Insulin action on glucose transport and plasma membrane GLUT4 content in skeletal muscle from patients with NIDDM

Zierath, Juleen R.; He, Lijing; Gumà, Anna; Wahlström, Erik; Klip, Amira; Wallberg-Henriksson, Harriet

doi:10.1007/bf02658504

Cited by 359 publications

(280 citation statements)

References 50 publications

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“…Tissue-specific regulation of GLUT4 has also been described in animals fed a high fat diet, which resulted in decreased GLUT4 mRNA expression in white adipose tissue but not skeletal muscle [51,52]. Further analysis has suggested that the defect in muscle glucose uptake in patients with Type 2 diabetes could be associated with impairments in trafficking and/or translocation of GLUT4 to the plasma membrane [53,54,55]. In agreement, high fat-induced skeletal muscle insulin resistance in animals has been associated with defects in the translocation and intrinsic activity of GLUT4.…”

Section: Discussionmentioning

confidence: 99%

Peripheral insulin resistance develops in transgenic rats overexpressing phosphoenolpyruvate carboxykinase in the kidney

et al. 2003

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Aims/hypothesis. To study the secondary consequences of impaired suppression of endogenous glucose production (EGP) we have created a transgenic rat overexpressing the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) in the kidney. The aim of this study was to determine whether peripheral insulin resistance develops in these transgenic rats. Methods. Whole body rate of glucose disappearance (R d ) and endogenous glucose production were measured basally and during a euglycaemic/hyperinsulinaemic clamp in phosphoenolpyruvate carboxykinase transgenic and control rats using [6-3 H]-glucose. Glucose uptake into individual tissues was measured in vivo using 2-[1-14 C]-deoxyglucose. Results. Phosphoenolpyruvate carboxykinase transgenic rats were heavier and had increased gonadal and infrarenal fat pad weights. Under basal conditions, endogenous glucose production was similar in phosphoenolpyruvate carboxykinase transgenic and control rats (37.4±1.1 vs 34.6±2.6 µmol/kg/min). Moderate hyperinsulinaemia (810 pmol/l) completely suppressed EGP in control rats (−0.6±5.5 µmol/kg/min, p<0.05) while there was no suppression in phosphoenolpyruvate carboxykinase rats (45.2±7.9 µmol/kg/min). Basal R d was comparable between PEPCK transgenic and control rats (37.4±1.1 vs 34.6±2.6 µmol/kg/min) but under insulin-stimulated conditions the increase in R d was greater in control compared to phosphoenolpyruvate carboxykinase transgenic rats indicative of insulin resistance (73.4±11.2 vs 112.0±8.0 µmol/kg/min, p<0.05). Basal glucose uptake was reduced in white and brown adipose tissue, heart and soleus while insulin-stimulated transport was reduced in white and brown adipose tissue, white quadriceps, white gastrocnemius and soleus in phosphoenolpyruvate carboxykinase transgenic compared to control rats. The impairment in both white and brown adipose tissue glucose uptake in phosphoenolpyruvate carboxykinase transgenic rats was associated with a decrease in GLUT4 protein content. In contrast, muscle GLUT4 protein, triglyceride and long-chain acylCoA levels were comparable between PEPCK transgenic and control rats. Conclusions/interpretation. A primary defect in suppression of EGP caused adipose tissue and muscle insulin resistance. [Diabetologia (2003[Diabetologia ( ) 46:1338[Diabetologia ( -1347

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Section: Discussionmentioning

confidence: 99%

Peripheral insulin resistance develops in transgenic rats overexpressing phosphoenolpyruvate carboxykinase in the kidney

et al. 2003

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“…Akt/protein kinase B is then phosphorylated through phosphorylation of the tyrosine site of IRS-1. In obese, insulin-resistant subjects, GLUT4 translocation to the plasma membrane is attenuated by the inhibition of insulin signaling pathways such as IR, IRS-1 and Akt activation (Zierath et al 1996). Therefore, to clarify the activation of GLUT4 translocation associated with improvement of insulin resistance by Fx, we investigated IR mRNA expression and Akt phosphorylation in the soleus and EDL muscles.…”

Section: Ir Mrna Expression and Akt Phosphorylation By Fx In Soleus Amentioning

confidence: 99%

Fucoxanthin promotes translocation and induction of glucose transporter 4 in skeletal muscles of diabetic/obese KK-A mice

2012

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Fucoxanthin (Fx) isolated from Undaria pinnatifida suppresses the development of hyperglycemia and hyperinsulinemia of diabetic/obese KK-A y mice after two weeks of feeding 0.2% Fx-containing diet. In the soleus muscle of KK-A y mice that were fed Fx, glucose transporter 4 (GLUT4) translocation to plasma membranes from cytosol was promoted. On the other hand, Fx increased GLUT4 expression levels in the extensor digitorum longus (EDL) muscle, although GLUT4 translocation tended to increase. The expression levels of insulin receptor (IR) mRNA and phosphorylation of Akt, which are in upstream of the insulin signaling pathway regulating GLUT4 translocation, were also enhanced in the soleus and EDL muscles of the mice fed Fx. Furthermore, Fx induced peroxisome proliferator activated receptor  coactivator-1 (PGC-1), which has been reported to increase GLUT4 expression, in both soleus and EDL muscles. These results suggest that in diabetic/obese KK-A y mice, Fx improves hyperglycemia by activating the insulin signaling pathway, including GLUT4 translocation, and inducing GLUT4 expression in the soleus and EDL muscles, respectively, of diabetic/obese KK-A y mice.

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“…Therefore, we determined the presence of the glucose transporter proteins GLUT1 and GLUT4 in the plasma membrane of rat skeletal muscle to assess whether in vivo glucose infusion induced the translocation of the transporters. Because insulin induces the translocation of GLUT4 particularly to the transversal tubules (TT) of the plasma membrane [42,50,51] this membrane compartment was also studied. The identity and purity of the TT fraction was assessed by the presence of a 1 dihydropyridine receptor which is exclusively located in the TT membranes [52].…”

Section: Insulin Signalling Cascadementioning

confidence: 99%

Prolonged glucose infusion into conscious rats inhibits early steps in insulin signalling and induces translocation of GLUT4 and protein kinase C in skeletal muscle

et al. 2002

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Impairment of the glucose transport in the insulinsensitive tissues contributes to the pathogenesis of Type II (non-insulin-dependent) diabetes mellitus [1,2]. Skeletal muscle represents the most important tissue for the maintenance of a balanced postprandial glucose homeostasis; about 80 % of insulin-stimulated glucose uptake is accounted for by muscle [3±5]. The influx of glucose into muscle is mediated by the glucose transporter proteins GLUT1 and the insulinsensitive GLUT4 [6±11]. Insulin induces the translocation of GLUT4 to the sarcolemma and to special- Abstract Aims/hypothesis. Previous studies on diabetic patients have shown that hyperglycaemia increases glucose uptake in an apparently insulin-independent manner. However, the molecular mechanism has not been clarified. Methods. We studied rats receiving continuous glucose infusion to address this question. In this animal model, rats accommodate systemic glucose oversupply and rapidly develop insulin resistance. Results. Glucose infusion increased both plasma glucose and insulin concentrations to peak after one day. In spite of continuous glucose infusion normoglycaemia was reached after 5 days while insulin concentrations remained higher. Focusing our studies in day 2 (hyperglycaemia/hyperinsulinaemia) and day 5 (normoglycaemia/hyperinsulinaemia) we found, particularly in day 5, that the early steps of the insulin signalling cascade in skeletal muscle of glucose-infused rats were not more activated when compared to control animals as assessed by a comparable phosphorylation of the insulin receptor, IRS-1 and PKB and by an unaltered IRS-1-associated Ptd(Ins) 3' kinase activity. Continuous glucose infusion induced GLUT4 protein expression and translocation to the plasma membrane while neither expression nor translocation of GLUT1 was affected. Translocation of PKC-bI, -bII (> threefold) and -a, -q (to a lesser extent) to the plasma membrane was significantly induced after 2 days but not after 5 days of glucose infusion when normoglycaemia was reached. Conclusions/interpretation. Our data support the hypothesis that continuous glucose infusion induces translocation of GLUT4 while the early steps of the insulin signalling cascade were not increased. These effects could be mediated by activation of PKC. [Diabetologia (2002) 45: 356±368]

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Insulin action on glucose transport and plasma membrane GLUT4 content in skeletal muscle from patients with NIDDM

Cited by 359 publications

References 50 publications

Peripheral insulin resistance develops in transgenic rats overexpressing phosphoenolpyruvate carboxykinase in the kidney

Peripheral insulin resistance develops in transgenic rats overexpressing phosphoenolpyruvate carboxykinase in the kidney

Fucoxanthin promotes translocation and induction of glucose transporter 4 in skeletal muscles of diabetic/obese KK-A mice

Prolonged glucose infusion into conscious rats inhibits early steps in insulin signalling and induces translocation of GLUT4 and protein kinase C in skeletal muscle

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