Maternal high-fat feeding primes steatohepatitis in adult mice offspring, involving mitochondrial dysfunction and altered lipogenesis gene expression

Hepatology ◽  
2009 ◽  
Vol 50 (6) ◽  
pp. 1796-1808 ◽  
Author(s):  
Kimberley D. Bruce ◽  
Felino R. Cagampang ◽  
Marco Argenton ◽  
Junlong Zhang ◽  
Priya L. Ethirajan ◽  
...  
2012 ◽  
Vol 98 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Frankie D. Heyward ◽  
R. Grace Walton ◽  
Matthew S. Carle ◽  
Mark A. Coleman ◽  
W. Timothy Garvey ◽  
...  

2012 ◽  
Vol 6 ◽  
pp. GRSB.S10371 ◽  
Author(s):  
Richard R. Almon ◽  
Debra C. DuBois ◽  
Siddharth Sukumaran ◽  
Xi Wang ◽  
Bai Xue ◽  
...  

2021 ◽  
Vol 320 (1) ◽  
pp. R19-R35
Author(s):  
Susana Rodriguez ◽  
Hannah C. Little ◽  
Parnaz Daneshpajouhnejad ◽  
Paride Fenaroli ◽  
Stefanie Y. Tan ◽  
...  

C1q/TNF-related protein 1 (CTRP1) is an endocrine factor with metabolic, cardiovascular, and renal functions. We previously showed that aged Ctrp1-knockout (KO) mice fed a control low-fat diet develop renal hypertrophy and dysfunction. Since aging and obesity adversely affect various organ systems, we hypothesized that aging, in combination with obesity induced by chronic high-fat feeding, would further exacerbate renal dysfunction in CTRP1-deficient animals. To test this, we fed wild-type and Ctrp1-KO mice a high-fat diet for 8 mo or longer. Contrary to our expectation, no differences were observed in blood pressure, heart function, or vascular stiffness between genotypes. Loss of CTRP1, however, resulted in an approximately twofold renal enlargement (relative to body weight), ∼60% increase in urinary total protein content, and elevated pH, and changes in renal gene expression affecting metabolism, signaling, transcription, cell adhesion, solute and metabolite transport, and inflammation. Assessment of glomerular integrity, the extent of podocyte foot process effacement, as well as renal response to water restriction and salt loading did not reveal significant differences between genotypes. Interestingly, blood platelet, white blood cell, neutrophil, lymphocyte, and eosinophil counts were significantly elevated, whereas mean corpuscular volume and hemoglobin were reduced in Ctrp1-KO mice. Cytokine profiling revealed increased circulating levels of CCL17 and TIMP-1 in KO mice. Compared with our previous study, current data suggest that chronic high-fat feeding affects renal phenotypes differently than similarly aged mice fed a control low-fat diet, highlighting a diet-dependent contribution of CTRP1 deficiency to age-related changes in renal structure and function.


2007 ◽  
Vol 177 (4S) ◽  
pp. 48-48
Author(s):  
Shintaro Narita ◽  
Norihiko Tsuchiya ◽  
Mitsuru Saito ◽  
Takamitsu Inoue ◽  
Teruaki Kumazawa ◽  
...  

2017 ◽  
Vol 11 ◽  
pp. 117762501771000 ◽  
Author(s):  
Jing Nie ◽  
Debra C DuBois ◽  
Bai Xue ◽  
William J Jusko ◽  
Richard R Almon

Author(s):  
Rotem Lahav ◽  
Yulia Haim ◽  
Nikhil Suresh Bhandarkar ◽  
Liron Levin ◽  
Vered Chalifa-Caspi ◽  
...  

In chronic obesity, activated adipose tissue pro-inflammatory cascades are tightly linked to metabolic dysfunction. Yet, close temporal analyses of the responses to obesogenic environment such as high-fat feeding (HFF) in susceptible mouse strains question the causal relationship between inflammation and metabolic dysfunction, and/or raises the possibility that certain inflammatory cascades play adaptive/homeostatic, rather than pathogenic roles. Here we hypothesized that CTRP6, a C1QTNF family member, may constitute an early responder to acute nutritional changes in adipose tissue, with potential physiological roles. Both 3 days high-fat feeding (3dHFF) and acute obesity reversal (2 weeks switch to low-fat diet after 8w-HFF) already induced marked changes in whole-body fuel utilization. While adipose tissue expression of classical pro-inflammatory cytokines (Tnf-α, Ccl2, Il1b) exhibited no, or only minor, change, C1qtnf6 uniquely increased, and decreased, in response to 3dHFF and acute obesity reversal, respectively. CTRP6 knockout (KO) mouse embryonic fibroblasts (MEF) exhibited increased adipogenic gene expression (Pparg, Fabp4, Adipoq) and markedly reduced inflammatory genes (Tnf-α, Ccl2, Il6) compared to wild-type MEF, and recombinant CTRP6 induced the opposite gene expression signature, as assessed by RNA-sequencing. Consistently, 3dHFF of CTRP6-KO mice induced a greater whole-body and adipose tissue weight gain compared to wild-type littermates. Collectively, we propose CTRP6 as a gene that rapidly responds to acute changes in caloric intake, acting in acute over-nutrition to induce a "physiological inflammatory response" that limits adipose tissue expansion.


2005 ◽  
Vol 275 (1-2) ◽  
pp. 109-115 ◽  
Author(s):  
I. P. Lopez ◽  
F. I. Milagro ◽  
A. Marti ◽  
M. J. Moreno-Aliaga ◽  
J. A. Martinez ◽  
...  

Amino Acids ◽  
2009 ◽  
Vol 37 (1) ◽  
pp. 187-198 ◽  
Author(s):  
Wenjuan Jobgen ◽  
Wenjiang J. Fu ◽  
Haijun Gao ◽  
Peng Li ◽  
Cynthia J. Meininger ◽  
...  

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