Canonical and Non-Canonical Mechanisms  of Insulin-Dependent Signaling Regulating Adipogenic  Differentiation in Adipose Tissue Renewal

Bondarev, A.D.; Kulebyakin, K.Y.; Gusev, N.B.; Tyurin-Kuzmin, P.A.

Авторы: Bondarev Andrey D., Kulebyakin Konstantin Yu, Gusev Nikolai B., Tyurin-Kuzmin Pyotr A.
Журнал: Biochemistry (Moscow)
Том: 91
Номер: 1
Год издания: 2026
Издательство: Pleiades Publishing, Ltd
Местоположение издательства: Road Town, United Kingdom
Первая страница: S355
Последняя страница: S372
DOI: 10.1134/S0006297925603727
Аннотация: Insulin exerts a complex effect on metabolism, cell growth, and differentiation interacting with its receptor. Adipose tissue is one of the key targets for insulin; in this tissue insulin regulates the processes of energy storage, as well as tissue renewal and emergence of new adipocytes. Insulin activates conversion of glucose into fatty acids, inhibits lipolysis, and induces adipogenic differentiation of adipose tissue stem cells. The insulin receptor is a classic tyrosine kinase receptor that activate phosphoinositide-3-kinase and mitogen-activated protein kinase signaling cascades. At the same time, insulin receptor activates several non-canonical signaling cascades that determine features of the receptor functioning. For example, insulin can affect phosphoinositide metabolism, as well as calcium and redox-dependent signaling. In addition, the insulin receptor can also interact with the trimeric G proteins-coupled receptors (GPCRs). Here, we review canonical and non-canonical signaling cascades activated by the insulin receptor and molecular mechanisms of their involvement in regulating the human adipose tissue renewal.
Добавил в систему: Бондарев Андрей Дмитриевич

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Canonical and Non-Canonical Mechanisms of Insulin-Dependent Signaling Regulating Adipogenic Differentiation in Adipose Tissue Renewalстатья

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