Effects of Growth Hormone and Prolactin on Adipose Tissue Development and Function

Pituitary ◽  
2003 ◽  
Vol 6 (2) ◽  
pp. 97-102 ◽  
Author(s):  
David J. Flint ◽  
Nadine Binart ◽  
John Kopchick ◽  
Paul Kelly
2008 ◽  
Vol 295 (5) ◽  
pp. R1671-R1679 ◽  
Author(s):  
Mireille Raccurt ◽  
Fannie Baudimont ◽  
Julien Tirard ◽  
Benjamin Rey ◽  
Elodie Moureaux ◽  
...  

Rapid growth is of crucial importance for Adélie penguin chicks reared during the short Antarctic summer. It partly depends on the rapid ontogenesis of fat stores that are virtually null at hatching but then develop considerably (×40) within a month to constitute both an isolative layer against cold and an energy store to fuel thermogenic and growth processes. The present study was aimed at identifying by RT-PCR the major transcriptional events that chronologically underlie the morphological transformation of adipocyte precursors into mature adipocytes from hatching to 30 days of age. The peak expression of GATA binding protein 3, a marker of preadipocytes, at day 7 posthatch indicates a key proliferation step, possibly in relation to the expression of C/EBPα (C/EBPα). High plasma total 3,5,3′-triiodo-l-thyronine (T3) levels and high levels of growth hormone receptor transcripts at hatching suggested that growth hormone and T3 play early activating roles to favor proliferation of preadipocyte precursors. Differentiation and growth of preadipocytes may occur around day 15 in connection with increased abundance of transcripts encoding IGF-1, proliferator-activated receptor-γ, and C/EBPβ, gradually leading to functional maturation of metabolic features of adipocytes including lipid uptake and storage (lipoprotein lipase, fatty-acid synthase) and late endocrine functions (adiponectin) by day 30. Present results show a close correlation between adipose tissue development and chick biology and a difference in the scheduled expression of regulatory factors controlling adipogenesis compared with in vitro studies using cell lines emphasizing the importance of in vivo approaches.


2018 ◽  
Author(s):  
Younghoon Jang ◽  
Chaochen Wang ◽  
Aaron Broun ◽  
Young-Kwon Park ◽  
Lenan Zhuang ◽  
...  

AbstractHistone H3K4 mono-methyltransferases MLL3 and MLL4 (MLL3/4) are required for enhancer activation during cell differentiation, though the mechanism is incompletely understood. To address MLL3/4 enzymatic activity in enhancer regulation, we have generated two mouse lines: one expressing H3.3K4M, a lysine-4-to-methionine (K4M) mutation of histone H3.3 that inhibits H3K4 methylation, and the other carrying conditional double knockout of MLL3/4 enzymatic SET domains. Expression of H3.3K4M in lineage-specific precursor cells depletes H3K4 methylation and prevents adipogenesis and adipose tissue development. Mechanistically, H3.3K4M prevents enhancer activation in adipogenesis by destabilizing MLL3/4 proteins but not other Set1-like H3K4 methyltransferases. Notably, deletion of the enzymatic SET domain of MLL3/4 in lineage-specific precursor cells mimics H3.3K4M expression and prevents adipose tissue development. Interestingly, destabilization of MLL3/4 by H3.3K4M in adipocytes does not affect adipose tissue maintenance and function. Together, our findings indicate that H3.3K4M destabilizes enhancer epigenomic writers MLL3/4 and impairs adipose tissue development.


Author(s):  
Justin J. Rochford

Appropriately functioning adipose tissue is essential for human health, a fact most clearly illustrated by individuals with lipodystrophy, who have impaired adipose development and often suffer severe metabolic disease as a result. Humans with obesity display a similar array of metabolic problems. This reflects failures in fat tissue function in obesity, which results in consequences similar to those seen when insufficient adipose tissue is present. Thus a better understanding of the molecules that regulate the development of fat tissue is likely to aid the generation of novel therapeutic strategies for the treatment of all disorders of altered fat mass. Single gene disruptions causing lipodystrophy can give unique insights into the importance of the proteins they encode in human adipose tissue development. Moreover, the mechanisms via which they cause lipodystrophy can reveal new molecules and pathways important for adipose tissue development and function as well as confirming the importance of molecules identified from studies of cellular and animal models.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Tiziana Squillaro ◽  
Gianfranco Peluso ◽  
Umberto Galderisi ◽  
Giovanni Di Bernardo

Complex interaction between genetics, epigenetics, environment, and nutrition affect the physiological activities of adipose tissues and their dysfunctions, which lead to several metabolic diseases including obesity or type 2 diabetes. Here, adipogenesis appears to be a process characterized by an intricate network that involves many transcription factors and long noncoding RNAs (lncRNAs) that regulate gene expression. LncRNAs are being investigated to determine their contribution to adipose tissue development and function. LncRNAs possess multiple cellular functions, and they regulate chromatin remodeling, along with transcriptional and post-transcriptional events; in this way, they affect gene expression. New investigations have demonstrated the pivotal role of these molecules in modulating white and brown/beige adipogenic tissue development and activity. This review aims to provide an update on the role of lncRNAs in adipogenesis and adipose tissue function to promote identification of new drug targets for treating obesity and related metabolic diseases.


2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Lenan Zhuang ◽  
Younghoon Jang ◽  
Young-Kwon Park ◽  
Ji-Eun Lee ◽  
Shalini Jain ◽  
...  

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