Ignet

Gene Information

Gene symbol: FSTL3

Gene name: follistatin-like 3 (secreted glycoprotein)

HGNC ID: 3973

Synonyms: FLRG, FSRP

Related Genes

#	Gene Symbol	Number of hits
1	FST	1 hits
2	INHBE	1 hits
3	INS	1 hits
4	MSTN	1 hits
5	TGFB1	1 hits

Related Sentences

#	PMID	Sentence
1	17229845	FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults.
2	17229845	Activin and myostatin are related members of the TGF-beta growth factor superfamily.
3	17229845	FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined.
4	17229845	We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients.
5	17229845	This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist.
6	17229845	Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity.
7	17229845	Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity.
8	17229845	FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults.
9	17229845	Activin and myostatin are related members of the TGF-beta growth factor superfamily.
10	17229845	FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined.
11	17229845	We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients.
12	17229845	This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist.
13	17229845	Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity.
14	17229845	Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity.
15	17229845	FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults.
16	17229845	Activin and myostatin are related members of the TGF-beta growth factor superfamily.
17	17229845	FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined.
18	17229845	We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients.
19	17229845	This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist.
20	17229845	Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity.
21	17229845	Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity.
22	17229845	FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults.
23	17229845	Activin and myostatin are related members of the TGF-beta growth factor superfamily.
24	17229845	FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined.
25	17229845	We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients.
26	17229845	This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist.
27	17229845	Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity.
28	17229845	Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity.
29	17229845	FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults.
30	17229845	Activin and myostatin are related members of the TGF-beta growth factor superfamily.
31	17229845	FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined.
32	17229845	We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients.
33	17229845	This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist.
34	17229845	Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity.
35	17229845	Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity.
36	20007937	First-trimester follistatin-like-3 levels in pregnancies complicated by subsequent gestational diabetes mellitus.
37	20007937	OBJECTIVE To determine whether maternal levels of follistatin-like-3 (FSTL3), an inhibitor of activin and myostatin involved in glucose homeostasis, are altered in the first trimester of pregnancies complicated by subsequent gestational diabetes mellitus (GDM).
38	20007937	First-trimester follistatin-like-3 levels in pregnancies complicated by subsequent gestational diabetes mellitus.
39	20007937	OBJECTIVE To determine whether maternal levels of follistatin-like-3 (FSTL3), an inhibitor of activin and myostatin involved in glucose homeostasis, are altered in the first trimester of pregnancies complicated by subsequent gestational diabetes mellitus (GDM).