scholarly journals PSXIII-33 Polyunsaturated fatty acid and their fetal programming effect on the FFARs from ewe lambs’ ovaries

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 364-365
Author(s):  
Ana Carranza Martin ◽  
Alejandro E Relling

Abstract Free fatty acids (FA) receptors (FFAR) are critical for metabolic functions and energy homeostasis. The FFAR1 and FFAR4 are activated by long-chain polyunsaturated FA, but FFAR2 and FFAR3 join to short-chain FA. There is no evidence fetal programming on nutritional effects on those receptors, insulin receptor (INS-R) and stereological enzyme in lambs’ ovaries. The objective of this study was to evaluate the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation to ewes during late gestation on finishing lamb ovary gene expression. Lambs born from ewes supplemented with Ca salts of EPA and DHA (PUFA), or palm FA distillate (PFAD) high in palmitic and oleic acid at 0.39% DM during the last 50d of gestation were used. After weaning and high concentrate diet adaptation (45d), 14 Hampshire x Dorset cross females lambs were blocked by initial BW and used in a 2x2 factorial arrangement of treatments using the factors of dam supplementation and lamb diets (PUFA or PFAD at 1.5% DM). At day 42, lambs were euthanized and ovary samples were obtained for FFARs, INS-R and steroid acute regulatory protein (STAR) mRNA concentration analysis. There was a dam diet effect on the abundance of FFAR4 mRNA (P = 0.05); lambs born from PUFA dams showed greater concentration than PFAD. Also, PUFA lambs tend to have greater concentration of FFAR4 (P = 0.07). The abundance of FFAR2, INS-R, and STAR mRNA was not significant for dam or lamb diet effect (P > 0.1). The mRNA of FFAR1 and FFAR3 were no found in the samples. However, mRNA concentration of FFAR2 and STAR were positively associated (r = 0.74 P < 0.05). In conclusion, dam and lamb diets modified FFAR4 mRNA concentration; and there might be a functional association between FFAR2 and STAR.

2000 ◽  
Vol 41 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Karin A. J.M. van der Lee ◽  
Michaël M. Vork ◽  
Johan E. De Vries ◽  
Peter H.M. Willemsen ◽  
Jan F.C. Glatz ◽  
...  

2002 ◽  
Vol 43 (6) ◽  
pp. 979-985 ◽  
Author(s):  
Syrah Khan ◽  
Anne-Marie Minihane ◽  
Philippa J. Talmud ◽  
John W. Wright ◽  
Margaret C. Murphy ◽  
...  

2021 ◽  
Vol 22 (12) ◽  
pp. 6292
Author(s):  
Rubén Tovar ◽  
Antonio Vargas ◽  
Jesús Aranda ◽  
Lourdes Sánchez-Salido ◽  
Laura González-González ◽  
...  

Maternal malnutrition in critical periods of development increases the risk of developing short- and long-term diseases in the offspring. The alterations induced by this nutritional programming in the hypothalamus of the offspring are of special relevance due to its role in energy homeostasis, especially in the endocannabinoid system (ECS), which is involved in metabolic functions. Since astrocytes are essential for neuronal energy efficiency and are implicated in brain endocannabinoid signaling, here we have used a rat model to investigate whether a moderate caloric restriction (R) spanning from two weeks prior to the start of gestation to its end induced changes in offspring hypothalamic (a) ECS, (b) lipid metabolism (LM) and/or (c) hypothalamic astrocytes. Monitorization was performed by analyzing both the gene and protein expression of proteins involved in LM and ECS signaling. Offspring born from caloric-restricted mothers presented hypothalamic alterations in both the main enzymes involved in LM and endocannabinoids synthesis/degradation. Furthermore, most of these changes were similar to those observed in hypothalamic offspring astrocytes in culture. In conclusion, a maternal low caloric intake altered LM and ECS in both the hypothalamus and its astrocytes, pointing to these glial cells as responsible for a large part of the alterations seen in the total hypothalamus and suggesting a high degree of involvement of astrocytes in nutritional programming.


1998 ◽  
Vol 83 (7) ◽  
pp. 2597-2600 ◽  
Author(s):  
M. Reincke ◽  
F. Beuschlein ◽  
E. Lalli ◽  
W. Arlt ◽  
S. Vay ◽  
...  

The DAX-1 gene encodes an orphan nuclear hormone receptor essential for normal fetal development of the adrenal cortex. Recently, DAX-1 has been shown to act as a transcriptional repressor of steroidogenic acute regulatory protein gene expression (StAR), suppressing steroidogenesis. We, therefore, investigated the expression of DAX-1 in a variety of adrenocortical tumors and compared the results with StAR mRNA expression. We found low or absent DAX-1 expression in aldosterone-producing adenomas (n=11: 35±11%; normal adrenals: 100±17%) and in aldosterone-producing adrenocortical carcinomas (n=2: 24 and 36%). Cortisol-producing adenomas showed intermediate DAX-1 expression (n=8; 92±16), as did 3 non-aldosterone-producing carcinomas (72, 132 and 132%). High DAX-1 expression was present in nonfunctional adenomas (n=3; 160±17%). In contrast to DAX-1, StAR mRNA expression did not show significant variations between groups. We did not detect the expected negative correlation between DAX-1 and StAR mRNA in adrenocortical tumors. These data suggest that high DAX-1 expression in adrenocortical tumors is associated with a non-functional phenotype whereas low DAX-1 expression favors mineralo-corticoid secretion. These effects on steroidogenesis are mediated by mechanisms other than repression of StAR gene expression. Our results indicate that DAX-1 may be one of the factors influencing the steroid biosynthesis of adrenocortical neoplasms.


1992 ◽  
Vol 12 (4) ◽  
pp. 1708-1718
Author(s):  
M Mietus-Snyder ◽  
F M Sladek ◽  
G S Ginsburg ◽  
C F Kuo ◽  
J A Ladias ◽  
...  

Apolipoprotein CIII (apoCIII), a lipid-binding protein involved in the transport of triglycerides and cholesterol in the plasma, is synthesized primarily in the liver and the intestine. A cis-acting regulatory element, C3P, located at -90 to -66 upstream from the apoCIII gene transcriptional start site (+1), is necessary for maximal expression of the apoCIII gene in human hepatoma (HepG2) and intestinal carcinoma (Caco2) cells. This report shows that three members of the steroid receptor superfamily of transcription factors, hepatocyte nuclear factor 4 (HNF-4), apolipoprotein AI regulatory protein 1 (ARP-1), and Ear3/COUP-TF, act at the C3P site. HNF-4 activates apoCIII gene expression in HepG2 and Caco2 cells, while ARP-1 and Ear3/COUP-TF repress its expression in the same cells. HNF-4 activation is abolished by increasing amounts of ARP-1 or Ear3/COUP-TF, and repression by ARP-1 or Ear3/COUP-TF is alleviated by increasing amounts of HNF-4. HNF-4 and ARP-1 bind with similar affinities to the C3P site, suggesting that their opposing transcriptional effects may be mediated by direct competition for DNA binding. HNF-4 and ARP-1 mRNAs are present within the same cells in the liver and intestine, and protein extracts from hepatic tissue, HepG2, and Caco2 cells contain significantly more HNF-4 than ARP-1 or Ear3/COUP-TF binding activities. These findings suggest that the transcription of the apoCIII gene in vivo is dependent, at least in part, upon the intracellular balance of these positive and negative regulatory factors.


Author(s):  
Ch. Shiva Prasad ◽  
R. Vinoo ◽  
R.N. Chatterjee ◽  
M. Muralidhar ◽  
D. Narendranath ◽  
...  

Background: Acetyl-CoA Carboxylase Beta (ACACB) plays a key role in fatty acid oxidation and was known to be involved in production of very-long-chain fatty acid and other compounds needed for proper development. This gene is mainly expressed in the tissues of heart, muscle, liver and colon. It chiefly involved in the production of malonyl-coA, a potent inhibitor of carnitine palmitoyl transferase I (CPT-I) enzyme needed in transport of long-chain fatty acyl-coAs to the mitochondria for β-oxidation.Methods: The present study was conducted to explore the expression pattern of the ACACB gene in breast muscle tissue during pre-hatch embryonic day (ED) 5th to 18th and post-hatch (18th, 22nd and 40th week of age) periods of White leghorn (IWI line) by using Quantitative real-time PCR (qPCR). Then, fold change of ACACB gene expression was calculated.Result: Our study showed that the ACACB gene expression was down-regulated during embryonic stages from ED6 to ED18. The gene expression was also down-regulated during adult stages i.e. on 22nd and 40th week of age. This result indicated that the initial expression of the ACACB gene is required for embryo development and during adult periods, low gene expression leads to the less fat deposition in muscle of layer chicken. Finally, it can be concluded that there was a differential expression pattern of the ACACB gene during the pre-hatch embryonic and post-hatch adult periods to mitigate varied requirements of lipids during different physiological stages in layer chicken.


1992 ◽  
Vol 12 (4) ◽  
pp. 1568-1577
Author(s):  
J V Paietta

The cys-3+ gene of Neurospora crassa encodes a bZIP (basic region-leucine zipper) regulatory protein that is essential for sulfur structural gene expression (e.g., ars-1+). Nuclear transcription assays confirmed that cys-3+ was under sulfur-regulated transcriptional control and that cys-3+ transcription was constitutive in sulfur controller (scon)-negative regulator mutants. Given these results, I have tested whether expression of cys-3+ under high-sulfur (repressing) conditions was sufficient to induce sulfur gene expression. The N. crassa beta-tubulin (tub) promoter was fused to the cys-3+ coding segment and used to transform a cys-3 deletion mutant. Function of the tub::cys-3 fusion in homokaryotic transformants grown under high-sulfur conditions was confirmed by Northern (RNA) and Western immunoblot analysis. The tub::cys-3 transformants showed arylsulfatase gene expression under normally repressing high-sulfur conditions. A tub::cys-3ts fusion encoding a temperature-sensitive CYS3 protein was used to confirm that the induced structural gene expression was due to CYS3 protein function. Constitutive CYS3 production did not induce scon-2+ expression under repressing conditions. In addition, a cys-3 promoter fusion to lacZ showed that CYS3 production was sufficient to induce its own expression and provides in vivo evidence for autoregulation. Finally, an apparent inhibitory effect observed with a strain carrying a point mutation at the cys-3 locus was examined by in vitro heterodimerization studies. These results support an interpretation of CYS3 as a transcriptional activator whose regulation is a crucial control point in the signal response pathway triggered by sulfur limitation.


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