KLF regulation of insulin pathway genes
Alteration in lipid metabolism can result in fat accumulation in adipose tissues, which may lead to two most important human diseases, obesity and diabetes. A shift in lipid metabolism deregulates signaling pathways which regulates obesity and/or diabetes. In this study, we examined the components o...
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Published in | 3 Biotech Vol. 13; no. 3; p. 87 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Cham
Springer International Publishing
01.03.2023
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Alteration in lipid metabolism can result in fat accumulation in adipose tissues, which may lead to two most important human diseases, obesity and diabetes. A shift in lipid metabolism deregulates signaling pathways which regulates obesity and/or diabetes. In this study, we examined the components of insulin/ TGF-β pathways and their genetic interaction with Krüppel-like transcription factors (KLFs). Their role in energy homeostasis were discussed. We separately created
klf/daf
genes double mutants by carrying out
klfs
RNAi on
daf-2 (e1391
),
daf-4 (e1364), daf-7 (e1372); dpy-1 (e1), daf-14 (m77), daf-16 (mgDf50)
mutants. And then conducted Oil O Red staining to assay the
klf/daf RNAi
worms for fat deposits and examine genetic interaction between
klfs
and
daf
genes. The results showed that worms bearing
klf-1, 2,
or
3
and
daf-2
, or
daf-4
mutations deposit large, but similar fat levels as individual mutants. The results suggested that they target the same molecular pathway of fat storage.
klf-1, 2
or
3
RNAi
/daf-7
worms showed higher fat deposits in
klf-1, 2, or 3 RNAi/daf-7
worms than
klf-1, 2, or 3 RNAi
or
daf-7
mutants alone, which showed a functional interaction between
klfs
and
daf-7
in perhaps TGF-β-like pathway. Altogether our study suggests a direct role of
klfs
in insulin signaling pathway. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2190-572X 2190-5738 |
DOI: | 10.1007/s13205-023-03502-5 |