Fermented extract of mealworm (Tenebrio molitor larvae) as a dietary protein source modulates hepatic proteomic profiles in C57BLKS/J-db/db mice

Turkyilmaz, A.; Lee, Y.; Lee, Hae-in

doi:10.3920/jiff2022.0162

Cited by 3 publications

(1 citation statement)

References 54 publications

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“…It plays a major role in regulating insulin content and may also contribute to glucose toxicity by affecting insulin production [121,168] so that loss-offunction variation in TXNDC5 elevates fasting blood glucose levels [178]. On the other side, casein as a dietary protein source for type 2 diabetes, can downregulate TXNDC5 [179]. TXNDC5 is closely associated and interacts with proinsulin in pancreatic islets.…”

Section: Txndc5 and Diabetes Mellitusmentioning

confidence: 99%

Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

Bidooki,

Navarro,

Fernandes

et al. 2024

CIMB

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This review focuses on the thioredoxin domain containing 5 (TXNDC5), also known as endoplasmic reticulum protein 46 (ERp46), a member of the protein disulfide isomerase (PDI) family with a dual role in multiple diseases. TXNDC5 is highly expressed in endothelial cells, fibroblasts, pancreatic β-cells, liver cells, and hypoxic tissues, such as cancer endothelial cells and atherosclerotic plaques. TXNDC5 plays a crucial role in regulating cell proliferation, apoptosis, migration, and antioxidative stress. Its potential significance in cancer warrants further investigation, given the altered and highly adaptable metabolism of tumor cells. It has been reported that both high and low levels of TXNDC5 expression are associated with multiple diseases, such as arthritis, cancer, diabetes, brain diseases, and infections, as well as worse prognoses. TXNDC5 has been attributed to both oncogenic and tumor-suppressive features. It has been concluded that in cancer, TXNDC5 acts as a foe and responds to metabolic and cellular stress signals to promote the survival of tumor cells against apoptosis. Conversely, in normal cells, TXNDC5 acts as a friend to safeguard cells against oxidative and endoplasmic reticulum stress. Therefore, TXNDC5 could serve as a viable biomarker or even a potential pharmacological target.

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Section: Txndc5 and Diabetes Mellitusmentioning

confidence: 99%

Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

Bidooki,

Navarro,

Fernandes

et al. 2024

CIMB

View full text Add to dashboard Cite

show abstract

Anti-muscle atrophy effect of fermented Tenebrio molitor larvae extract by modulating the PI3K-Akt-mTOR/FoxO3α pathway in mice treated with dexamethasone

Han,

Choi,

Choi

et al. 2024

Biomedicine & Pharmacotherapy

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Anti‑osteoclastogenic effect of fermented mealworm extract by inhibiting RANKL‑induced NFATc1 action

Ham,

Lee

2024

Exp Ther Med

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Augmented osteoclast activity and differentiation can lead to destructive bone diseases, such as arthritis and osteoporosis. Therefore, modulating osteoclastogenesis and differentiation may serve to be a possible strategy for treating such diseases. Tenebrio molitor larvae, also known as mealworms, are considered a good source of protein with nutritional value, digestibility, flavor and functional properties, such as antioxidant, anti-diabetic and anti-obesity effects. However, the role of mealworms in osteoclastogenesis remains poorly understood. The present study therefore investigated the effects of fermented mealworm extract (FME) on receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived macrophages (BMMs) whilst also attempting to understand the underlying mechanism, if any. The cells treated with RANKL were used as the negative control. To prepare FME, defatted mealworm powder was fermented with a Saccharomyces cerevisiae strain, and then extracted with fermented alcohol. Cell viability of BMMs isolated from 5-week-old Institute of Cancer Research mice was measured using Cell Counting Kit-8 assay. Subsequently, the effects of FME on osteoclast differentiation were measured using tartrate-resistant acid phosphatase (TRAP) staining. In addition, expression of markers associated with osteoclast differentiation was assessed by reverse transcription-quantitative PCR. Expression of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) was assessed by western blotting. TRAP staining revealed that FME inhibited osteoclast differentiation in a dose-dependent manner (10-100 µg/ml) without causing cytotoxicity. Specifically, the formation of osteoclasts appear to have been suppressed by FME as indicated by the reduction in the number of TRAP-positive multinucleated cells observed. Furthermore, FME treatment significantly decreased the mRNA expression of c-Fos, whilst also significantly decreasing the expression of NFATc1 on both protein and mRNA levels. c-Fos and NFATc1 are transcription factors that can regulate osteoclast differentiation. FME treatment also reduced the expression of genes associated with osteoclast differentiation and function, including dendritic cell-specific transmembrane protein , osteoclast associated Ig-like receptor , Cathepsin K and TRAP , compared with that in the control group. Subsequently, FME was found to effectively suppress RANKL-induced osteoclast differentiation compared with that by the non-fermented mealworm extract. These findings suggest that FME may confer anti-osteoclastogenic effects, providing insights into its potential application in treatment of osteoporosis.

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Fermented extract of mealworm (Tenebrio molitor larvae) as a dietary protein source modulates hepatic proteomic profiles in C57BLKS/J-db/db mice

Cited by 3 publications

References 54 publications

Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

Anti-muscle atrophy effect of fermented Tenebrio molitor larvae extract by modulating the PI3K-Akt-mTOR/FoxO3α pathway in mice treated with dexamethasone

Anti‑osteoclastogenic effect of fermented mealworm extract by inhibiting RANKL‑induced NFATc1 action

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