Leptin and adiponectin synthesis and secretion in mature 3T3-L1 adipocytes are differentially down-regulated by arsenic and palmitic acid exposure throughout different stages of adipogenesis

Ceja-Galicia, Zeltzin Alejandra; Calderón-DuPont, Diana; Daniel, Alberto; Chiu, Luz María; Dı́az-Villaseñor, Andrea

doi:10.1016/j.lfs.2021.120262

Cited by 8 publications

(10 citation statements)

References 63 publications

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“…First, 3T3‐L1 cells, also known as preadipocytes, were used to differentiate into mature adipocytes by adding adipogenic induction medium as reported previously (Figure 3A,B). The amount of LEP secreted by differentiated adipocytes was much higher than that of the 3T3‐L1 preadipocytes, 20–22 which provided a theoretical basis for the establishment of BC cells and an adipocyte co‐culture model in the next step.…”

Section: Resultsmentioning

confidence: 95%

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Baicalein enhances immune response in TNBC by inhibiting leptin expression of adipocytes

Liu,

Li,

et al. 2023

Cancer Science

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Triple‐negative breast cancer (TNBC) is a special pathological type of breast cancer (BC) with poor prognosis. Obesity is shown to be involved in TNBC tumor progression. The interaction between obesity and BC has generated great attention in recent years, however, the mechanism is still unclear. Here, we showed that leptin secreted by adipocytes upregulated PD‐L1 expression in TNBC through the p‐STAT3 signaling pathway and that baicalein inhibited PD‐L1 expression in tumor microenvironment by suppressing leptin transcription of adipocytes. Collectively, our findings suggest that leptin may be the key factor participating in obesity‐related tumor progression and that baicalein can break through the dilemma to boost the anti‐tumor immune response.

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Section: Resultsmentioning

confidence: 95%

“…The amount of LEP secreted by differentiated adipocytes was much higher than that of the 3T3-L1 preadipocytes, [20][21][22] which provided a theoretical basis for the establishment of BC cells and an adipocyte co-culture model in the next step.…”

Section: Adipocytes Upregulate Pd-l1 Expression In 4t1 Cells By Secre...mentioning

confidence: 94%

Baicalein enhances immune response in TNBC by inhibiting leptin expression of adipocytes

Liu,

Li,

et al. 2023

Cancer Science

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“…72 Accordingly, leptin was downregulated in adipocytes by PA exposure, indicating the synergistic regulation of leptin expression by diabetes and fatty acids. 73 However, its role in periodontitis remains controversial. Some studies have reported that leptin accelerates periodontitis by increasing M1 macrophage polarization, promoting IL-6 and IL-8 expression in PDLSCs, and accelerating bone resorption.…”

Section: Adipokinesmentioning

confidence: 99%

Lipotoxicity: The missing link between diabetes and periodontitis?

Sun,

Yin,

Yang

et al. 2024

J of Periodontal Research

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Lipotoxicity refers to the accumulation of lipids in tissues other than adipose tissue (body fat). It is one of the major pathophysiological mechanisms responsible for the progression of diabetes complications such as non‐alcoholic fatty liver disease and diabetic nephropathy. Accumulating evidence indicates that lipotoxicity also contributes significantly to the toxic effects of diabetes on periodontitis. Therefore, we reviewed the current in vivo, in vitro, and clinical evidence of the detrimental effects of lipotoxicity on periodontitis, focusing on its molecular mechanisms, especially oxidative and endoplasmic reticulum stress, inflammation, ceramides, adipokines, and programmed cell death pathways. By elucidating potential therapeutic strategies targeting lipotoxicity and describing their associated mechanisms and clinical outcomes, including metformin, statins, liraglutide, adiponectin, and omega‐3 PUFA, this review seeks to provide a more comprehensive and effective treatment framework against diabetes‐associated periodontitis. Furthermore, the challenges and future research directions are proposed, aiming to contribute to a more profound understanding of the impact of lipotoxicity on periodontitis.

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“…These molecules participate in systemic energy balance, regulating appetite signals in the central nervous system, systemic insulin sensitivity and metabolic activity in peripheral tissues ( 40 ). The levels and secretion of leptin and adiponectin were decreased by sodium arsenite alone (1 µM for 72 h in vitro ) or in combination with palmitate (200 µM) when the treatment occurred during adipogenic differentiation of 3T3-L1 cells, but not by treating fully differentiated 3T3-L1 adipocytes, indicating that the effect depends on the differentiation window of the adipocyte lineage at which exposure began ( 41 ). Perilipin is a protein associated to the surface of lipid droplets, acting as a barrier that prevents lipase access to triglycerides, regulating lipolysis in the adipocytes.…”

Section: Arsenic As An Obesogenic Pollutantmentioning

confidence: 99%

“…Regarding the effects of arsenic and obesity, most of the evidence indicates that arsenic’s metabolic and endocrine effects are independent of weight gain and increased adiposity. Nevertheless, in vitro and in vivo evidence points to the notion that arsenic induces adipocyte hypertrophy, adipose tissue metabolic dysfunction, and alterations in adipokine secretion ( 41 , 42 , 99 ). Thus, even without increasing adiposity, arsenic can affect the functions of adipose tissue, mimicking alterations associated with obesity and MS.…”

Section: Unifying Mechanisms Across Tissuesmentioning

confidence: 99%

Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms

et al. 2022

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Exposure to arsenic in drinking water is a worldwide health problem. This pollutant is associated with increased risk of developing chronic diseases, including metabolic diseases. Metabolic syndrome (MS) is a complex pathology that results from the interaction between environmental and genetic factors. This condition increases the risk of developing type 2 diabetes, cardiovascular diseases, and cancer. The MS includes at least three of the following signs, central obesity, impaired fasting glucose, insulin resistance, dyslipidemias, and hypertension. Here, we summarize the existing evidence of the multiple mechanisms triggered by arsenic to developing the cardinal signs of MS, showing that this pollutant could contribute to the multifactorial origin of this pathology.

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Leptin and adiponectin synthesis and secretion in mature 3T3-L1 adipocytes are differentially down-regulated by arsenic and palmitic acid exposure throughout different stages of adipogenesis

Cited by 8 publications

References 63 publications

Baicalein enhances immune response in TNBC by inhibiting leptin expression of adipocytes

Baicalein enhances immune response in TNBC by inhibiting leptin expression of adipocytes

Lipotoxicity: The missing link between diabetes and periodontitis?

Is Arsenic Exposure a Risk Factor for Metabolic Syndrome? A Review of the Potential Mechanisms

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