scholarly journals Increased Maternal Nutrition Stimulates Peroxisome Proliferator Activated Receptor-γ, Adiponectin, and Leptin Messenger Ribonucleic Acid Expression in Adipose Tissue before Birth

Endocrinology ◽  
2007 ◽  
Vol 148 (2) ◽  
pp. 878-885 ◽  
Author(s):  
B. S. Muhlhausler ◽  
J. A. Duffield ◽  
I. C. McMillen
Keyword(s):  
Adipose Tissue ◽  
Ribonucleic Acid ◽  
Maternal Nutrition ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Messenger Ribonucleic Acid

195 Maternal Impact on Fetal Muscle and Adipose Tissue Development

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 103-104
Author(s):  
Min Du
Keyword(s):  
Adipose Tissue ◽  
Production Efficiency ◽  
Maternal Nutrition ◽  
Maternal Stress ◽  
Adipogenic Differentiation ◽  
Peroxisome Proliferator ◽  
Offspring Performance ◽  
Peroxisome Proliferator Activated Receptor ◽  
Brown Adipose ◽  
Fetal Muscle

Abstract Tissues and organs are actively developing during the fetal stage, which is sensitive to nutritional alteration and exerts long-term impacts on offspring performance. Both muscle and adipose tissue are derived from the dermomyotome during the early embryonic stage, and their common origins provide an opportunity to promote myogenic instead of adipogenic differentiation, which enhances the lean/fat ratio of offspring. In previous studies with sheep and cattle, we found that maternal nutrient deficiency reduces fetal myogenesis and the lean/fat ratio of offspring. Stress is common in animals during pregnancy, and we examined the impacts of maternal stress induced by dexamethasone on fetal muscle and adipose development. We found that maternal stress impairs fetal muscle and brown adipose tissue (BAT) development. Mechanistically, we found that maternal stress suppresses mitochondrial biogenesis during fetal muscle and BAT development by elevating DNA methylation in the promoter of peroxisome proliferator-activated receptor-gamma coactivator α (PGC-1α), which persists in offspring muscle and BAT, generating lasting effects on the functions of muscle and adipose tissue. In short, available data clearly show that maternal nutrition and other physiological factors have profound impacts on fetal development, which programs offspring performance. Understanding related mechanisms are important for effective and precise management of animals during gestation in order to enhance production efficiency of offspring.

scholarly journals Programmed regulation of rat offspring adipogenic transcription factor (PPARγ) by maternal nutrition

2015 ◽  
Vol 6 (6) ◽  
pp. 530-538 ◽  
Author(s):  
M. Desai ◽  
J. K. Jellyman ◽  
G. Han ◽  
R. H. Lane ◽  
M. G. Ross
Keyword(s):  
Transcription Factor ◽  
Adipose Tissue ◽  
Birth Weight ◽  
Protein Expression ◽  
Maternal Nutrition ◽  
Female Rats ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Altered Expression ◽  
Adipogenic Transcription Factor

We determined the protein expression of adipogenic transcription factor, peroxisome proliferator-activated receptor gamma (PPARγ) and its co-repressor and co-activator complexes in adipose tissue from the obese offspring of under- and over-nourished dams. Female rats were fed either a high-fat (60% kcal) or control (10% kcal) diet before mating, and throughout pregnancy and lactation (Mat-OB). Additional dams were 50% food-restricted from pregnancy day 10 to term [intrauterine growth-restricted (IUGR)]. Adipose tissue protein expression was analyzed in newborn and adult male offspring. Normal birth weight Mat-OB and low birth weight IUGR newborns had upregulated PPARγ with variable changes in co-repressors and co-activators. As obese adults, Mat-OB and IUGR offspring had increased PPARγ with decreased co-repressor and increased co-activator expression. Nutritionally programmed increased PPARγ expression is associated with altered expression of its co-regulators in the newborn and adult offspring. Functional studies of PPARγ co-regulators are necessary to establish their role in PPARγ-mediated programmed obesity.

scholarly journals Is the Mitochondrial Function of Keloid Fibroblasts Affected by Cytoglobin?

2021 ◽  
Vol 28 (2) ◽  
pp. 39-47
Author(s):  
Sri Widia A Jusman ◽  
Isma Nur Azzizah ◽  
Mohamad Sadikin ◽  
Novi Silvia Hardiany
Keyword(s):  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Ribonucleic Acid ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Messenger Ribonucleic Acid ◽  
Keloid Fibroblast ◽  
Excessive Proliferation ◽  
Keloid Fibroblasts

Background: A keloid is a benign skin tumour characterised by excessive proliferation of fibroblasts, a process that requires a sufficient amount of energy. The energy needs are associated with adequate oxygen (O2) flow and well-functioning mitochondria. It is known that cytoglobin (CYGB) has a function in O2 distribution. The aim of the present study was to explore whether the inhibition of CYGB expression caused impaired mitochondrial function of keloid fibroblasts. Methods: An in vitro study was conducted on a keloid fibroblast derived from our previous study. The study was carried out in the laboratory of the Biochemistry & Molecular Biology Department, Faculty of Medicine, Universitas Indonesia (FMUI), from July to December 2018. CYGB expression was inhibited by small interfering ribonucleic acid (siRNA) and CYGB. Analysis of mitochondrial function was observed through peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), a mitochondrial biogenesis marker and the activity of the succinate dehydrogenase (SDH) enzyme in mitochondria. Results: The CYGB gene and protein were downregulated after treatment with CYGB siRNA. Inhibition of CYGB expression with siRNA also tended to decrease the levels of PGC-1α messenger ribonucleic acid (mRNA) and protein, as well as SDH enzyme activity. Conclusion: Inhibition of CYGB expression with siRNA tended to decrease mitochondrial biogenesis and function. This may be useful for understanding the excessive proliferation of fibroblasts in keloids and for development of treatment for keloids.

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