Hepatocyte Growth Factor Induces Glucose Uptake in 3T3-L1 Adipocytes through A Gab1/Phosphatidylinositol 3-Kinase/Glut4 Pathway

Bertola, Adeline; Bonnafous, Stéphanie; Cormont, Mireille; Anty, Rodolphe; Tanti, Jean‐François; Tran, Albert; Marchand-Brustel, Y. Le; Gual, Philippe

doi:10.1074/jbc.m611770200

Cited by 36 publications

(33 citation statements)

References 39 publications

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“…It has recently been reported that HGF enhances glucose transport in pancreatic beta cells and adipocytes (3,6). The current studies demonstrate for the first time that HGF also acutely increases glucose uptake in mouse soleus muscle ex vivo and rat L6 myotubes in vitro and that this effect is translated into an augmentation of glucose utilization, but not storage, in L6 myotubes.…”

Section: Discussionsupporting

confidence: 48%

“…HGF has also been shown to up-regulate the Na ϩ /glucose co-transporter SGLT1 and the facilitative glucose transporter Glut-5 in rat intestine epithelial cells (5). Furthermore, HGF promotes Glut-4 translocation to the cellular membrane and enhances glucose uptake through phosphatidylinositol 3-kinase (PI3K) activation in 3T3-L1 adipocytes (6). Taken together, these studies demonstrate HGFmediated regulatory effects on glucose transport in three different cells types: beta cells, intestinal epithelial cells, and adipocytes.…”

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confidence: 99%

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Hepatocyte Growth Factor Is a Novel Stimulator of Glucose Uptake and Metabolism in Skeletal Muscle Cells

Perdomo¹,

Martínez-Brocca²,

Bhatt

et al. 2008

Journal of Biological Chemistry

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Skeletal muscle plays a major role in glucose and lipid metabolism. Active hepatocyte growth factor (HGF) is present in the extracellular matrix in skeletal muscle. However, the effects of HGF on glucose and lipid metabolism in skeletal muscle are completely unknown. We therefore examined the effects of HGF on deoxyglucose uptake (DOGU), glucose utilization, and fatty acid oxidation (FAO) in skeletal muscle cells. HGF significantly enhanced DOGU in mouse soleus muscles in vitro. Furthermore, HGF significantly increased: (i) DOGU in a time-and dose-dependent manner; (ii) glucose utilization; and (iii) plasma membrane expression of Glut-1 and Glut-4 in the rat skeletal muscle model of L6 myotubes. HGF-mediated effect on DOGU was dependent on the activation of phosphatidylinositol 3-kinase signaling pathway. On the other hand, HGF markedly and significantly decreased FAO in L6 myotubes without affecting the activities of carnitine palmitoyltransferase I and II. Collectively, these results indicate that HGF is a potent activator of glucose transport and metabolism and also a strong inhibitor of FAO in rodent myotubes. HGF, through its ability to stimulate glucose transport and metabolism and to impair FAO, may participate in the regulation of glucose disposal in skeletal muscle.

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Section: Discussionsupporting

confidence: 48%

mentioning

confidence: 99%

Hepatocyte Growth Factor Is a Novel Stimulator of Glucose Uptake and Metabolism in Skeletal Muscle Cells

Perdomo¹,

Martínez-Brocca²,

Bhatt

et al. 2008

Journal of Biological Chemistry

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“…Growth factors, including HGF, EGF and TNF-, have been shown to increase glucose utilization in a variety of cells (Bertola et al, 2007;Boussouar and Benahmed, 1999;Hsu and Sabatini, 2008;Perdomo et al, 2008;Véga et al, 2002). Furthermore, Kaplan and colleagues (Kaplan et al, 2000) have shown that HGF also enhances glycolysis and oxidative phosphorylation in murine mammary cells.…”

Section: Hgf Increases Proton Production Inducing Acidification Of Tmentioning

confidence: 99%

HGF-induced invasion by prostate tumor cells requires anterograde lysosome trafficking and activity of Na+-H+ exchangers

Steffan

Williams

Welbourne

et al. 2010

Journal of Cell Science

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SummaryHepatocyte growth factor (HGF) is found in tumor microenvironments, and interaction with its tyrosine kinase receptor Met triggers cell invasion and metastasis. It was previously shown that acidic extracellular pH stimulated peripheral lysosome trafficking, resulting in increased cathepsin B secretion and tumor cell invasion, which was dependent upon sodium-proton exchanger (NHE) activity. We now demonstrate that HGF induced the trafficking of lysosomes to the cell periphery, independent of HGF-induced epithelialmesenchymal transition. HGF-induced anterograde lysosome trafficking depended upon the PI3K pathway, microtubules and RhoA, resulting in increased cathepsin B secretion and invasion by the cells. HGF-induced NHE activity via increased net acid production, and inhibition of NHE activity with 5-(N-ethyl-N-isopropyl)-amiloride (EIPA), or a combination of the NHE1-specific drug cariporide and the NHE3-specific drug s3226 prevented HGF-induced anterograde trafficking and induced retrograde trafficking in HGFoverexpressing cells. EIPA treatment reduced cathepsin B secretion and HGF-induced invasion by the tumor cells. Lysosomes were located more peripherally in Rab7-shRNA-expressing cells and these cells were more invasive than control cells. Overexpression of the Rab7 effector protein, RILP, resulted in a juxtanuclear location of lysosomes and reduced HGF-induced invasion. Together, these results suggest that the location of lysosomes is an inherently important aspect of invasion by tumor cells.

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“…Proteins (50 g) were separated by SDS-PAGE using a 10% resolving gel. The Western blotting was performed as previously described (27). The proteins were probed with anti-OPN (AKm2A1) or anti-GAPDH (FL-335) antibodies (Santa Cruz Biotechnology, Santa Cruz, CA) at 1 g/ml.…”

Section: Methodsmentioning

confidence: 99%

Elevated Expression of Osteopontin May Be Related to Adipose Tissue Macrophage Accumulation and Liver Steatosis in Morbid Obesity

et al. 2009

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OBJECTIVE-Osteopontin (OPN) plays an important role in the development of insulin resistance and liver complications in dietary murine models. We aimed to determine the expression pattern of OPN and its receptor CD44 in obese patients and mice according to insulin resistance and liver steatosis.RESEARCH DESIGN AND METHODS-OPN and CD44 expressions were studied in 52 morbidly obese patients and in mice. Cellular studies were performed in HepG2 cells. RESULTS-HepaticOPN and CD44 expressions were strongly correlated with liver steatosis and insulin resistance in obese patients and mice. This increased OPN expression could be due to the accumulation of triglycerides, since fat loading in HepG2 promotes OPN expression. In contrast, OPN expression in adipose tissue (AT) was enhanced independently of insulin resistance and hepatic steatosis in obese patients. The elevated OPN expression in AT was paralleled with the AT macrophage infiltration, and both phenomena were reversed after weight loss. The circulating OPN level was slightly elevated in obese patients and was not related to liver steatosis. Further, AT did not appear to secrete OPN. In contrast, bariatric surgery-induced weight loss induced a strong increase in circulating OPN. CONCLUSIONS-The modestly elevated circulating OPN levels in morbidly obese patients were not related to liver steatosis and did not appear to result from adipose tissue secretion. In subcutaneous AT, expression of OPN was directly related to macrophage accumulation independently from liver complications. In contrast, hepatic OPN and CD44 expressions were related to insulin resistance and steatosis, suggesting their local implication in the progression of liver injury. Diabetes 58: 125-133, 2009

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Hepatocyte Growth Factor Induces Glucose Uptake in 3T3-L1 Adipocytes through A Gab1/Phosphatidylinositol 3-Kinase/Glut4 Pathway

Cited by 36 publications

References 39 publications

Hepatocyte Growth Factor Is a Novel Stimulator of Glucose Uptake and Metabolism in Skeletal Muscle Cells

Hepatocyte Growth Factor Is a Novel Stimulator of Glucose Uptake and Metabolism in Skeletal Muscle Cells

HGF-induced invasion by prostate tumor cells requires anterograde lysosome trafficking and activity of Na+-H+ exchangers

Elevated Expression of Osteopontin May Be Related to Adipose Tissue Macrophage Accumulation and Liver Steatosis in Morbid Obesity

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