scholarly journals Relationship between body condition score loss and mRNA of genes related to fatty acid metabolism and the endocannabinoid system in adipose tissue of periparturient cows

animal ◽  
2020 ◽  
Vol 14 (8) ◽  
pp. 1724-1732
Author(s):  
E. Dirandeh ◽  
M. Ghorbanalinia ◽  
A. Rezaei-Roodbari ◽  
M.G. Colazo
2005 ◽  
Vol 85 (1) ◽  
pp. 101-105 ◽  
Author(s):  
A. Arana ◽  
J. A. Mendizabal ◽  
R. Delfa ◽  
P. Eguinoa ◽  
B. Soret ◽  
...  

The aim of the study was to assess the effect of body condition score on tissue and metabolic characteristics of the adipose depots in sheep of Rasa Aragonesa breed. Ewes were uniformly assigned according to their body condition score (BCS) (scale 0 to 5), to four groups: 0.75–1.75, 2–2.75, 3–3.75, and 4–4.5. The amount of fat and the adipocyte size in the different adipose depots increased as BCS did (P < 0.001) while the number of adipocytes did not change. The greatest ability to accumulate or mobilize fat was the subcutaneous depot (slope of the regression between amount of fat and BCS, b = 1.92; P < 0.001). Fatty acid synthase (FAS) lipogenic enzyme activity was affected by BCS, while G3-PDH and G6-PDH activities were not. Key words: Adipose tissue, body condition score, adipocyte size, lipogenic enzyme activity, ewes


2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 387-387
Author(s):  
R. M. Humphrey ◽  
A. T. Sukumaran ◽  
R. L. Lemire ◽  
E. N. Ferjak ◽  
C. Cavinder ◽  
...  

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1674
Author(s):  
Ilona Strączek ◽  
Krzysztof Młynek ◽  
Agata Danielewicz

A significant factor in improving the performance of dairy cows is their physiological ability to correct a negative energy balance (NEB). This study, using Simmental (SIM) and Holstein-Friesian (HF) cows, aimed to assess changes in NEB (non-esterified fatty acid; body condition score; and C16:0, C18:0, and C18:1) and its effect on the metabolic efficiency of the liver (β-hydroxybutyrate and urea). The effects of NEB on daily yield, production at peak lactation and its duration, and changes in selected milk components were assessed during complete lactation. Up to peak lactation, the loss of the body condition score was similar in both breeds. Subsequently, SIM cows more efficiently restored their BCS. HF cows reached peak lactation faster and with a higher milk yield, but they were less able to correct NEB. During lactation, their non-esterified fatty acid, β-hydroxybutyrate, C16:0, C18:0, C18:1, and urea levels were persistently higher, which may indicate less efficient liver function during NEB. The dynamics of NEB were linked to levels of leptin, which has anorectic effects. Its content was usually higher in HF cows and during intensive lactogenesis. An effective response to NEB may be exploited to improve the production and nutritional properties of milk. In the long term, it may extend dairy cows’ productive life and increase lifetime yield.


2009 ◽  
Vol 34 (3) ◽  
pp. 315-322 ◽  
Author(s):  
Gregory R. Steinberg

During moderate-intensity exercise, fatty acids are the predominant substrate for working skeletal muscle. The release of fatty acids from adipose tissue stores, combined with the ability of skeletal muscle to actively fine tune the gradient between fatty acid and carbohydrate metabolism, depending on substrate availability and energetic demands, requires a coordinated system of metabolic control. Over the past decade, since the discovery that AMP-activated protein kinase (AMPK) was increased in accordance with exercise intensity, there has been significant interest in the proposed role of this ancient stress-sensing kinase as a critical integrative switch controlling metabolic responses during exercise. In this review, studies examining the role of AMPK as a regulator of fatty acid metabolism in both adipose tissue and skeletal muscle during exercise will be discussed. Exercise induces activation of AMPK in adipocytes and regulates triglyceride hydrolysis and esterfication through phosphorylation of hormone sensitive lipase (HSL) and glycerol-3-phosphate acyl-transferase, respectively. In skeletal muscle, exercise-induced activation of AMPK is associated with increases in fatty acid uptake, phosphorylation of HSL, and increased fatty acid oxidation, which is thought to occur via the acetyl-CoA carboxylase-malony-CoA-CPT-1 signalling axis. Despite the importance of AMPK in regulating fatty acid metabolism under resting conditions, recent evidence from transgenic models of AMPK deficiency suggest that alternative signalling pathways may also be important for the control of fatty acid metabolism during exercise.


2019 ◽  
Vol 20 (6) ◽  
pp. 1462 ◽  
Author(s):  
Reem Atawia ◽  
Haroldo Toque ◽  
Mohamed Meghil ◽  
Tyler Benson ◽  
Nicole Yiew ◽  
...  

Visceral adipose tissue (VAT) inflammation and metabolic dysregulation are key components of obesity-induced metabolic disease. Upregulated arginase, a ureahydrolase enzyme with two isoforms (A1-cytosolic and A2-mitochondrial), is implicated in pathologies associated with obesity and diabetes. This study examined A2 involvement in obesity-associated metabolic and vascular disorders. WT and globally deleted A2(−/−) or A1(+/−) mice were fed either a high fat/high sucrose (HFHS) diet or normal diet (ND) for 16 weeks. Increases in body and VAT weight of HFHS-fed WT mice were abrogated in A2−/−, but not A1+/−, mice. Additionally, A2−/− HFHS-fed mice exhibited higher energy expenditure, lower blood glucose, and insulin levels compared to WT HFHS mice. VAT and adipocytes from WT HFHS fed mice showed greater A2 expression and adipocyte size and reduced expression of PGC-1α, PPAR-γ, and adiponectin. A2 deletion blunted these effects, increased levels of active AMPK-α, and upregulated genes involved in fatty acid metabolism. A2 deletion prevented HFHS-induced VAT collagen deposition and inflammation, which are involved in adipocyte metabolic dysfunction. Endothelium-dependent vasorelaxation, impaired by HFHS diet, was significantly preserved in A2−/− mice, but more prominently maintained in A1+/− mice. In summary, A2 is critically involved in HFHS-induced VAT inflammation and metabolic dysfunction.


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