Role of protease inhibitors and acylation stimulating protein in the adipogenesis in 3T3-L1 cells

Soliman, Mohamed Mohamed; El-Senosi, Yakut Abdel-Fattah; Salem, Maysara M.; Hamid, Omniya Mahmoud Abdel; Kimura, Kazuhiro

doi:10.4142/jvs.2009.10.3.197

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…This is in concordance with previous data [26][27][28][29], but we also found that the differentiation levels varied at the two study points depending on the insulin used to induce the adipogenesis.…”

Section: Discussionsupporting

confidence: 94%

Effect of insulin analogues on 3t3-l1 adipogenesis and lipolysis

García‐Escobar

Rodríguez‐Pacheco

Haro‐Mora

et al. 2011

European Journal of Clinical Investigation

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Detemir insulin was the least adipogenic of the insulins tested, whereas treatment with glargine insulin tended to produce the highest lipolysis levels. Under these experimental conditions, the modifications made in commercial insulins to improve glycaemic control also affect adipocyte differentiation, the lipolysis level of differentiated cells, and the expression of different genes that can modify metabolic pathways independently of glucose metabolism.

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Section: Discussionsupporting

confidence: 94%

Effect of insulin analogues on 3t3-l1 adipogenesis and lipolysis

García‐Escobar

Rodríguez‐Pacheco

Haro‐Mora

et al. 2011

European Journal of Clinical Investigation

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“…Forced expression of NEDD8 decreased the expression of C/EBP and PPAR , possibly acting on the differentiation program throughout the NEDD8/p27/beta-catenin pathway [30]. PIs also altered protein expression of two proteins involved in lipid droplet formation, ASP (acylation stimulating protein) [57] and perilipin [58].…”

Section: Introduction: Early Occurrence Of Lipodystrophy After Art Inmentioning

confidence: 96%

Adipose Tissue as a Target of HIV-1 Antiretroviral Drugs. Potential Consequences on Metabolic Regulations

Caron-Debarle¹,

Boccara²,

Lagathu³

et al. 2010

CPD

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Adipose tissue redistribution occurred at first in HIV-infected patients about 15 years ago after initiation of combination antiretroviral treatment (ART) and the responsibility of drugs was rapidly considered. This lipodystrophic syndrome can associate lipoatrophy, affecting subcutaneous adipose tissue in priority with fat hypertrophy, in particular in the upper part of the body, and metabolic alterations, dyslipidemia and altered glucose tolerance with insulin resistance. The primary role of thymidine analogue reverse transcriptase inhibitors (tNRTI) in peripheral lipoatrophy has been clearly shown in vitro and in vivo, these drugs inducing a severe mitochondrial dysfunction and an increased oxidative stress together with fat inflammation leading to fat loss. In vitro and in vivo studies suggest that some protease inhibitors (PI) or non-NRTIs also exert adverse effects on adipocytes and could act in synergy to amplify the effect of tNRTI. While severe lipoatrophy is now less prevalent in HIV-infected patients, fat hypertrophy is frequently observed: a role for drugs from the different classes acting in synergy to induce fat hyperplasia and hypertrophy is suggested, with milder mitochondrial dysfunction but increased inflammation and activation of the cortisol system. In addition, it is now considered that long-term viral infection, even if controlled, could induce low-grade inflammation and prepare fat to the deleterious effect of ART. Both lipoatrophy and lipohypertrophy are involved in metabolic disorders and increased cardio-metabolic risk that likely participate to early aging reported in these patients. ART can also be directly responsible for metabolic alterations. Strategies to revert or reduce lipodystrophy are important to consider in these patients in addition to the required control of the metabolic disorders.

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