Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
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Target Concepts:
Gene/Protein
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Query: UNIPROT:P56851 (
epididymal
)
11,273
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK-2/FBPase) catalyzes the synthesis and degradation of fructose 2,6-bisphosphate (F2,6BP), which is a powerful activator of 6-phosphofructo-1-kinase, the rate-limiting enzyme of glycolysis. Four genes encode PFK-2/FBPase (PFKFB1-4), and an inducible isoform (iPFK-2/
PFKFB3
) has been found to mediate F2,6BP production in proliferating cells. We have investigated the role of iPFK-2/
PFKFB3
and related isoforms in the regulation of glycolysis in adipocytes. Human visceral fat cells express
PFKFB3
mRNA, and three alternatively spliced isoforms of iPFK-2/
PFKFB3
are expressed in the
epididymal
fat pad of the mouse. Forced expression of the iPFK-2/
PFKFB3
in COS-7 cells resulted in increased glucose uptake and cellular F2,6BP content. Prolonged insulin treatment of 3T3-L1 adipocytes led to reduced
PFKFB3
mRNA expression, and
epididymal
fat pads from db/db mice also showed decreased expression of
PFKFB3
mRNA. Finally, anti-phospho-iPFK-2(Ser461) Western blotting revealed strong reactivity in insulin-treated 3T3-L1 adipocyte, suggesting that insulin induces the phosphorylation of
PFKFB3
protein. These data expand the role of these structurally unique iPFK-2/
PFKFB3
isoforms in the metabolic regulation of adipocytes.
...
PMID:Expression of inducible 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase/PFKFB3 isoforms in adipocytes and their potential role in glycolytic regulation. 1630 49
Little is known about gene regulation by fasting in human adipose tissue. Accordingly, the objective of this study was to investigate the effects of fasting on adipose tissue gene expression in humans. To that end, subcutaneous adipose tissue biopsies were collected from 11 volunteers 2 and 26 h after consumption of a standardized meal. For comparison,
epididymal
adipose tissue was collected from C57Bl/6J mice in the ab libitum-fed state and after a 16 h fast. The timing of sampling adipose tissue roughly corresponds with the near depletion of liver glycogen. Transcriptome analysis was carried out using Affymetrix microarrays. We found that,
1
) fasting downregulated numerous metabolic pathways in human adipose tissue, including triglyceride and fatty acid synthesis, glycolysis and glycogen synthesis, TCA cycle, oxidative phosphorylation, mitochondrial translation, and insulin signaling;
2
) fasting downregulated genes involved in proteasomal degradation in human adipose tissue;
3
) fasting had much less pronounced effects on the adipose tissue transcriptome in humans than mice;
4
) although major overlap in fasting-induced gene regulation was observed between human and mouse adipose tissue, many genes were differentially regulated in the two species, including genes involved in insulin signaling (
PRKAG2
,
PFKFB3
), PPAR signaling (
PPARG
,
ACSL1
,
HMGCS2
,
SLC22A5
,
ACOT1
), glycogen metabolism (
PCK1
,
PYGB
), and lipid droplets (
PLIN1
,
PNPLA2
,
CIDEA
,
CIDEC
). In conclusion, although numerous genes and pathways are regulated similarly by fasting in human and mouse adipose tissue, many genes show very distinct responses to fasting in humans and mice. Our data provide a useful resource to study adipose tissue function during fasting.
...
PMID:Transcriptomic signature of fasting in human adipose tissue. 3286 87
