Monosodium glutamate restricts the adipogenic potential of 3T3‐L1 preadipocytes through mitotic clonal expansion

Abstract

Recent epidemiologic studies pointed out a significant correlation between dietary monosodium glutamate (MSG) and increased body mass index. Corroborating evidences came from animal studies depicting a clear association between dietary MSG intake and increased abdominal fat, dyslipidemia, adipocyte hypertrophy, and total body weight gain. Taken together with the inferred absence of conspicuous hypothalamic neuropathies the hallmark of disease etiopathogenesis in MSG‐obese animals, these animal studies with dietary MSG strongly argue for the presence of an alternative non‐neuronal route for MSG to mediate its adipose tissue‐specific phenotype and body weight gain. On the basis of this hypothesis, we investigated the direct effect of physiologically relevant low (100 µM), moderate (250 µM), and high dosages (2.5 and 25 mM) of MSG on distinct phases of adipocyte differentiation. MSG‐dependent changes in cell proliferation and lipid accumulation were analyzed by cell proliferation assays, flow cytometry, and biochemical methods, respectively. Physiologically relevant high dosages MSG demonstrated a significant potential in reducing MCE and thereof adipogenic capacity of preadipocytes in a dose‐dependent manner by restricting the availability of critical mitogenic proteins, CCAAT/enhancer‐binding protein β (CEBPβ), and the mitotic cyclin B. Our findings warrant further investigations to unravel the effect of long‐term dietary MSG intake on capacity of preadipocytes in different fat depots to undergo mitotic clonal expansion and hyperplasia in rodent models and human subjects, respectively.

Alterations in APC, BECN1, and TP53 gene expression levels in colon cancer cells caused by monosodium glutamate

“…In the present study, the recorded increase of CRC viability in MSG-treated cells can be attributed to intestinal epithelial dysfunction as toxic effect of MSG recently recognised by Türküner and Özcan (2020). Induced epithelial dysfunction, in turn can be related to the remarkable increase of gut bacterial translocation, increase of hepatic lipid droplets, and decrease of rough endoplasmic reticulum activity, collectively induce proliferation of CRC (Türküner and Özcan, 2020).…”

“…This may explain the increase in viable CRC cells measured through MTT assay. On the other hand, the non-significant increase of SW620 CRC might be attributed to the dose and time dependent effect of MSG on mitotic colonal expansion phase (MCE) phase leading to complete inhibition of mitotic activity after 48 hours (Türküner and Özcan, 2020) .Beclin 1 has a central role in autophagy in mammalian cells and is considered as a key regulator of autophagosome formation. In this experiment, BECN1 showed an increase in expression and according to a study conducted in China by Wu and colleagues they observed an increase in both gene and protein expression of BECN1 in CRC tissues compared to that in normal tissues.…”

Elecampane (Inula helenium) Root Extract and Its Major Sesquiterpene Lactone, Alantolactone, Inhibit Adipogenesis of 3T3-L1 Preadipocytes

“…The initiation of MCE involves the expression and activation of immediate early genes, such as transcription factors (CEBPβ and CEBPδ) and cell cycle regulators (p27, cyclin A, cyclin D1, etc.) which induce G1/S transition in 3T3-L1 cells, and many of these genes are known to be regulated by AMPK and Nur77 [ 1 , 2 , 15 , 16 , 17 , 18 ].…”