Free Fatty Acid Liberation and Cellular Swelling During Cerebral Ischemia: the Role of Excitatory Amino Acids

1994 ◽  
pp. 242-245 ◽  
Author(s):  
Yoichi Katayama ◽  
T. Kawamata ◽  
T. Maeda ◽  
T. Tsubokawa
Keyword(s):  
Amino Acids ◽  
Fatty Acid ◽  
Cerebral Ischemia ◽  
Free Fatty Acid ◽  
Excitatory Amino Acids ◽  
Cellular Swelling

Cardiovascular responses to global cerebral ischemia: role of excitatory amino acids in the ventrolateral medullary pressor area

1993 ◽  
Vol 78 (6) ◽  
pp. 922-928 ◽  
Author(s):  
Robert F. Heary ◽  
Allen H. Maniker ◽  
Abbott J. Krieger ◽  
Hreday N. Sapru
Keyword(s):  
Amino Acids ◽  
Cerebral Ischemia ◽  
Excitatory Amino Acids ◽  
Excitatory Amino Acid ◽  
Cardiovascular Responses ◽  
Global Cerebral Ischemia ◽  
Content Type ◽  
Acid Receptor ◽  
Male Wistar Rats

✓ The object of this study was to investigate the role of the ventrolateral medullary pressor area in mediating the cardiovascular responses to experimentally induced global cerebral ischemia, and to test if excitatory amino acids or acetylcholine are the transmitters released in this brain region during these responses. The cerebral ischemic response was elicited in pentobarbital-anesthetized, artificially ventilated male Wistar rats by bilateral ligation of vertebral arteries followed by temporary clamping of the common carotid arteries. The pressor area was identified by microinjections of L-glutamate. Inhibition of neurons in this area by microinjections of muscimol, a γ-aminobutyric acid receptor agonist, abolished the ischemic response, which demonstrated that this area is important in mediating these responses. Microinjections of a broad-spectrum excitatory amino acid receptor blocker (kynurenate), of specific antagonists for N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors (injected alone or in combination), and of atropine failed to block the ischemic responses. These results indicate that: 1) the ventrolateral medullary pressor area mediates pressor responses to cerebral ischemia, and 2) excitatory amino acids or acetylcholine in this area do not mediate the cardiovascular responses to cerebral ischemia.

Early cellular swelling during cerebral ischemia in vivo is mediated by excitatory amino acids released from nerve terminals

1992 ◽  
Vol 577 (1) ◽  
pp. 121-126 ◽  
Author(s):  
Yoichi Katayama ◽  
Toru Tamura ◽  
Donald P. Becker ◽  
Takashi Tsubokawa
Keyword(s):  
Amino Acids ◽  
Cerebral Ischemia ◽  
Excitatory Amino Acids ◽  
Nerve Terminals ◽  
Cellular Swelling

Role of Excitatory Amino Acids in the Control of Growth Hormone Secretion

Endocrine ◽  
2005 ◽  
Vol 28 (3) ◽  
pp. 295-302 ◽  
Author(s):  
Enrique Aguilar ◽  
Manuel Tena-Sempere ◽  
Leonor Pinilla
Keyword(s):  
Amino Acids ◽  
Growth Hormone ◽  
Excitatory Amino Acids ◽  
Hormone Secretion ◽  
Growth Hormone Secretion

The role of excitatory amino acids in synaptic transmission in the hippocampus

1989 ◽  
Vol 93 (1) ◽  
pp. 195-201 ◽  
Author(s):  
J.D.C Lambert ◽  
R.S.G Jones ◽  
M Andreasen ◽  
M.S Jensen ◽  
U Heinemann
Keyword(s):  
Amino Acids ◽  
Synaptic Transmission ◽  
Excitatory Amino Acids

Regulation of free fatty acid metabolism by insulin in humans: role of lipolysis and reesterification

2006 ◽  
Vol 263 (6) ◽  
pp. E1063-E1069 ◽  
Author(s):  
P. J. Campbell ◽  
M. G. Carlson ◽  
J. O. Hill ◽  
N. Nurjhan
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Acid Metabolism ◽  
Insulin Dose ◽  
Healthy Humans ◽  
Constant Rate ◽  
Free Fatty Acid Metabolism ◽  
Plasma Ffa ◽  
Maximal Suppression

The regulation of lipolysis, free fatty acid appearance into plasma (FFA R(a)), an FFA reesterification and oxidation were examined in seven healthy humans infused intravenously with insulin at rates of 4, 8, 25, and 400 mU.m-2.min-1. Glycerol and FFA R(a) were determined by isotope dilution methods, and FFA oxidation was calculated by indirect calorimetry or by measurement of expired 14CO2 from infused [1-14C]palmitate. These measurements were used to calculate total FFA reesterification, primary FFA reesterification occurring within the adipocyte, and secondary reesterification of circulating FFA molecules. Lipolysis, FFA R(a), and secondary FFA reesterification were exquisitely insulin sensitive [the insulin concentrations that produced half-maximal suppression (EC50), 106 +/- 26, 91 +/- 20 vs. 80 +/- 16 pM, P = not significant] in contrast to insulin suppression of FFA oxidation (EC50, 324 +/- 60, all P < 0.01). The absolute rate of primary FFA reesterification was not affected by the increase in insulin concentration, but the proportion of FFA molecules undergoing primary reesterification doubled over the physiological portion of the insulin dose-response curve (from 0.23 +/- 0.06 to 0.44 +/- 0.07, P < 0.05). This served to magnify insulin suppression of FFA R(a) twofold. In conclusion, insulin regulates FFA R(a) by inhibition of lipolysis while maintaining a constant rate of primary FFA reesterification.

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.

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