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

1973 ◽  
Vol 52 (8) ◽  
pp. 1979-1984 ◽  
Author(s):  
Stephen R. Crespin ◽  
William B. Greenough ◽  
Daniel Steinberg


1972 ◽  
Vol 128 (5) ◽  
pp. 1057-1067 ◽  
Author(s):  
E. D Saggerson

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.



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


2006 ◽  
Vol 119 (7) ◽  
pp. 574-580 ◽  
Author(s):  
Jing-yan TIAN ◽  
Guo LI ◽  
Yan-yun GU ◽  
Hong-li ZHANG ◽  
Wen-zhong ZHOU ◽  
...  


2002 ◽  
Vol 3 (2) ◽  
pp. 103-112 ◽  
Author(s):  
S. Zraika ◽  
M. Dunlop ◽  
J. Proietto ◽  
S. Andrikopoulos






2020 ◽  
Vol 522 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Katsutoshi Nishino ◽  
Haruka Uesugi ◽  
Akira Hirasawa ◽  
Anna Ohtera ◽  
Yusaku Miyamae ◽  
...  


2010 ◽  
Vol 299 (3) ◽  
pp. E475-E485 ◽  
Author(s):  
Nicolai M. Doliba ◽  
Wei Qin ◽  
Sergei A. Vinogradov ◽  
David F. Wilson ◽  
Franz M. Matschinsky

Fatty acids, acetylcholine, and GLP-1 enhance insulin secretion in a glucose-dependent manner. However, the interplay between glucose, fatty acids, and the neuroendocrine regulators of insulin secretion is not well understood. Therefore, we studied the acute effects of PA (alone or in combination with glucose, acetylcholine, or GLP-1) on isolated cultured mouse islets. Two different sets of experiments were designed. In one, a fixed concentration of 0.5 mM of PA bound to 0.15 mM BSA was used; in the other, a PA ramp from 0 to 0.5 mM was applied at a fixed albumin concentration of 0.15 mM so that the molar PA/BSA ratio changed within the physiological range. At a fixed concentration of 0.5 mM, PA markedly inhibited acetylcholine-stimulated insulin release, the rise of intracellular Ca2+, and enhancement of cAMP production but did not influence the effects of GLP-1 on these parameters of islet cell function. 2-ADB, an IP3 receptor inhibitor, reduced the effect of acetylcholine on insulin secretion and reversed the effect of PA on acetylcholine-stimulated insulin release. Islet perfusion for 35–40 min with 0.5 mM PA significantly reduced the calcium storage capacity of ER measured by the thapsigargin-induced Ca2+ release. Oxygen consumption due to low but not high glucose was reduced by PA. When a PA ramp from 0 to 0.5 mM was applied in the presence of 8 mM glucose, PA at concentrations as low as 50 μM significantly augmented glucose-stimulated insulin release and markedly reduced acetylcholine's effects on hormone secretion. We thus demonstrate that PA acutely reduces the total oxygen consumption response to glucose, glucose-dependent acetylcholine stimulation of insulin release, Ca2+, and cAMP metabolism, whereas GLP-1's actions on these parameters remain unaffected or potentiated. We speculate that acute emptying of the ER calcium by PA results in decreased glucose stimulation of respiration and acetylcholine potentiation of insulin secretion.





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