ArticleMolecular medicine reports2019
Inhibitory effect of 17β‑estradiol on triglyceride synthesis in skeletal muscle cells is dependent on ESR1 and not ESR2.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Pooled it
- Exogenous adiponectin attenuates lipid accumulation and is associated with enhanced TG and VLDL secretion in primary chicken hepatocytes.Poultry science · 2026Article
- The role ofArchives animal breeding · 2026Article
- Diabetes mellitus in breast cancer survivors: metabolic effects of endocrine therapy.Nature reviews. Endocrinology · 2024Review
- Role of Fish Oil in Preventing Paternal Obesity and Improving Offspring Skeletal Muscle Health.Biomedicines · 2023Article
- Mechanisms of Estrogen Influence on Skeletal Muscle: Mass, Regeneration, and Mitochondrial Function.Sports medicine (Auckland, N.Z.) · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the inhibitory effects and the mechanisms underlying 17β‑estradiol (E2) effects on triglyceride synthesis and insulin resistance in skeletal muscle tissues and cells. Ovariectomy (OVX) was performed on 6‑month‑old female rats treated with or without E2. Subsequently, various serum biochemical markers were measured. Additionally, pathological alterations of the uterus, liver and skeletal muscle were analyzed, and the content of triglycerides (TG) in muscle was detected. Differentiated myotubes formed by C2C12 cells were treated with palmitic acid (PA) or pretreated with E2, estrogen receptor (ESR) 1 agonist propylpyrazoletriol (PPT) and ESR2 agonist diarylpropionitrile (DPN). Subsequently, the mRNA or protein expression levels of ESR1/2, peroxisome proliferator activated receptor α (PPARα), CD36 molecule (CD36), fatty acid synthase (FASN), perilipin 2 (PLIN2), phosphorylated acetyl‑CoA carboxylase α (p‑ACACA), p‑AKT serine/threonine kinase (p‑AKT) and p‑mitogen‑activated protein kinase 8 (p‑MAPK8) were analyzed in skeletal muscle or in C2C12 cells by reverse transcription‑semi‑quantitative polymerase chain reaction and western blotting. The present results suggested that treatment with E2 inhibited OVX‑induced body weight gain, TG accumulation and insulin resistance. The protein or mRNA expression levels of ESR1, CD36, PPARα, p‑ACACA and p‑AKT were decreased, whereas the protein or mRNA expression levels of ESR2, PLIN2, FASN and p‑MAPK8 were increased in the OVX group. Of note, treatment with E2 restored the expression levels of the aforementioned factors. In C2C12 cells, treatment with E2 or PPT reversed the alterations induced by treatment with PA. In contrast, pretreatment with DPN did not influence the effect of PA. Collectively, E2 was able to interact with ESR1, thus activating the CD36‑PPARα pathway, decreasing the level of TG in the muscles and improving insulin resistance in skeletal muscles and C2C12 cells.
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