Insulin and Insulin Receptors in Adipose Tissue Development

Insulin is a major endocrine hormone also involved in the regulation of energy and lipid metabolism via the activation of an intracellular signaling cascade involving the insulin receptor (INSR), insulin receptor substrate (IRS) proteins, phosphoinositol 3-kinase (PI3K) and protein kinase B (AKT). Specifically, insulin regulates several aspects of the development and function of adipose tissue and stimulates the differentiation program of adipose cells. Insulin can activate its responses in adipose tissue through two INSR splicing variants: INSR-A, which is predominantly expressed in mesenchymal and less-differentiated cells and mainly linked to cell proliferation, and INSR-B, which is more expressed in terminally differentiated cells and coupled to metabolic effects. Recent findings have revealed that different distributions of INSR and an altered INSR-A:INSR-B ratio may contribute to metabolic abnormalities during the onset of insulin resistance and the progression to type 2 diabetes. In this review, we discuss the role of insulin and the INSR in the development and endocrine activity of adipose tissue and the pharmacological implications for the management of obesity and type 2 diabetes.

Medienart:

E-Artikel

Erscheinungsjahr:

2019

Erschienen:

2019

Enthalten in:

Zur Gesamtaufnahme - volume:20

Enthalten in:

International journal of molecular sciences - 20(2019), 3 vom: 11. Feb.

Sprache:

Englisch

Beteiligte Personen:

Cignarelli, Angelo [VerfasserIn]
Genchi, Valentina Annamaria [VerfasserIn]
Perrini, Sebastio [VerfasserIn]
Natalicchio, Annalisa [VerfasserIn]
Laviola, Luigi [VerfasserIn]
Giorgino, Francesco [VerfasserIn]

Links:

Volltext

Themen:

Adipocyte
Adipose tissue
EC 2.7.10.1
IGF1R protein, human
Insulin
Insulin receptor
Journal Article
Receptor, IGF Type 1
Receptor, Insulin
Receptor isoform
Receptors, Somatomedin
Review

Anmerkungen:

Date Completed 29.05.2019

Date Revised 09.12.2020

published: Electronic

Citation Status MEDLINE

doi:

10.3390/ijms20030759

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM293803544