Molecular and Functional Characterization of Human SW 872 Adipocytes as a Model System for Testing Nutraceutical Products

Olivieri, Chiara; Ruzza, Marco; Tolaj, Fationa; Dalt, L. Da; Magni, Paolo

doi:10.3390/iecn2022-12370

Cited by 2 publications

(2 citation statements)

References 17 publications

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“…SW872 is a human model of preadipocytes with the ability to differentiate into mature adipocytes. These cells have been employed in vitro to study adipose tissue dysfunction associated metabolic conditions such as obesity [39]. The effect of Lampaya medicinalis in PA-treated SW872 adipocytes is demonstrated for the first time in this in vitro study.…”

Section: Discussionmentioning

confidence: 90%

Effect of Lampaya medicinalis Phil. (Verbenaceae) and Palmitic Acid on Insulin Signaling and Inflammatory Marker Expression in Human Adipocytes

Yuri,

Cifuentes,

Cisternas

et al. 2024

Pharmaceuticals

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Background: Aging and obesity are associated with insulin resistance (IR) and low-grade inflammation. Molecularly, IR is characterized by a reduction in glucose uptake and insulin signaling (IRS-1/Akt/AS160 pathway), while inflammation may result from upregulated NF-κB pathway after low Tyr-IκBα phosphorylation. Upregulated phosphatase activity of PTP1B is associated with impaired insulin signaling and increased inflammation. Plasma levels of palmitic acid (PA) are elevated in obesity, triggering inflammation and disruption of insulin signaling. Traditional medicine in Northern Chile uses oral infusions of Lampaya medicinalis Phil. (Verbenaceae) to treat inflammatory conditions. Significant amounts of flavonoids are found in the hydroethanolic extract of Lampaya (HEL), which may account for its biological activity. The aim of this work was to study the effect of HEL and PA on insulin signaling and glucose uptake as well as inflammatory marker expression in human adipocytes. Methods: We studied HEL effects on PA-induced impairment on insulin signaling, glucose uptake and inflammatory marker content in human SW872 adipocytes. HEL cytotoxicity was assessed in adipocytes at different concentrations (0.01 to 10 g/mL). Adipocytes were incubated or not with PA (0.4 mM, 24 h) with or without HEL (2 h pre-incubation), and then stimulated with insulin (10 min, 100 mM) or a vehicle. Phospho-IRS-1, phospho-Akt, phospho-AS160, phospho-NF-κB and phospho-IκBα, as well as protein levels of PTP1B, were assessed using Western blotting, and glucose uptake was evaluated using the 2-NBDG analogue. Results: At the assessed HEL concentrations, no cytotoxic effects were observed. PA decreased insulin-stimulated phospho-Akt and glucose uptake, while co-treatment with HEL increased such markers. PA decreased phospho-IRS-1 and phospho-Tyr-IκBα. On the other hand, incubation with HEL+PA decreased phospho-AS160 and phospho-NF-κB compared with cells treated with PA alone. Conclusion: Our results suggest a beneficial effect of HEL by improving PA-induced impairment on molecular markers of insulin signaling, glucose uptake and inflammation in adipocytes. Further studies are necessary to elucidate whether lampaya may constitute a preventive strategy for people whose circulating PA levels contribute to IR and inflammation during aging and obesity.

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Section: Discussionmentioning

confidence: 90%

Effect of Lampaya medicinalis Phil. (Verbenaceae) and Palmitic Acid on Insulin Signaling and Inflammatory Marker Expression in Human Adipocytes

Yuri,

Cifuentes,

Cisternas

et al. 2024

Pharmaceuticals

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“…The expression of LRP1 in hepatocytes is also required to limit fat-induced hepatic steatosis, lipotoxicity, insulin resistance, and steatohepatitis [116,117]. In adipose tissues, LRP1 has been shown to be essential for the maturation of preadipocytes into mature adipocytes, as well as for the appropriate storage of lipids by these mature adipocytes [118,119]. Diet-induced obesity and insulin resistance are decreased by the inactivation of LRP1 in mature white and brown adipocytes by shifting lipid resources to the muscle to enhance thermogenesis [120]; however, hyperlipidemic animals with normal LRP1 expression in the artery wall also have increased inflammation and accelerated atherosclerosis due to the lack of LRP1 in mature adipocytes [121].…”

Section: Low-density Lipoprotein Receptor (Ldlr)mentioning

confidence: 99%

Molecular Mechanisms and Mediators of Hepatotoxicity Resulting from an Excess of Lipids and Non-Alcoholic Fatty Liver Disease

Finelli

2023

Gastrointestinal Disorders

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The paper reviews some of the mechanisms implicated in hepatotoxicity, which is induced by an excess of lipids. The paper spans a wide variety of topics: from the molecular mechanisms of excess lipids, to the therapy of hyperlipidemia, to the hepatotoxicity of lipid-lowering drugs. NAFLD is currently the leading cause of chronic liver disease in Western countries; the molecular mechanisms leading to NAFLD are only partially understood and there are no effective therapeutic interventions. The prevalence of liver disease is constantly increasing in industrialized countries due to a number of lifestyle variables, including excessive caloric intake, unbalanced diet, lack of physical activity, and abuse of hepatotoxic medicines. Considering the important functions of cell death and inflammation in the etiology of the majority, if not all, liver diseases, one efficient therapeutic treatment may include the administration of hepatoprotective and anti-inflammatory drugs, either alone or in combination. Clinical trials are currently being conducted in cohorts of patients with different liver diseases in order to explore this theory.

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Molecular and Functional Characterization of Human SW 872 Adipocytes as a Model System for Testing Nutraceutical Products

Cited by 2 publications

References 17 publications

Effect of Lampaya medicinalis Phil. (Verbenaceae) and Palmitic Acid on Insulin Signaling and Inflammatory Marker Expression in Human Adipocytes

Effect of Lampaya medicinalis Phil. (Verbenaceae) and Palmitic Acid on Insulin Signaling and Inflammatory Marker Expression in Human Adipocytes

Molecular Mechanisms and Mediators of Hepatotoxicity Resulting from an Excess of Lipids and Non-Alcoholic Fatty Liver Disease

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