Regulation of lipid accumulation in 3T3-L1 cells: insulin-independent and combined effects of fatty acids and insulin

Kokta, Theresa A.; Strat, Aurel L.; Papasani, Madhusudhan R.; Szasz, J. I.; Dodson, M. V.; Hill, Rodney A.

doi:10.1017/s1751731107000936

Cited by 23 publications

(31 citation statements)

References 45 publications

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“…This property of trehalose is considered to result in the suppression of adipocyte hypertrophy. Insulin promotes storage of lipids in adipocytes, and its excessive secretion can cause hypertrophy of these cells (13,14). Thus, the results of this study suggest the possibility that excessive insulin secretion can be reduced by ingesting trehalose with meals.…”

Section: Discussionmentioning

confidence: 68%

Daily Intake of Trehalose Is Effective in the Prevention of Lifestyle-Related Diseases in Individuals with Risk Factors for Metabolic Syndrome

Mizote

Yamada

Yoshizane

et al. 2016

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryWe previously performed animal studies that suggested that trehalose potentially prevents the development of metabolic syndrome in humans. To evaluate this possibility, we examined whether trehalose suppressed the progression of insulin resistance in a placebo-controlled, double-blind trial in 34 subjects with a body mass index (BMI) $23. The subjects were divided into two groups and were assigned to ingest either 10 g/d of trehalose or sucrose with meals for 12 wk. During the study, body composition and blood biochemical parameters were measured at week 0, 8, and 12. These parameters were also measured 4 wk after the end of intake to confirm the washout of test substances. In the trehalose group, blood glucose concentrations after a 2-h oral glucose tolerance test significantly decreased following 12 wk of intake in comparison with baseline values (0 wk). When a stratified analysis was performed in the subjects whose percentage of truncal fat approached the high end of the normal range, the change in body weight, waist circumference, and systolic blood pressure were significantly lower in the trehalose group than in the sucrose group. Our data indicated that a daily intake of 10 g of trehalose improved glucose tolerance and progress to insulin resistance. Furthermore, these results suggested that trehalose can potentially reduce the development of metabolic syndrome and associated lifestyle-related diseases, such as type 2 diabetes.

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Section: Discussionmentioning

confidence: 68%

Daily Intake of Trehalose Is Effective in the Prevention of Lifestyle-Related Diseases in Individuals with Risk Factors for Metabolic Syndrome

Mizote

Yamada

Yoshizane

et al. 2016

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…Both anti-adipogenic effects of conjugated linoleic acids (reviewed in [31]) and adipogenic effects of other polyunsaturated fatty acids (PUFA) and monounsaturated fatty acids (MUFA) [11,12,35,46] have been reported. Several of these studies have also focused on induction of gene expression of the key transcription factors that regulate adipogenesis, PPARγ and C/EBPα [22,35,61]. Amri et al [3], demonstrated that α-linolenate can induce ap2 (adipocyte fatty acid binding protein or FABP4) gene expression in Ob1771 cells.…”

Section: Introductionmentioning

confidence: 99%

“…Short-chain and medium-chain fatty acids (MCFA) showed weaker induction of ap2 gene expression than longchain fatty acids (LCFA) [3]. Recently, we have shown that OA and LA induced triglyceride accumulation, PPARγ, and GLUT4 (glucose transporter 4) protein expression in 3T3-L1 cells [35]. In addition, MCFA, octanoate (C8:0) and decanoate (C10:0), were shown to induce gene expression of AD specific transcription factors such as, PPARγ, C/ EBPα, SREBP-1c, FABP4, and LPL [22,61].…”

Section: Introductionmentioning

confidence: 99%

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Adipocyte differentiation-specific gene transcriptional response to C18 unsaturated fatty acids plus insulin

Cheguru

Chapalamadugu

Doumit

et al. 2012

Pflugers Arch - Eur J Physiol

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Adipocyte differentiation (AD) and AD-specific gene expression was studied in 3T3-L1 cells in response to oleic acid (OA) or linoleic acid (LA) alone and in combination with insulin. This system facilitated the study of key regulators of adipogenesis PPARγ and C/EBPα and other AD-specific genes, in the absence of dexamethasone (DEX) and isobutyl-1-methyl xanthine (IBMX) (components of the traditional AD medium, DMI). Lipid accumulation and expression levels of AD-specific genes were enhanced by both OA and LA in the presence of insulin but not by OA or LA alone. Gene expression levels of PPARγ, C/EBPα, FABP4, and SREBP1c induced by OA plus insulin, were comparable to DMI medium, by study day 10. The response to long-chain fatty acids (LCFA) plus insulin in the presence or absence of LY294002 demonstrated that the insulin-induced PI 3-kinase pathway regulates AD and AD-specific gene expression levels. Insulin treatment in the presence or absence of genistein suggested that genistein invoked inhibition of AD and AD-specific gene expression. In contrast when LCFA were also included with insulin, the presence of genistein invoked a pronounced and opposite effect on AD to that in the absence of LCFA. This effect may be modulated via C/EBPα as C/EBPα but not PPARγ expression patterns closely reflected the changes in AD. DMI invoked a rapid expression of all genes studied, and LCFA plus insulin invoke more gradual increases in gene expression, to similar levels to those invoked by DMI. The model system is valuable for study of transactivators and response elements of PPARγ and C/EBPα genes.

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“…Oil Red O-stained fat droplets are observed in the differentiated ADC. Unsaturated fatty acids as inducers of adipogenic differentiation were demonstrated in various kinds of cells including multipotent muscle stem cells (Wada et al, 2002), immortalized human myogenic progenitors (Hashimoto et al, 2006) and human cancer cells (Ruiz-Vela et al, 2011), as was validated by de novo biogenesis of lipid droplets (Fujimoto et al, 2007) and the adipogenic marker PPAR-gamma expression (Kokta et al, 2008). PPAR-gamma expression in ADC is shown in Fig.…”

Section: Resultsmentioning

confidence: 92%

JNK implication in adipocyte-like cell death induced by chemotherapeutic drug cisplatin

Krestnikova¹,

Stulpinas²,

Imbrasaitė³

et al. 2015

J. Toxicol. Sci.

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-Recent evidence shows that tumor microenvironment containing heterogeneous cells may be involved in cancer initiation, growth and tumor cell response to anticancer therapy. Chemotherapy was designed to make toxic impact on malicious cells in organisms, however, the means to protect healthy cells against chemical toxicity are still unsuccessful. As known, the majority of tumor surrounding cells are cancer-associated adipocytes which influence cancer development, progression and treatment. Targeting the components of tumor microenvironment in combination with conventional cancer treatment may become an effective cancer therapy strategy. However, little is known about adipocyte death mechanisms during combined chemo-and targeted therapy. The importance of c-Jun-NH 2 -terminal kinase (JNK) signaling in tumor development and treatment has been demonstrated using various in vitro and in vivo cancer models. The aim of this study was to ascertain adipocyte viability during simultaneous stress kinase JNK inhibition and exposure to one of the most commonly used anticancer drugs cis-diamminedichloroplatinum II (cisplatin). Our model involved adipocyte-like cells (ADC) which were obtained during in vitro differentiation of adult rabbit muscle-derived stem cells. Cisplatin induced apoptotic cell death. During 24-hr cisplatin treatment gradual, strong and prolonged increase of both JNK and its target protein c-Jun phosphorylation was found in ADC. Pre-treatment of cells with SP600125 decreased cisplatin-induced activation of c-Jun and promoted apoptosis. Upregulation of proapoptotic Bax and downregulation of antiapoptotic Bcl-2 proteins were found to be regulated in JNK-dependent manner. Thus, the results prove the antiapoptotic role of activated JNK in adipocyte-like cells treated with cisplatin.

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Regulation of lipid accumulation in 3T3-L1 cells: insulin-independent and combined effects of fatty acids and insulin

Cited by 23 publications

References 45 publications

Daily Intake of Trehalose Is Effective in the Prevention of Lifestyle-Related Diseases in Individuals with Risk Factors for Metabolic Syndrome

Daily Intake of Trehalose Is Effective in the Prevention of Lifestyle-Related Diseases in Individuals with Risk Factors for Metabolic Syndrome

Adipocyte differentiation-specific gene transcriptional response to C18 unsaturated fatty acids plus insulin

JNK implication in adipocyte-like cell death induced by chemotherapeutic drug cisplatin

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