Role of 5′-AMP-activated protein kinase in stimulation of glucose transport in response to inhibition of oxidative phosphorylation

Jing, Ming; Ismail‐Beigi, Faramarz

doi:10.1152/ajpcell.00321.2005

Cited by 23 publications

(28 citation statements)

References 33 publications

(54 reference statements)

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“…AMPK also phosphorylates and activates eNOS and the CFTR, both of which have been implicated as essential triggering elements in the development of IPC (10,16). Furthermore, antecedent ethanol ingestion, which induces late-phase PC and prevents postischemic leukocyte rolling and adhesion by an eNOS-dependent mechanism, also activates AMPK (21). These observations led us to postulate that direct pharmacological activation of AMPK should induce development of an anti-inflammatory state similar to that seen with ethanol or IPC.…”

Section: Discussionmentioning

confidence: 93%

“…These results are intriguing due to their divergence from the canonical view that NO release prevents both leukocyte rolling and adhesion (34) and that PC stimuli, such as antecedent ethanol ingestion, treatment with exogenous adenosine or adenosine A 2 receptor agonists, calcitonin gene-related peptide, bradykinin, or NO donors, which utilize NO to trigger entrance into an inflammatory state, prevent both types of adhesive interactions (12,21,22,33,43). Kubes and coworkers (25) have presented evidence that adherent leukocytes are almost exclusively recruited from the rolling cell population and that reductions in rolling by Ͼ90% are required before a significant effect on leukocyte adhesion is noted.…”

Section: Discussionmentioning

confidence: 99%

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5′-AMP-activated protein kinase activation prevents postischemic leukocyte-endothelial cell adhesive interactions

Gaskin

Kamada²,

Yusof³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

5′-AMP-activated protein kinase activation prevents postischemic leukocyte-endothelial cell adhesive interactions

Gaskin

Kamada²,

Yusof³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Several researchers have reported that stimulation of AMPK activity is associated with enhancement of GLUT1-mediated glucose transport. 6,7,28) The underlying mechanism shows that the enhanced response of glucose transport is mediated by activation of GLUT1 preexisting in the plasma membrane without affecting the cell-surface concentration of GLUT1. Collectively, the role of AMPK is critical in stimulation of glucose transport via GLUT1 activation and AMPK is involved in berberine-stimulated glucose transport, leading to a conclusion that berberine may augment the ability of GLUT1 to accelerate glucose transport by activating AMPK.…”

Section: Discussionmentioning

confidence: 99%

Berberine Activates GLUT1-Mediated Glucose Uptake in 3T3-L1 Adipocytes

Kim

Shin

Kim

et al. 2007

Biological & Pharmaceutical Bulletin

119

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Glucose uptake in insulin-sensitive tissues, which is dependent on the activity of glucose transporters (GLUTs), is a major regulatory process in the homeostatic control of blood glucose levels. GLUT1 is ubiquitously expressed for fulfilling basal glucose uptake, whereas GLUT4 is expressed in the insulin sensitive tissues in which glucose uptake is acutely stimulated by insulin.1) The regulatory mechanisms for the activity of glucose transporters have been extensively studied. It has been known that, at least two distinct signaling pathways are implicated in insulin-stimulated GLUT4 translocation and glucose uptake. One pathway results from the tyrosine phosphorylation of insulin receptor substrate (IRS) protein, leading to the activation of phosphatidylinositol 3-kinase (PI 3-K), and a second pathway occurs through the tyrosine phosphorylation of Clb, followed by the activation of TC10.2) Recent evidence has demonstrated that atypical protein kinase C (PKCz/l) is known to be a convergent target of the insulin-stimulated PI 3-K and TC10 pathways. 3)Related to GLUT1, it has been reported that activation of extracellular signal-regulated kinase (ERK) up-regulates GLUT1 expression, resulting in augmentation of basal glucose uptake in the absence of acute insulin stimulation. 4,5) In addition, an enhancement of GLUT1-mediated glucose transport is reportedly associated with an stimulation of AMP-activated protein kinase (AMPK). 6,7)Berberine, an isoquinoline alkaloid isolated from some Chinese medicinal herbs such as Coptidis Rhizoma and Cortex Phellodendri, has been used for the treatment of diarrhea an other gastrointestinal infections as an antibacterial drug in Chinese medicine. 8) Recently, it has been reported that berberine reduces serum cholesterol, triglycerides, and LDLcholesterol in hypercholesterolemic patients, with being suggested as a novel cholesterol-lowing drug.9) Recent studies have also shown that berberine has antihyperglycemic effects.10-12) However, elucidations of berberine action are not in agreement between research groups. One suggested an insulin-independent effect, 10) whereas others showed an insulin-secretion stimulating 11) or insulin-sensitizing effects. 13)Although the mechanism underlying the berberine effect is not known in detail, it might involve the activation of AMPK. Lee et al. suggested that berberine has beneficial effects in diabetes and obesity in part via activation of AMPK.14)Presently, we found that berberine displays an enhancing effect on GLUT1-mediated glucose transport in 3T3-L1 adipocytes. To explore a yet unidentified mechanism, we analyzed related signal transduction pathways that are activated by berberine. MATERIALS AND METHODS MaterialsAntibodies against IR, IRS-1, phospho-IRS-1 (Ser636/639), PKCz/l, phospho-PKCz/l (Thr410/403), p38, phospho-p38 (Thr180/Tyr182), ERK1/2, phospho-ERK1/2 (Thr202/Tyr204), AMPK, and phospho-AMPK (Thr172) were purchased from Cell Signaling Technology (Beverly, MA, U.S.A.). Anti-GLUT1 and anti-GLUT4 antibodies were purchased from San...

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“…production was decreased (Cunningham et al 1990). Thirdly, ethanol enhances intracellular AMP levels as well ( Jing & Ismail-Beigi 2006). As it is described above, the AMP/ATP ratio is increased, which leads to PRKAA2 activation.…”

Section: Discussionmentioning

confidence: 99%

Long-term moderate ethanol consumption restores insulin sensitivity in high-fat-fed rats by increasing SLC2A4 (GLUT4) in the adipose tissue by AMP-activated protein kinase activation

Gao

Guan

et al. 2008

Journal of Endocrinology

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The sole effect of either saturated fatty acid or moderate ethanol consumption on SLC2A4 (GLUT4) expression is widely reported but the combined effects of them remain obscure. Here, we observed their combined effects on SLC2A4 expression, explored the underlying mechanism mediated by AMP-activated protein kinase a (PRKAA2) and myocyte enhancer factor 2 (MEF2) both in vivo and in vitro. In the in vivo experiments, 36 male Wistar rats, divided into three groups, were fed with normal diet, high-fat (HF) diet, or HF diet plus ethanol for 22 weeks. We measured the expressions of total-PRKAA2 (T-PRKAA2), phosphorylated-PRKAA2 (pPRKAA2, activated form of PRKAA2), MEF2, and SLC2A4 in epididymal adipose tissues. In the in vitro experiments, primary adipocytes, isolated from normal Wistar rats, were incubated in the presence or absence of palmitate, ethanol, and compound C (an PRKAA2 inhibitor) for 1 h. Thereafter, T-PRKAA2, pPRKAA2, MEF2, and SLC2A4 expressions were measured. We found that both HF diet and in vitro exposition to palmitate impaired SLC2A4 expression in rat adipocytes with a parallel reduction in PRKAA2 activation and MEF2 expression. This impairment was reversed by ethanol administration. We further demonstrated that ethanol-mediated PRKAA2 activation stimulates MEF2 and SLC2A4 expressions in adipocytes, as evidenced by compound C blockade of these effects. In summary, long-term moderate ethanol consumption reversed the adverse effect of saturated fatty acid on SLC2A4 expression in adipocytes, which was likely to be a result of PRKAA2 activation and subsequent up-regulation of MEF2 and SLC2A4 expressions.

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Role of 5′-AMP-activated protein kinase in stimulation of glucose transport in response to inhibition of oxidative phosphorylation

Cited by 23 publications

References 33 publications

5′-AMP-activated protein kinase activation prevents postischemic leukocyte-endothelial cell adhesive interactions

5′-AMP-activated protein kinase activation prevents postischemic leukocyte-endothelial cell adhesive interactions

Berberine Activates GLUT1-Mediated Glucose Uptake in 3T3-L1 Adipocytes

Long-term moderate ethanol consumption restores insulin sensitivity in high-fat-fed rats by increasing SLC2A4 (GLUT4) in the adipose tissue by AMP-activated protein kinase activation

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