scholarly journals Fatty Acids Stimulate Glucose Uptake by the PI3K/AMPK/Akt and PI3K/ERK1/2 Pathways

10.5772/52456 ◽  
2012 ◽  
Author(s):  
Jing Pu ◽  
Pingsheng Liu
Keyword(s):  
Fatty Acids ◽  
Glucose Uptake

scholarly journals Insulinomimetic Zn(II) Complexes as Evaluated by Both Glucose-Uptake Activity and Inhibition of Free Fatty Acids Release in Isolated Rat Adipocytes

2008 ◽  
Vol 56 (8) ◽  
pp. 1181-1183 ◽  
Author(s):  
Midori Nishide ◽  
Yutaka Yoshikawa ◽  
Eriko U. Yoshikawa ◽  
Kinuyo Matsumoto ◽  
Hiromu Sakurai ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Rat Adipocytes ◽  
Uptake Activity ◽  
Isolated Rat

scholarly journals Distinct effects of oleic acid and itstrans-isomer elaidic acid on the expression of myokines and adipokines in cell models

2011 ◽  
Vol 105 (8) ◽  
pp. 1226-1234 ◽  
Author(s):  
Nuria Granados ◽  
Jaume Amengual ◽  
Joan Ribot ◽  
Andreu Palou ◽  
M. Luisa Bonet
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Oleic Acid ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Elaidic Acid ◽  
C2c12 Myotubes ◽  
Cell Models ◽  
Monounsaturated Fat ◽  
Expression Levels

Trans-fatty acids (TFA) andcis-monounsaturated fat appear to exert detrimental and beneficial effects, respectively, on glucose metabolism and insulin sensitivity. Adipose tissue and skeletal muscle are a source of signalling proteins (adipokines and myokines), some of which have been related to the control of insulin sensitivity. Here, we investigated the possible differential effects of elaidic acid (EA;trans-9-18 : 1) – the major component in industrially produced TFA – and oleic acid (OA;cis-9-18 : 1) – itscis-isomer naturally present in food – on cellular glucose uptake and the expression of selected myokines and adipokines using cell models. Differentiated C2C12 myotubes and 3T3-L1 adipocytes were pretreated with the vehicle (control cells) or fatty acids for 24 h, after which basal and insulin-stimulated 2-deoxyglucose uptake and the expression of selected signalling proteins were measured. In C2C12 myotubes, pretreatment with OA, but not with EA, led to increased insulin-stimulated 2-deoxyglucose uptake and IL-6 expression levels, while pretreatment with EA, but not with OA, led to reduced IL-15 mRNA levels and increased TNF-α expression levels. In 3T3-L1 adipocytes, exposure to OA, but not to EA, resulted in reduced resistin gene expression and increased adiponectin gene expression. The results show evidence of distinct, direct effects of OA and EA on muscle glucose uptake and the expression of target myokines and adipokines, thus suggesting novel mechanisms by whichcis- andtrans-monounsaturated fat may differentially affect systemic functions.

scholarly journals Free Fatty acids receptors (FFAR2 and FFAR3) control cell proliferation by regulating cellular glucose uptake

2019 ◽  
Author(s):  
Mohammad Aziz ◽  
Saeed Al Mahri ◽  
Amal Alghamdi ◽  
Maaged AlAkiel ◽  
Monira Al Aujan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Fatty Acids ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Free Fatty Acids ◽  
Glucose Uptake ◽  
Microarray Data ◽  
Free Fatty Acid Receptors

Abstract Background Colorectal cancer is a worldwide problem which has been associated with changes in diet and lifestyle pattern. As a result of colonic fermentation of dietary fibres, short chain free fatty acids are generated which activate Free Fatty Acid Receptors 2 and 3 (FFAR2 and FFAR3). FFAR2 and FFAR3 genes are abundantly expressed in colonic epithelium and play an important role in the metabolic homeostasis of colonic epithelial cells. Earlier studies point to the involvement of FFAR2 in colorectal carcinogenesis. Methods Transcriptome analysis console was used to analyse microarray data from patients and cell lines. We employed shRNA mediated down regulation of FFAR2 and FFAR3 genes which was assessed using qRT-PCR. Assays for glucose uptake and cAMP generation was done along with immunofluorescence studies. For measuring cell proliferation, we employed real time electrical impedance based assay available from xCelligence. Results Microarray data analysis of colorectal cancer patient samples showed a significant down regulation of FFAR2 gene expression. This prompted us to study the FFAR2 in colorectal cancer. Since, FFAR3 shares significant structural and functional homology with FFAR2, we knocked down both these receptors in colorectal cancer cell line HCT 116. These modified cell lines exhibited higher proliferation rate and were found to have increased glucose uptake as well as increased level of GLUT1. Since, FFAR2 and FFAR3 signal through G protein subunit (Gαi), knockdown of these receptors was associated with increased cAMP. Inhibition of PKA did not alter the growth and proliferation of these cells indicating a mechanism independent of cAMP/PKA pathway. Conclusion: Our results suggest role of FFAR2/FFAR3 genes in increased proliferation of colon cancer cells via enhanced glucose uptake and exclude the role of protein kinase A mediated cAMP signalling. Alternate pathways could be involved that would ultimately result in increased cell proliferation as a result of down regulated FFAR2/FFAR3 genes. This study paves the way to understand the mechanism of action of short chain free fatty acid receptors in colorectal cancer.

Environmental influences on adiponectin levels in humans

2007 ◽  
Vol 32 (3) ◽  
pp. 505-511 ◽  
Author(s):  
Pascal Imbeault
Keyword(s):  
Fatty Acids ◽  
Weight Loss ◽  
Food Intake ◽  
Lipid Oxidation ◽  
Glucose Uptake ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Environmental Influences ◽  
Nonesterified Fatty Acids ◽  
Glucose Output

In addition to its classic role in the storage and release of nonesterified fatty acids, the adipocyte is now recognized as a critical source of many endocrine signals. Of these signals, adiponectin has been found to promote lipid oxidation and glucose uptake in skeletal muscles and to reduce glucose output in the liver. Because of the effects of adiponectin on these organs, the search for factors or conditions that could positively influence the synthesis of this adipocyte-derived protein has drawn a great deal of interest. This brief review explores the effects of environmental influences such as weight loss, acute food intake, exercise, and cold exposure on circulating adiponectin levels in humans.

Saturated, but not n-6 polyunsaturated, fatty acids induce insulin resistance: role of intramuscular accumulation of lipid metabolites

2006 ◽  
Vol 100 (5) ◽  
pp. 1467-1474 ◽  
Author(s):  
Jong Sam Lee ◽  
Srijan K. Pinnamaneni ◽  
Su Ju Eo ◽  
In Ho Cho ◽  
Jae Hwan Pyo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Polyunsaturated Fatty Acids ◽  
Glucose Uptake ◽  
High Fat ◽  
Insulin Resistant ◽  
L6 Myotubes ◽  
Lipid Metabolites

Consumption of a Western diet rich in saturated fats is associated with obesity and insulin resistance. In some insulin-resistant phenotypes this is associated with accumulation of skeletal muscle fatty acids. We examined the effects of diets high in saturated fatty acids (Sat) or n-6 polyunsaturated fatty acids (PUFA) on skeletal muscle fatty acid metabolite accumulation and whole-body insulin sensitivity. Male Sprague-Dawley rats were fed a chow diet (16% calories from fat, Con) or a diet high (53%) in Sat or PUFA for 8 wk. Insulin sensitivity was assessed by fasting plasma glucose and insulin and glucose tolerance via an oral glucose tolerance test. Muscle ceramide and diacylglycerol (DAG) levels and triacylglycerol (TAG) fatty acids were also measured. Both high-fat diets increased plasma free fatty acid levels by 30%. Compared with Con, Sat-fed rats were insulin resistant, whereas PUFA-treated rats showed improved insulin sensitivity. Sat caused a 125% increase in muscle DAG and a small increase in TAG. Although PUFA also resulted in a small increase in DAG, the excess fatty acids were primarily directed toward TAG storage (105% above Con). Ceramide content was unaffected by either high-fat diet. To examine the effects of fatty acids on cellular lipid storage and glucose uptake in vitro, rat L6 myotubes were incubated for 5 h with saturated and polyunsaturated fatty acids. After treatment of L6 myotubes with palmitate (C16:0), the ceramide and DAG content were increased by two- and fivefold, respectively, concomitant with reduced insulin-stimulated glucose uptake. In contrast, treatment of these cells with linoleate (C18:2) did not alter DAG, ceramide levels, and glucose uptake compared with controls (no added fatty acids). Both 16:0 and 18:2 treatments increased myotube TAG levels (C18:2 vs. C16:0, P < 0.05). These results indicate that increasing dietary Sat induces insulin resistance with concomitant increases in muscle DAG. Diets rich in n-6 PUFA appear to prevent insulin resistance by directing fat into TAG, rather than other lipid metabolites.

scholarly journals Palmitate and oleate exert differential effects on insulin signalling and glucose uptake in human skeletal muscle cells

2017 ◽  
Vol 6 (5) ◽  
pp. 331-339 ◽  
Author(s):  
Selina Mäkinen ◽  
Yen H Nguyen ◽  
Paulina Skrobuk ◽  
Heikki A Koistinen
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Er Stress ◽  
Glucose Uptake ◽  
Insulin Signalling ◽  
Ros Production ◽  
Human Myotubes ◽  
Human Skeletal Muscle Cells ◽  
Concomitant Exposure

Saturated fatty acids are implicated in the development of insulin resistance, whereas unsaturated fatty acids may have a protective effect on metabolism. We tested in primary human myotubes if insulin resistance induced by saturated fatty acid palmitate can be ameliorated by concomitant exposure to unsaturated fatty acid oleate. Primary human myotubes were pretreated with palmitate, oleate or their combination for 12 h. Glucose uptake was determined by intracellular accumulation of [3H]-2-deoxy-d-glucose, insulin signalling and activation of endoplasmic reticulum (ER) stress by Western blotting, and mitochondrial reactive oxygen species (ROS) production by fluorescent dye MitoSOX. Exposure of primary human myotubes to palmitate impaired insulin-stimulated Akt-Ser473, AS160 and GSK-3β phosphorylation, induced ER stress signalling target PERK and stress kinase JNK 54 kDa isoform. These effects were virtually abolished by concomitant exposure of palmitate-treated myotubes to oleate. However, an exposure to palmitate, oleate or their combination reduced insulin-stimulated glucose uptake. This was associated with increased mitochondrial ROS production in palmitate-treated myotubes co-incubated with oleate, and was alleviated by antioxidants MitoTempo and Tempol. Thus, metabolic and intracellular signalling events diverge in myotubes treated with palmitate and oleate. Exposure of human myotubes to excess fatty acids increases ROS production and induces insulin resistance.

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