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ACACA — INS
Text-mined interactions from Literome
Liang et al., J Biol Chem 2002
:
Thus, SREBP-2 and/or SREBP-1a can substitute partially for SREBP-1c in permitting an
insulin mediated
increase in
ACC and FAS mRNAs
Witters et al., J Biol Chem 1992
(Liver Neoplasms, Experimental) :
In the present study, we have examined, in Fao hepatoma cells, the
effects of
insulin on
ACC and AMPK activity, the latter measured with a synthetic peptide corresponding to one of the phosphorylation sites on ACC for AMPK ... Taken together, these data are consistent with the hypothesis that the 5'-AMP activated protein kinase is a regulated component of the insulin signal transduction pathway and may be the major target for
insulin regulation of
ACC
Bianchi et al., J Cell Biochem 1992
(Liver Neoplasms, Experimental) :
During investigations in different clonal lines of these cells, we have uncovered marked intercellular variability in the activity, enzyme content, and
insulin regulation of
ACC paralleled by differences in cellular neutral lipid ( triglyceride ) content
Foufelle et al., J Biol Chem 1992
:
Insulin ( 100 nM ) added in the presence of lactate and pyruvate did not
stimulate the expression of FAS and
ACC
Kim et al., J Nutr Sci Vitaminol (Tokyo) 2005
:
Therefore,
insulin , Dex, T3, glucose, and PUFA
regulate ACC gene expression, at least in part, through the PI promoter
MacDonald et al., Arch Biochem Biophys 2008
:
Inhibitors of
ACC and fatty acid synthase
inhibited insulin release in islets and INS-1 cells
Ronnebaum et al., J Biol Chem 2008
:
To investigate the
effects of
ACC1 inhibition on
insulin secretion, three small interfering RNA ( siRNA ) duplexes targeting ACC1 ( siACC1 ) were transfected into the INS-1 derived cell line, 832/13 ; the most efficacious duplex was also cloned into an adenovirus and used to transduce isolated rat islets
Berggreen et al., Am J Physiol Endocrinol Metab 2009
:
The
regulation of the rate limiting lipogenic enzyme
acetyl-CoA carboxylase (ACC) by
insulin through dephosphorylation of S79, which is a target for AMP activated protein kinase (AMPK), was dependent on the presence of active PKB
Han et al., J Exp Biol 2009
:
Compared with the control group, 100 and 150 nmol l ( -1 )
insulin increased TG accumulation, acetyl-CoA carboxylase-alpha (ACCalpha) and fatty acid synthase (FAS) activity, and the mRNA levels of sterol regulatory element binding protein-1 ( SREBP-1 ), FAS and
ACCalpha genes ...
Insulin at 200 nmol l ( -1 ) had an inhibiting effect on TG accumulation and the activity of ACC and FAS, but
increased the gene expression of SREBP-1, FAS and
ACCalpha
Hoehn et al., Cell Metab 2010
:
Hence, AMPK and
ACC have become major drug
targets for weight loss and improved
insulin action
de Castro Barbosa et al., Metabolism 2013
:
L-NAME treatment suppressed Arg effects on : 1 ) nitrite and c-GMP content ; 2 ) glycogen synthesis and glucose uptake ; 3 ) basal and
insulin stimulated p-Akt ( Ser ( 473 ) ), total and p-AMPK-a and
ACC , and nNOS expression
Witters et al., Arch Biochem Biophys 1987
:
The possible mechanisms underlying the
insulin activation of
ACC and the role of intracellular nucleotides in insulin action are discussed
Girard et al., FASEB J 1994
:
An increased glucose metabolism is necessary for the expression of
insulin effects on fatty acid synthase (FAS) and
acetyl-CoA carboxylase (ACC) mRNA accumulation in white adipose tissue, as insulin is ineffective in vitro in the absence of glucose
Brun et al., J Biol Chem 1993
:
Activation of the Ca2+, cAMP, and C-kinase pathways with high K+, forskolin, and phorbol 12-myristate 13 acetate, respectively, caused
insulin release but not
ACC mRNA
induction ... The data strengthen the view that
ACC plays a pivotal role in nutrient induced
insulin release
Zhang et al., Biochem Biophys Res Commun 1996
:
Since acetyl-CoA carboxylase (ACC) is the only enzyme which synthesizes malonyl-CoA, we generated transfectants of INS-1 cells which express antisense ACC mRNA in order to unequivocally establish that
ACC is
involved in glucose induced
insulin secretion
Makinde et al., Circ Res 1997
:
In 1-day-old hearts, the presence of
insulin resulted in a significant decrease in AMPK activity, an increase in
ACC activity, and a decrease in fatty acid oxidation rates