scholarly journals JNK Inhibition by SP600125 Attenuates trans-10, cis-12 Conjugated Linoleic Acid-Mediated Regulation of Inflammatory and Lipogenic Gene Expression

Lipids ◽  
2011 ◽  
Vol 46 (10) ◽  
pp. 885-892 ◽  
Author(s):  
Kristina Martinez ◽  
Arion Kennedy ◽  
Michael K. McIntosh
Keyword(s):  
Gene Expression ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Lipogenic Gene ◽  
Lipogenic Gene Expression

scholarly journals Trans-10, cis-12 conjugated linoleic acid reduces milk fat content and lipogenic gene expression in the mammary gland of sows without altering litter performance

2019 ◽  
Vol 123 (6) ◽  
pp. 610-618 ◽  
Author(s):  
E. C. Sandri ◽  
K. J. Harvatine ◽  
D. E. Oliveira
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Milk Fat ◽  
Fat Content ◽  
Lipogenic Gene ◽  
Lipogenic Genes ◽  
Lipogenic Gene Expression

AbstractTrans-10, cis-12 conjugated linoleic acid (CLA) decreases milk fat synthesis in lactating sows and involves, at least in part, the down-regulation of lipogenic genes. The objective was to evaluate the effect of CLA on milk composition and lipogenic gene expression. Twenty multiparous sows were randomly assigned to one of the two treatments for 18 d (from day 7 to day 25 of lactation): (1) control (no CLA added) and (2) 1 % of CLA mixed into the ration. CLA treatment decreased milk fat and protein content by 20 % (P = 0·004) and 11 % (P = 0·0001), respectively. However, piglet weight did not differ between treatments (P = 0·60). Dietary CLA increased the concentration of SFA in milk fat by 16 % (P < 0·0001) and decreased MUFA by 17·6 % (P < 0·0001). In the mammary gland, CLA reduced gene expression of acetyl-CoA carboxylase-α by 37 % (P = 0·003), fatty acid synthase by 64 % (P = 0·002), stearoyl-CoA desaturase 1 by 52 % (P = 0·003), lipoprotein lipase by 26 % (P = 0·03), acyl glycerol phosphate acyltransferase 6 by 15 % (P = 0·02) and diacylglycerol acyltransferase 1 by 27 % (P = 0·02), whereas the expression of fatty acid binding protein 3 was not altered by CLA treatment (P = 0·09). Mammary expression of casein-β and α-lactalbumin was reduced by CLA by 68 % (P = 0·0004) and 62 % (P = 0·005), respectively. Additionally, CLA had no effect on the expression of lipogenic genes evaluated in adipose tissue. In summary, CLA reduced milk fat content without negatively affecting litter performance and it affected mammary expression of genes involved in all lipogenic pathways studied.

scholarly journals Conjugated Linoleic Acid Reduces Body Fat Accretion and Lipogenic Gene Expression in Neonatal Pigs Fed Low- or High-Fat Formulas

2008 ◽  
Vol 138 (3) ◽  
pp. 449-454 ◽  
Author(s):  
Benjamin A. Corl ◽  
Susan A. Mathews Oliver ◽  
Xi Lin ◽  
William T. Oliver ◽  
Yongxi Ma ◽  
...  
Keyword(s):  
Gene Expression ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Body Fat ◽  
High Fat ◽  
Lipogenic Gene ◽  
Neonatal Pigs ◽  
Lipogenic Gene Expression ◽  
Fat Accretion

scholarly journals Carbohydrate-response-element-binding protein (ChREBP) and not the liver X receptor α (LXRα) mediates elevated hepatic lipogenic gene expression in a mouse model of glycogen storage disease type 1

2010 ◽  
Vol 432 (2) ◽  
pp. 249-254 ◽  
Author(s):  
Aldo Grefhorst ◽  
Marijke Schreurs ◽  
Maaike H. Oosterveer ◽  
Victor A. Cortés ◽  
Rick Havinga ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Protein ◽  
Glycogen Storage Disease Type ◽  
Glycogen Storage ◽  
Hepatic Glycogen ◽  
Lipogenic Gene ◽  
Lipogenic Gene Expression ◽  
Liver X Receptor Α ◽  
Element Binding Protein

GSD-1 (glycogen storage disease type 1) is caused by an inherited defect in glucose-6-phosphatase activity, resulting in a massive accumulation of hepatic glycogen content and an induction of de novo lipogenesis. The chlorogenic acid derivative S4048 is a pharmacological inhibitor of the glucose 6-phosphate transporter, which is part of glucose-6-phosphatase, and allows for mechanistic studies concerning metabolic defects in GSD-1. Treatment of mice with S4048 resulted in an ~60% reduction in blood glucose, increased hepatic glycogen and triacylglycerol (triglyceride) content, and a markedly enhanced hepatic lipogenic gene expression. In mammals, hepatic expression of lipogenic genes is regulated by the co-ordinated action of the transcription factors SREBP (sterol-regulatory-element-binding protein)-1c, LXRα (liver X receptor α) and ChREBP (carbohydrate-response-element-binding protein). Treatment of Lxra−/− mice and Chrebp−/− mice with S4048 demonstrated that ChREBP, but not LXRα, mediates the induction of hepatic lipogenic gene expression in this murine model of GSD-1. Thus ChREBP is an attractive target to alleviate derangements in lipid metabolism observed in patients with GSD-1.

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