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Developing of glucose-consuming adipocytes by interleukin 4 gene deliveryстатья Электронная публикация Тезисы
Статья опубликована в высокорейтинговом журнале
Статья опубликована в журнале из списка Web of Science и/или ScopusДата последнего поиска статьи во внешних источниках: 8 апреля 2022 г.
- Авторы: Michurina S.S., Stafeev I.S., Mamontova E.D., Menshikov M.Y., Parfyonova Y.V.
- Журнал: Human Gene Therapy
- Том: 32
- Номер: 19-20
- Год издания: 2021
- Издательство: Mary Ann Liebert Inc.
- Местоположение издательства: United States
- Номер статьи: P390
- DOI: 10.1089/hum.2021.29180.abstracts
- Аннотация: Energy metabolism of adipose tissue is essential for whole body glucose homeostasis. Adipocytes' insulin sensitivity and storage function is strongly regulated by inflammatory status of the tissue and can be altered during latent inflammation, developing in obesity and type 2 diabetes. Using lentiviral gene delivery we produced adipocytes 3T3‐L1 expressing anti‐inflammatory cytokine interleukin 4 (IL‐4), and closely examined their adipogenic differentiation and insulin sensitivity.3T3‐L1 cells were transduced before or after differentiation to determine the effect of IL‐4 on preadipocytes and mature cells. White adipogenic differentiation was performed with insulin, dexamethasone, isobutylmethylxanthine and rosiglitazone; during beige adipogenic differentiation isoproterenol and triiodothyronine were added. Insulin sensitivity was analyzed by 3H‐2deoxyglucose uptake and immunoblotting. Adipogenic differentiation was determined by OilRedO staining and real time PCR.Adipocytes expressing IL‐4 exhibited higher basal and insulin‐stimulated glucose consumption, elevated phosphorylation of insulin signaling proteins. IL‐4 production during white and brown adipogenic differentiation increased expression of respiratory chain proteins (NDUFA1, Cox7) and mitochondrial biogenesis factor PGC1a, but had no effect on lipid metabolism (hormone sensitive lipase, perilipin, fatty acid synthase) and lipid accumulation.This suggests that IL‐4 activates oxidative metabolism through mitochondria potentiation. Furthermore, it increases glucose uptake by adipocytes without an increase of lipid droplets content. These results emphasize that IL‐4 is a mediator of oxidative metabolism in adipocytes and a potential activator of glucose‐consuming adipocytes, beneficial for type 2 diabetes prevention.This work was supported by RFBR grant #20‐015‐00100.
- Добавил в систему: Мамонтова Елизавета Денисовна