scholarly journals Chickens from lines selected for high and low body weight show differences in fatty acid oxidation efficiency and metabolic flexibility in skeletal muscle and white adipose tissue

2014 ◽  
Vol 38 (10) ◽  
pp. 1374-1382 ◽  
Author(s):  
S Zhang ◽  
R P McMillan ◽  
M W Hulver ◽  
P B Siegel ◽  
L H Sumners ◽  
...  

2014 ◽  
Vol 46 (9) ◽  
pp. 315-327 ◽  
Author(s):  
Bo Ji ◽  
Jesse L. Middleton ◽  
Ben Ernest ◽  
Arnold M. Saxton ◽  
Susan J. Lamont ◽  
...  

Domestic broiler chickens rapidly accumulate fat and are naturally hyperglycemic and insulin resistant, making them an attractive model for studies of human obesity. We previously demonstrated that short-term (5 h) fasting rapidly upregulates pathways of fatty acid oxidation in broiler chickens and proposed that activation of these pathways may promote leanness. The objective of the current study was to characterize adipose tissue from relatively lean and fatty lines of chickens and determine if heritable leanness in chickens is associated with activation of some of the same pathways induced by fasting. We compared adipose gene expression and metabolite profiles in white adipose tissue of lean Leghorn and Fayoumi breeds to those of fattier commercial broiler chickens. Both lipolysis and expression of genes involved in fatty acid oxidation were upregulated in lean chickens compared with broilers. Although there were strong similarities between the lean lines compared with broilers, distinct expression signatures were also found between Fayoumi and Leghorn, including differences in adipogenic genes. Similarities between genetically lean and fasted chickens suggest that fatty acid oxidation in white adipose tissue is adaptively coupled to lipolysis and plays a role in heritable differences in fatness. Unique signatures of leanness in Fayoumi and Leghorn lines highlight distinct pathways that may provide insight into the basis for leanness in humans. Collectively, our results provide a number of future directions through which to fully exploit chickens as unique models for the study of human obesity and adipose metabolism.



Adipocyte ◽  
2016 ◽  
Vol 6 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Emmanuelle Torchon ◽  
Rodney Ray ◽  
Matthew W. Hulver ◽  
Ryan P. McMillan ◽  
Brynn H. Voy


2005 ◽  
Vol 289 (4) ◽  
pp. E617-E626 ◽  
Author(s):  
Pipeng Li ◽  
Zhengxian Zhu ◽  
Yuyan Lu ◽  
James G. Granneman

Chronic activation of adipocyte β-adrenergic receptors induces remodeling of white adipose tissue (WAT) that includes a transient inflammatory response followed by mitochondrial biogenesis, induction of fatty acid oxidation genes, and elevation of tissue oxidative metabolism. Gene profiling experiments of WAT during remodeling induced by the β3-adrenergic receptor agonist CL-316,243 (CL) suggested that peroxisome proliferator-activated receptor-α (Ppara), which is upregulated by CL, might be an important transcriptional regulator of that process. Histological, physiological, and molecular analysis of CL-induced remodeling in wild-type mice and mice lacking Ppara demonstrated that Ppara was important for inducing adipocyte mitochondrial biogenesis and upregulating genes involved in fatty acid oxidation. Furthermore, Ppara-deficient mice exhibited sustained WAT inflammation during CL treatment, indicating that upregulation of Ppara limits proinflammatory signaling during chronic lipolytic activation. Together, these data support the hypothesis that WAT remodeling is an adaptive response to excessive fatty acid mobilization whereby Ppara and its downstream targets elevate fatty acid catabolism and suppress proinflammatory signaling.



2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Emmanuelle Torchon ◽  
Matthew Hulver ◽  
Ryan McMillan ◽  
Brynn Voy


2007 ◽  
Vol 194 (2) ◽  
pp. 293-304 ◽  
Author(s):  
Sabina Paglialunga ◽  
Patrick Schrauwen ◽  
Christian Roy ◽  
Esther Moonen-Kornips ◽  
Huiling Lu ◽  
...  

Activation of C5L2, a G-protein-coupled receptor, by acylation-stimulating protein/complement C3adesArg (ASP/C3adesArg) has been shown to stimulate triglyceride (TG) synthesis in both mature adipocytes and preadipocytes. ASP is an adipocyte-derived hormone that acts by increasing diacylglycerol acyltransferase activity and glucose transport. ASP-deficient mice (C3KO, precursor protein) are lean, display delayed postprandial TG clearance, increased food intake, and increased energy expenditure. The present study shows that C5L2KO mice on a low fat diet are hyperphagic (~60% increase in total food intake) yet maintain the same body weight and adipose tissue mass as wild-type (WT) controls. However, on a high fat diet, average adipocyte size and adipose tissue TG/DNA content were significantly reduced and postprandial TG clearance was delayed in C5L2KO. Adipose tissue TG synthesis (WT: 47.2 ± 5.6 versus C5L2KO: 7.8 ± 1.8 pmol/μg protein, P < 0.001), TG lipolysis (WT: 227.6 ± 36.4 versus C5L2KO: 45.8 ± 5.0 nmol/μg protein, P < 0.001), and fatty acid re-esterification (WT: 85.3 ± 2.4% versus C5L2KO: 59.5 ± 6.8%, P < 0.001) were significantly reduced in C5L2KO mice. Indirect calorimetry measurements revealed C5L2KO mice have unchanged oxygen consumption levels yet reduced respiratory quotient value, suggesting preferential fatty acid utilization over carbohydrate. In agreement, fatty acid oxidation was elevated in heart and skeletal muscle tissue in C5L2KO mice and skeletal muscle levels of uncoupling protein 3 (425.5 ± 86.3%, P < 0.0001), CD36 (277.6 ± 49.5%, P < 0.05), cytochrome c (252.6 ± 33.9%, P < 0.05), and phospho-acetyl CoA carboxylase (118.4 ± 9.3%, P < 0.05) were significantly increased in C5L2KO mice versus WT (100%). The study shows that in response to reduced TG storage in white adipose tissue, C5L2KO mice have developed a compensatory mechanism of increased muscle fat oxidation.



2018 ◽  
Vol 315 (6) ◽  
pp. R1096-R1106 ◽  
Author(s):  
Lidan Zhao ◽  
Ryan P. McMillan ◽  
Guohao Xie ◽  
Samantha G. L. W. Giridhar ◽  
Lance H. Baumgard ◽  
...  

Heat-stressed pigs experience metabolic alterations, including altered insulin profiles, reduced lipid mobilization, and compromised intestinal integrity. This is bioenergetically distinct from thermal neutral pigs on a similar nutritional plane. To delineate differences in substrate preferences between direct and indirect (via reduced feed intake) heat stress effects, skeletal muscle fuel metabolism was assessed. Pigs (35.3 ± 0.8 kg) were randomly assigned to three treatments: thermal neutral fed ad libitum (TN; 21°C, n = 8), heat stress fed ad libitum (HS; 35°C, n = 8), and TN, pair-fed/HS intake (PF; n = 8) for 7 days. Body temperature (TB) and feed intake (FI) were recorded daily. Longissimus dorsi muscle was biopsied for metabolic assays on days −2, 3, and 7 relative to initiation of environmental treatments. Heat stress increased TBand decreased FI ( P < 0.05). Heat stress inhibited incomplete fatty acid oxidation and glucose oxidation ( P < 0.05). Metabolic flexibility decreased in HS pigs compared with TN and PF controls ( P < 0.05). Both phosphofructokinase and pyruvate dehydrogenase (PDH) activities increased in PF ( P < 0.05); however, TN and HS did not differ. Heat stress inhibited citrate synthase and β-hydroxyacyl-CoA dehydrogenase (β-HAD) activities ( P < 0.05). Heat stress did not alter PDH phosphorylation or carnitine palmitoyltransferase 1 abundance but reduced acetyl-CoA carboxylase 1 (ACC1) protein abundance ( P < 0.05). In conclusion, HS decreased skeletal muscle fatty acid oxidation and metabolic flexibility, likely involving β-HAD and ACC regulation.





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