scholarly journals Stimulation of Insulin Secretion by Long-Chain Free Fatty Acids. A DIRECT PANCREATIC EFFECT

1973 ◽  
Vol 52 (8) ◽  
pp. 1979-1984 ◽  
Author(s):  
Stephen R. Crespin ◽  
William B. Greenough ◽  
Daniel Steinberg
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Long Chain ◽  
Stimulation Of

Effects of Long Chain Free Fatty Acids on Glucose-Induced Insulin Secretion in the Perfused Rat Pancreas

1993 ◽  
Vol 25 (11) ◽  
pp. 596-597 ◽  
Author(s):  
O. Mokuda ◽  
Y. Sakamoto ◽  
H.-Y. Hu ◽  
R. Kawagoe ◽  
N. Shimizu
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Long Chain

scholarly journals Stimulation of insulin secretion by infusion of free fatty acids

1969 ◽  
Vol 48 (10) ◽  
pp. 1934-1943 ◽  
Author(s):  
Stephen R. Crespin ◽  
William B. Greenough ◽  
Daniel Steinberg
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Stimulation Of

scholarly journals The regulation of glyceride synthesis in isolated white-fat cells. The effects of palmitate and lipolytic agents

1972 ◽  
Vol 128 (5) ◽  
pp. 1057-1067 ◽  
Author(s):  
E. D Saggerson
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Fat Cells ◽  
Glyceride Synthesis ◽  
Glucose Incorporation ◽  
High Concentrations ◽  
Stimulation Of

1. 0.5mm-Palmitate stimulated incorporation of [U-14C]glucose into glyceride glycerol and fatty acids in normal fat cells in a manner dependent upon the glucose concentration. 2. In the presence of insulin the incorporation of 5mm-glucose into glyceride fatty acids was increased by concentrations of palmitate, adrenaline and 6-N-2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate up to 0.5mm, 0.5μm and 0.5mm respectively. Higher concentrations of these agents produced progressive decreases in the rate of glucose incorporation into fatty acids. 3. The effects of palmitate and lipolytic agents upon the measured parameters of glucose utilization were similar, suggesting that the effects of lipolytic agents are mediated through increased concentrations of free fatty acids. 4. In fat cells from 24h-starved rats, maximal stimulation of glucose incorporation into fatty acids was achieved with 0.25mm-palmitate. Higher concentrations of palmitate were inhibitory. In fat cells from 72h-starved rats, palmitate only stimulated glucose incorporation into fatty acids at high concentrations of palmitate (1mm and above). 5. The ability of fat cells to incorporate glucose into glyceride glycerol in the presence of palmitate decreased with increasing periods of starvation. 6. It is suggested that low concentrations of free fatty acids stimulate fatty acid synthesis from glucose by increasing the utilization of ATP and cytoplasmic NADH for esterification of these free fatty acids. When esterification of free fatty acids does not keep pace with their provision, inhibition of fatty acid synthesis occurs. Provision of free fatty acids far in excess of the esterification capacity of the cells leads to uncoupling of oxidative phosphorylation and a secondary stimulation of fatty acid synthesis from glucose.

scholarly journals Associations of Free Fatty Acids With Insulin Secretion and Action Among African-American and European-American Girls and Women

Obesity ◽  
2010 ◽  
Vol 18 (2) ◽  
pp. 247-253 ◽  
Author(s):  
Laura Lee T. Goree ◽  
Betty E. Darnell ◽  
Robert A. Oster ◽  
Marian A. Brown ◽  
Barbara A. Gower
Keyword(s):  
Fatty Acids ◽  
African American ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
European American

Stimulation of myocardial coenzyme A degradation by fatty acids

1987 ◽  
Vol 253 (1) ◽  
pp. H41-H46
Author(s):  
G. D. Lopaschuk ◽  
J. R. Neely
Keyword(s):  
Fatty Acids ◽  
Coenzyme A ◽  
Future Studies ◽  
Isolated Hearts ◽  
Tissue Content ◽  
Chain Acyl ◽  
Long Chain ◽  
Stimulation Of

Coenzyme A (CoA) levels were increased in isolated hearts from 537 +/- 14 to 818 +/- 44 nmol/g dry wt by perfusion for 45 min under conditions known to stimulate CoA synthesis (5). Subsequently, perfusion of these hearts with buffer containing glucose (11 mM) and pyruvate (5 mM) for 3 min had no effect on CoA levels (789 +/- 42 nmol/g dry wt). However, perfusion with a buffer containing glucose (11 mM) and palmitate (1.2 mM) decreased CoA levels to 683 +/- 34 nmol/g dry wt within 3 min. This decrease in CoA appeared to occur in the cytosolic compartment with no change in mitochondrial CoA content and was associated with a rise in tissue content of long-chain acyl-CoA. An increased incorporation of fatty acids into triglycerides was associated with the rise in total acyl-CoA suggesting that long-chain acyl-CoA levels were elevated in the cytosolic compartment. Perfusion conditions which maximally increased acyl-CoA levels also maximally stimulated CoA degradation. These observations suggest that the cytosolic degradation of CoA is related to high levels of long-chain acyl-CoA in this compartment. Use of these perfusion conditions in future studies should help define the pathway of CoA degradation and determine the mechanisms which control cellular levels of CoA.

scholarly journals Role and mechanism of rosiglitazone on the impairment of insulin secretion induced by free fatty acids on isolated rat islets

2006 ◽  
Vol 119 (7) ◽  
pp. 574-580 ◽  
Author(s):  
Jing-yan TIAN ◽  
Guo LI ◽  
Yan-yun GU ◽  
Hong-li ZHANG ◽  
Wen-zhong ZHOU ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Isolated Rat

scholarly journals Free Fatty Acids Interfere with the DNA Binding Activity of the Virulence Regulator PrfA of Listeria monocytogenes

2020 ◽  
Vol 202 (15) ◽  
Author(s):  
Patrícia T. dos Santos ◽  
Rikke S. S. Thomasen ◽  
Mathias S. Green ◽  
Nils J. Færgeman ◽  
Birgitte H. Kallipolitis
Keyword(s):  
Fatty Acids ◽  
Dna Binding ◽  
Free Fatty Acids ◽  
Antimicrobial Agents ◽  
Virulence Gene ◽  
Binding Activity ◽  
Content Type ◽  
Dna Binding Activity ◽  
Virulence Regulator ◽  
Long Chain

ABSTRACT Naturally occurring free fatty acids (FFAs) are recognized as potent antimicrobial agents that also affect the production of virulence factors in bacterial pathogens. In the foodborne pathogen Listeria monocytogenes, some medium- and long-chain FFAs act as antimicrobial agents as well as signaling compounds, causing a repression of transcription of virulence genes. We previously observed that the master virulence regulator PrfA is involved in both the antimicrobial and virulence-inhibitory response of L. monocytogenes to selected FFAs, but the underlying mechanisms are presently unknown. Here, we present a systematic analysis of the antimicrobial and PrfA-inhibitory activities of medium- and long-chain FFAs of various carbon chain lengths and degrees of saturation. We observed that exposure to specific antimicrobial and nonantimicrobial FFAs prevented PrfA-dependent activation of virulence gene transcription and reduced the levels of PrfA-regulated virulence factors. Thus, an antimicrobial activity was not compulsory for the PrfA-inhibitory ability of an FFA. In vitro binding experiments revealed that PrfA-inhibitory FFAs were also able to prevent the constitutively active variant PrfA* from binding to the PrfA box in the promoter region of the virulence gene hly, whereas noninhibitory FFAs did not affect its ability to bind DNA. Notably, the unsaturated FFAs inhibited the DNA binding activity of PrfA* most efficiently. Altogether, our findings support a model in which specific FFAs orchestrate a generalized reduction of the virulence potential of L. monocytogenes by directly targeting the key virulence regulator PrfA. IMPORTANCE Listeria monocytogenes is a Gram-positive pathogen able to cause foodborne infections in humans and animals. Key virulence genes in L. monocytogenes are activated by the transcription regulator PrfA, a DNA binding protein belonging to the CRP/FNR family. Various signals from the environment are known to affect the activity of PrfA, either positively or negatively. Recently, we found that specific medium- and long-chain free fatty acids act as antimicrobial agents as well as signaling compounds in L. monocytogenes. Here, we show that both antimicrobial and nonantimicrobial free fatty acids inhibit PrfA-dependent activation of virulence gene transcription by interfering with the DNA binding activity of PrfA. Our findings suggest that free fatty acids could be candidates for alternative therapies against L. monocytogenes.

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