scholarly journals Heat stress and β-adrenergic agonists alter the adipose transcriptome and fatty acid mobilization in ruminant livestock1

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. S141-S144
Author(s):  
Rachel R Reith ◽  
Renae L Sieck ◽  
Pablo C Grijalva ◽  
Erin M Duffy ◽  
Rebecca M Swanson ◽  
...  
2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 195-196
Author(s):  
Rachel R Reith ◽  
Renae L Sieck ◽  
Pablo C Grijalva ◽  
Erin M Duffy ◽  
Rebecca M Swanson ◽  
...  

Abstract Heat stress (HS) negatively impacts livestock performance and carcass traits while beta-adrenergic agonist (βAA) supplementation improves animal production and efficiency; both can stimulate lipolysis in adipose. The objective of this study was to understand the independent and interacting effects of HS and βAA on the subcutaneous adipose transcriptome in lambs and on visceral adipose fatty acid mobilization in steers. For study 1, 24 wethers were assigned to thermal neutral (TN THI = 65) or HS (THI = 80) conditions and supplemented without (NS) or with ractopamine hydrochloride (RH) for 30d in a 2 x 2 factorial. TN lambs were pair-fed the average intake of HS. RNA collected from subcutaneous fat at harvest was sequenced. Differential expression (DE) analyses identified 71 (Padj < 0.05) loci altered due to the interaction of environment and supplement. No DE genes were observed for the main effect of supplement, but HS reduced expression (P < 0.05) of RBM3 and increased expression (P < 0.05) of ATXN7L1. HS was predicted by pathway analyses to impair adipogenesis and fatty acid mobilization. In study 2, 24 steers were assigned to TN (THI = 65) or HS (THI = 83) and NS or zilpaterol hydrochloride (ZH) treatments for 21d in a 2 x 2 factorial. TN steers were pair-fed the intake of their HS cohort. Ex vivo fatty acid mobilization from visceral adipose in response to 0 or 1µM epinephrine was quantified at harvest. Fatty acid mobilization did not differ among groups when unstimulated, but epinephrine-stimulated mobilization was less (P = 0.05) in HS and greater (P < 0.01) in ZH steers. These findings indicate that heat stress-induced reduction of fatty acid mobilization from adipose may be associated with increased expression of stress-responsive genes. Moreover, the stimulatory effect of ZH on epinephrine-induced fatty acid mobilization was present after chronic treatment. Our data have yet to identify an interaction between HS and βAA supplementation that demonstrably impacts well-being.


Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 731-P
Author(s):  
MICHAEL W. SCHLEH ◽  
BENJAMIN J. RYAN ◽  
JENNA B. GILLEN ◽  
PALLAVI VARSHNEY ◽  
KATIE FOUG ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zolian S. Zoong Lwe ◽  
Ruth Welti ◽  
Daniel Anco ◽  
Salman Naveed ◽  
Sachin Rustgi ◽  
...  

AbstractUnderstanding the changes in peanut (Arachis hypogaea L.) anther lipidome under heat stress (HT) will aid in understanding the mechanisms of heat tolerance. We profiled the anther lipidome of seven genotypes exposed to ambient temperature (AT) or HT during flowering. Under AT and HT, the lipidome was dominated by phosphatidylcholine (PC), phosphatidylethanolamine (PE), and triacylglycerol (TAG) species (> 50% of total lipids). Of 89 lipid analytes specified by total acyl carbons:total carbon–carbon double bonds, 36:6, 36:5, and 34:3 PC and 34:3 PE (all contain 18:3 fatty acid and decreased under HT) were the most important lipids that differentiated HT from AT. Heat stress caused decreases in unsaturation indices of membrane lipids, primarily due to decreases in highly-unsaturated lipid species that contained 18:3 fatty acids. In parallel, the expression of Fatty Acid Desaturase 3-2 (FAD3-2; converts 18:2 fatty acids to 18:3) decreased under HT for the heat-tolerant genotype SPT 06-07 but not for the susceptible genotype Bailey. Our results suggested that decreasing lipid unsaturation levels by lowering 18:3 fatty-acid amount through reducing FAD3 expression is likely an acclimation mechanism to heat stress in peanut. Thus, genotypes that are more efficient in doing so will be relatively more tolerant to HT.


2019 ◽  
Vol 70 (1) ◽  
pp. e522
Author(s):  
David Carneros Trujillo ◽  
Cristina Morilla ◽  
Emilio Jimenez ◽  
Matilde Bustos

2006 ◽  
Vol 290 (6) ◽  
pp. E1227-E1236 ◽  
Author(s):  
Hyunsook Kim ◽  
Patricia A. Pennisi ◽  
Oksana Gavrilova ◽  
Stephanie Pack ◽  
William Jou ◽  
...  

The antiobesity and antidiabetic effects of the β3-adrenergic agonists were investigated on nonobese type 2 diabetic MKR mice after injection with a β3-adrenergic agonist, CL-316243. An intact response to acute CL-316243 treatment was observed in MKR mice. Chronic intraperitoneal CL-316243 treatment of MKR mice reduced blood glucose and serum insulin levels. Hyperinsulinemic euglycemic clamps exhibited improvement of the whole body insulin sensitivity and glucose homeostasis concurrently with enhanced insulin action in liver and adipose tissue. Treating MKR mice with CL-316243 significantly lowered serum and hepatic lipid levels, in part due to increased whole body triglyceride clearance and fatty acid oxidation in adipocytes. A significant reduction in total body fat content and epididymal fat weight was observed along with enhanced metabolic rate in both wild-type and MKR mice after treatment. These data demonstrate that β3-adrenergic activation improves the diabetic state of nonobese diabetic MKR mice by potentiation of free fatty acid oxidation by adipose tissue, suggesting a potential therapeutic role for β3-adrenergic agonists in nonobese diabetic subjects.


2021 ◽  
Vol 12 ◽  
Author(s):  
Chaoyue Wen ◽  
Siyu Li ◽  
Jiaojiao Wang ◽  
Yimin Zhu ◽  
Xin Zong ◽  
...  

BackgroundHeat stress has negative effects on the intestinal health of humans and animals. However, the impact of heat stress on intestinal microbial and metabolic changes remains elusive. Here, we investigated the cecal microbial and metabolic profiles in mice in response to heat stress.MethodsThe mouse heat stress model was constructed by simulating a high-temperature environment. Twenty mice were randomly assigned to two groups, the control group (CON, 25°C) and the heat treatment group (HS, 40°C from 13:00 to 15:00 every day for 7 days). Serum and cecal contents were collected from the mice for serum biochemical analysis, 16S rRNA high-throughput sequencing, and non-targeted metabolomics.ResultsBoth core body temperature and water intake were significantly increased in the HS group. Serum biochemical indicators were also affected, including significantly increased triglyceride and decreased low-density lipoprotein in the heat stress group. The composition and structure of intestinal microbiota were remarkably altered in the HS group. At the species level, the relative abundance of Candidatus Arthromitus sp. SFB-mouse-Japan and Lactobacillus murinus significantly reduced, while that of Lachnospiraceae bacterium 3-1 obviously increased after HS. Metabolomic analysis of the cecal contents clearly distinguished metabolite changes between the groups. The significantly different metabolites identified were mainly involved in the fatty acid synthesis, purine metabolism, fatty acid metabolism, cyanoamino acid metabolism, glyceride metabolism, and plasmalogen synthesis.ConclusionIn summary, high temperature disrupted the homeostatic balance of the intestinal microbiota in mice and also induced significant alterations in intestinal metabolites. This study provides a basis for treating intestinal disorders caused by elevated temperature in humans and animals and can further formulate nutritional countermeasures to reduce heat stress-induced damage.


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