Highlighting “Withered Tree” Concept Host, Achieved by Global Contraception and Abortion, Secondary to Fragmented Germ Cells, Agonizingly Reduced Endogenous Estrogen/Androgen, Defaulted Genomic Repertoire, Deranged Cell Metabolism, Metabolic Syndrome, Result in Failure of Pharmacological Therapeutics with Advanced Technologies

Mitochondria are critical regulator of cell metabolism; thus, mitochondrial dysfunction is associated with many metabolic disorders. Defects in oxidative phosphorylation, ROS production, or mtDNA mutations are the main causes of mitochondrial dysfunction in many pathological conditions such as IR/diabetes, metabolic syndrome, cardiovascular diseases, and cancer. Thus, targeting mitochondria has been proposed as therapeutic approach for these conditions, leading to the development of small molecules to be tested in the clinical scenario. Here we discuss therapeutic interventions to treat mitochondrial dysfunction associated with two major metabolic disorders, metabolic syndrome, and cancer. Finally, novel mechanisms of regulation of mitochondrial function are discussed, which open new scenarios for mitochondria targeting.

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Studies on Increased Prevalence of Hernia, Uterine Descent, Fibrous Adhesions, Retroperitoneal Fibrosis and Germ Cells with Endogenous Estrogen

Highlights on Medicine and Medical Science Vol. 8 ◽

10.9734/bpi/hmms/v8/2394f ◽

2021 ◽

pp. 92-100

Author(s):

Elizabeth JeyaVardhini Samuel

Keyword(s):

Germ Cells ◽

Retroperitoneal Fibrosis ◽

Uterine Descent ◽

Endogenous Estrogen

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Metabolo-epigenetics: The interplay of metabolism and epigenetics during early germ cells development

Biology of Reproduction ◽

10.1093/biolre/ioab118 ◽

2021 ◽

Author(s):

Roxane Verdikt ◽

Patrick Allard

Keyword(s):

Cell Fate ◽

Germ Cells ◽

Current Knowledge ◽

Cell Metabolism ◽

Primordial Germ Cells ◽

Epigenetic Inheritance ◽

Cell Fate Determination ◽

Specific Context ◽

Control Of Gene Expression ◽

Multiple Stages

Abstract Metabolites control epigenetic mechanisms and, conversly, cell metabolism is regulated at the epigenetic level in response to changes in the cellular environnement. In recent years, this metabolo-epigenetic control of gene expression has been implicated in the regulation of multiple stages of embryonic development. The developmental potency of stem cells and their embryonic counterparts is directly determined by metabolic rewiring. Here, we review the current knowledge on the interplay between epigenetics and metabolism in the specific context of early germ cells development. We further develop the implications of metabolic rewiring in primordial germ cells in light of their epigenetic remodelling during cell fate determination. Finally, we discuss the relevance of concerted metabolic and epigenetic regulation of primordial germ cells in the context of mammalian transgenerational epigenetic inheritance.

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Increasing Incidence of Diabetes Mellitus, Systemic Hypertension and Germ Cells with Endogenous Estrogen

Open Journal of Preventive Medicine ◽

10.4236/ojpm.2014.46056 ◽

2014 ◽

Vol 04 (06) ◽

pp. 481-488 ◽

Cited By ~ 1

Author(s):

Elizabeth Jeya Vardhini Samuel ◽

Nagarajan Natarajan ◽

Sanjoy George ◽

Kiran Gkulirankal ◽

George Eapen

Keyword(s):

Diabetes Mellitus ◽

Germ Cells ◽

Systemic Hypertension ◽

Endogenous Estrogen

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Metformin Increases Proliferative Activity and Viability of Multipotent Stromal Stem Cells Isolated from Adipose Tissue Derived from Horses with Equine Metabolic Syndrome

Cells ◽

10.3390/cells8020080 ◽

2019 ◽

Vol 8 (2) ◽

pp. 80 ◽

Cited By ~ 9

Author(s):

Agnieszka Smieszek ◽

Katarzyna Kornicka ◽

Jolanta Szłapka-Kosarzewska ◽

Peter Androvic ◽

Lukas Valihrach ◽

...

Keyword(s):

Metabolic Syndrome ◽

Membrane Potential ◽

Mitochondrial Membrane Potential ◽

Proliferative Activity ◽

Mitochondrial Membrane ◽

Cell Metabolism ◽

Brdu Incorporation ◽

Population Doubling ◽

Population Doubling Time ◽

Equine Metabolic Syndrome

In this study, we investigated the influence of metformin (MF) on proliferation and viability of adipose-derived stromal cells isolated from horses (EqASCs). We determined the effect of metformin on cell metabolism in terms of mitochondrial metabolism and oxidative status. Our purpose was to evaluate the metformin effect on cells derived from healthy horses (EqASCHE) and individuals affected by equine metabolic syndrome (EqASCEMS). The cells were treated with 0.5 μM MF for 72 h. The proliferative activity was evaluated based on the measurement of BrdU incorporation during DNA synthesis, as well as population doubling time rate (PDT) and distribution of EqASCs in the cell cycle. The influence of metformin on EqASC viability was determined in relation to apoptosis profile, mitochondrial membrane potential, oxidative stress markers and BAX/BCL-2 mRNA ratio. Further, we were interested in possibility of metformin affecting the Wnt3a signalling pathway and, thus, we determined mRNA and protein level of WNT3A and β-catenin. Finally, using a two-tailed RT-qPCR method, we investigated the expression of miR-16-5p, miR-21-5p, miR-29a-3p, miR-140-3p and miR-145-5p. Obtained results indicate pro-proliferative and anti-apoptotic effects of metformin on EqASCs. In this study, MF significantly improved proliferation of EqASCs, which manifested in increased synthesis of DNA and lowered PDT value. Additionally, metformin improved metabolism and viability of cells, which correlated with higher mitochondrial membrane potential, reduced apoptosis and increased WNT3A/β-catenin expression. Metformin modulates the miRNA expression differently in EqASCHE and EqASCEMS. Metformin may be used as a preconditioning agent which stimulates proliferative activity and viability of EqASCs.

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