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

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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