Adipogenesis

Sarjeant, K.; Stephens, Jacqueline M.

doi:10.1101/cshperspect.a008417

Cited by 269 publications

(256 citation statements)

References 192 publications

(235 reference statements)

Supporting

Mentioning

250

Contrasting

Unclassified

Order By: Relevance

“…Adipose tissue expansion can also result from an increase in the size (hypertrophy) of adipocytes in a depot-dependent fashion (12,31,36). Thus, we determined whether hypertrophy contributed to adipose tissue accumulation in the HFWD and HFWDϩF/S groups.…”

Section: Discussionmentioning

confidence: 99%

“…The capacity of adipose tissue to form new adipocytes (hyperplasia), which accumulate excess energy, can prevent ectopic lipid deposition in critical organs including visceral adipose tissue, liver, and muscle (12,31,36). Adipose tissue expansion can also result from an increase in the size (hypertrophy) of adipocytes in a depot-dependent fashion (12,31,36).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Metabolic phenotype and adipose and liver features in a high-fat Western diet-induced mouse model of obesity-linked NAFLD

Luo

Burrington

Graff

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Metabolic phenotype and adipose and liver features in a high-fat Western diet-induced mouse model of obesity-linked NAFLD

Luo

Burrington

Graff

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

“…These factors include positive effectors such as AP-1 and Kruppel-like factor (KLFs 4 and 6) and negative regulators such as KLFs 2and 7 that are induced during clonal expansion. Other positive effectors such as PPARγ and C/EBPα and negative effectors such as Wnt-5a and Wnt-10b are induced during differentiation stage (24). We have previously shown that PPARγ and C/EBPα are TR-regulated genes that are repressed by TRα1PV in WAT of Thra1 PV/+ mice (17,19).…”

Section: Discussionmentioning

confidence: 99%

Nuclear receptor corepressor (NCOR1) regulates in vivo actions of a mutated thyroid hormone receptor α

Fozzatti

Kim

Park

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Genetic evidence from patients with mutations of the thyroid hormone receptor α gene (THRA) indicates that the dominant negative activity of mutants underlies the pathological manifestations. However, the molecular mechanisms by which TRα1 mutants exert dominant negative activity in vivo are not clear. We tested the hypothesis that the severe hypothyroidism in patients with THRA mutations is due to an inability of TRα1 mutants to properly release the nuclear corepressors (NCORs), thereby inhibiting thyroid hormone-mediated transcription activity. We crossed Thra1 PV mice, expressing a dominant negative TRα1 mutant (TRα1PV), with mice expressing a mutant Ncor1 allele (Ncor1 ΔID mice) that cannot recruit the TR or PV mutant. TRα1PV shares the same C-terminal mutated sequences as those of patients with frameshift mutations of the THRA gene. Remarkably, NCOR1ΔID ameliorated abnormalities in the thyroid-pituitary axis of Thra1 PV/+ mice. The severe retarded growth, infertility, and delayed bone development were partially reverted in Thra1 PV/+ mice expressing NCOR1ΔID. The impaired adipogenesis was partially corrected by de-repression of peroxisome-proliferator activated receptor γ and CCAAT/enhancerbinding protein α gene, due to the inability of TRα1PV to recruit NCOR1ΔID to form a repressor complex. Thus, the aberrant recruitment of NCOR1 by TRα1 mutants could lead to clinical hypothyroidism in humans. Therefore, therapies aimed at the TRα1-NCOR1 interaction or its downstream actions could be tested as potential targets in treating TRα1 mutant-mediated hypothyroidism in patients.growth retardation | lipid metabolism | fertility defect T he thyroid hormone T3 regulates growth and development and maintains metabolic homeostasis in humans. The genomic signaling by T3 is via the thyroid hormone receptor (TR) isoforms α1, β1, and β2, which are encoded by the THRA and THRB genes located on two different chromosomes. These TR isoforms share extensive sequence homology in the DNA and T3 binding domains but differ in the amino terminal A/B domains (1). TR binds to the thyroid hormone response elements (TREs) and recruits nuclear coregulatory proteins to regulate gene transcription. In the absence of T3, TRs recruit the nuclear corepressors (NCOR1 and NCOR2) for transcriptional repression on the T3 positively regulated genes. In the presence of T3, the T3-bound TR undergoes structural changes, resulting in the release of corepressors, allowing recruitment of nuclear receptor coactivators (e.g., SRC-1) to facilitate transcription activation (2, 3).The critical roles of TR in mediating biological functions of T3 are clearly evident, in that mutations of the THRB gene cause resistance to thyroid hormone (RTH) (3). The intriguing observation that no mutations of the THRA gene were ever found in RTH patients raised the possibilities that mutations of the THRA gene could be embryonic lethal or could confer different clinical manifestations. These possibilities were explored by using a powerful mouse genetic approach. Targeting a ...

show abstract

“…Hepatocytes-GCs are required for adipocyte differentiation (44). Excess GCs in circulation, such as occurs during Cushing disease or chronic GC therapy, promote both visceral fat deposition and hepatic insulin resistance (45,46).…”

Section: Ms4 Does Not Promote Adipogenesis or Gluconeogenic Gene Exprmentioning

confidence: 99%

Thiobenzothiazole-modified Hydrocortisones Display Anti-inflammatory Activity with Reduced Impact on Islet β-Cell Function

Burke

May

Noland³

et al. 2015

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Glucocorticoids impair islet ␤-cell function via glucocorticoid receptor (GR) activation. Results: Thiobenzothiazole-modified hydrocortisone compounds exhibit anti-inflammatory properties with reduced impact on insulin secretion. Conclusion: Novel glucocorticoids can be engineered to reduce impact on ␤-cell mass and function. Significance: Improved GR agonists will be beneficial in a variety of clinical settings.

show abstract

Adipogenesis

Cited by 269 publications

References 192 publications

Metabolic phenotype and adipose and liver features in a high-fat Western diet-induced mouse model of obesity-linked NAFLD

Metabolic phenotype and adipose and liver features in a high-fat Western diet-induced mouse model of obesity-linked NAFLD

Nuclear receptor corepressor (NCOR1) regulates in vivo actions of a mutated thyroid hormone receptor α

Thiobenzothiazole-modified Hydrocortisones Display Anti-inflammatory Activity with Reduced Impact on Islet β-Cell Function

Contact Info

Product

Resources

About