In addition, lactoferrin led to increased p172Thr AMPK during 3T3-L1 differentiation and to decreased adipogenesis (as shown by decreased expression of fatty acid synthase, acetyl-coenzyme A carboxylase-a and peroxisome proliferator-activated receptor-g in parallel with decreased formation of lipid droplets). Lactoferrin also increased dose-dependent Rb activity (expression and hypophosphorylation) during 3T3-L1 differentiation. Conclusion: Lactoferrin administration increased insulin-induced 473Ser AKT phosphorylation, even in those conditions wherein the response to insulin was downregulated, and led to blunted adipogenesis in the context of increased p172Thr AMPK and Rb activity.

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“…However, translocation of GLUT 4 to the cell surface in response to insulin and to other stimuli (e.g. hypoxia) is inhibited in the presence of glucocorticoids [29][30][31][32][33].…”

Section: Metabolic Determinants Of Peripheral Glucose Uptakementioning

confidence: 99%

Glucocorticoids and insulin resistance: old hormones, new targets

1999

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Insulin resistance has been proposed as a mediator of the association between risk factors for cardiovascular disease in the population. The clinical syndrome of glucocorticoid excess (Cushing's syndrome) is associated with glucose intolerance, obesity and hypertension. By opposing the actions of insulin, glucocorticoids could contribute to insulin resistance and its association with other cardiovascular risk factors. In this review, we describe briefly the known mechanisms of insulin resistance and highlight the potential mechanisms for the effect of glucocorticoids. We then discuss factors which modulate the influence of glucocorticoids on insulin sensitivity; this highlights a novel therapeutic strategy to manipulate glucocorticoid action which may prove to be a useful tool in treating subjects with insulin resistance. Finally, we describe evidence from human studies that glucocorticoids make an important contribution to the pathophysiology of insulin resistance in the population.

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Dexamethasone-induced changes in glucose transporter 4 in rat heart muscle, skeletal muscle and adipocytes

Cited by 27 publications

References 22 publications

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Adipose tissue compensates for defect of phosphatidylinositol 3′-kinase induced in liver and muscle by dietary fish oil in fed rats

Lactoferrin increases 172ThrAMPK phosphorylation and insulin-induced p473SerAKT while impairing adipocyte differentiation

Glucocorticoids and insulin resistance: old hormones, new targets

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