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Special Issue Information

Dear Colleagues,

Reduced insulin receptor (Insr) signaling, especially in key metabolic tissues, i.e., the liver, skeletal muscle, and adipose, is associated with type 2 diabetes mellitus due to impaired glucose uptake in cells. However, the Insr may have important roles in other tissues, e.g., vasculature, heart, and kidney, with less-defined effects. The human Insr cDNA was first cloned in 1985. The receptor is composed of two subunits: alpha and beta—both derived by the proteolytic processing of a 1382-amino-acid pre-proreceptor. Insr signaling proceeds primarily through autophosphorylation on key tyrosine residues, with the eventual activation of Akt kinase. On the other hand, the phosphorylation of Insr on several serine residues is associated with the reduced activation of this signaling cascade.

In addition, the insulin receptor exists in two isoforms (InsrA and InsrB) generated by the alternative splicing of exon 11. The two isoforms may have different tissue expression with different biological effects in several diseases. The dysregulation of the InsrA:InsrB ratio is associated with insulin resistance and increased proliferative activity of normal and neoplastic tissues.

This Special Issue focuses on Insr modifications with disease (expression, post-translational modifications, and downstream signaling), as well as hypothetical, experimental, and tested therapies to restore, alter, or enhance signaling.

We welcome submissions, including original papers and reviews, on this widely discussed topic.

Dr. Carolyn M. Ecelbarger
Guest Editor

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Keywords

metabolic syndrome
hypertension
insulin resistance
type 2 diabetes
obesity
tyrosine-kinase receptor
type 1 diabetes

Published Papers (2 papers)

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Research

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15 pages, 3782 KiB

Open AccessArticle

Insulin-like Peptide Receptor (ILPR) in the Cuttlefish Sepiella japonica: Characterization, Expression, and Regulation of Reproduction

by Zhenming Lü, Yantao Liu, Jun Yan, Yao Zhang, Li Gong, Bingjian Liu, Jing Liu, Zhijin Xu and Liqin Liu

Int. J. Mol. Sci. 2022, 23(21), 12903; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232112903 - 26 Oct 2022

Cited by 2 | Viewed by 1306

Abstract

Insulin-like peptide receptor (ILPR) can effectively regulate ovarian development in invertebrates, but its effect in cuttlefish has not been reported. We isolated and characterized a ILPR gene from Sepiella japonica, referred to as SjILPR. This gene displayed significant homologies to Octopus bimaculoides ILPR, and contained all typical features of insulin receptors and tyrosine kinase domain structure. SjILPR is expressed in all detected tissues, with the highest expression in the ovary. During ovarian development stages, its expression levels in the ovary, pancreas, and liver were correlated to the female reproductive cycle. After the silencing of SjILPR in vivo, comparative transcriptome analysis identified 4314 differentially expressed genes (DEGs) in the injected group, including 2586 down-regulated genes and 1728 up-regulated genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed that 832 DEGs were assigned to 222 pathways, many pathways of which were related to gonadal development. Four down-regulated genes relevant to ovarian development (Vitellogenin 1, Vitellogenin 2, Cathepsin L1-like, and Follistatin) were selected to confirm the accuracy of RNA-seq data by qRT-PCR. These results showed that SjILPR might regulate ovarian development to control reproduction by affecting the expression of the relevant genes in female S. japonica. Full article

(This article belongs to the Special Issue New Advances in Insulin and Insulin Receptor Biology)

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Review

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13 pages, 1030 KiB

Open AccessReview

Insulin Metabolism in Polycystic Ovary Syndrome: Secretion, Signaling, and Clearance

by Rok Herman, Jaka Sikonja, Mojca Jensterle, Andrej Janez and Vita Dolzan

Int. J. Mol. Sci. 2023, 24(4), 3140; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24043140 - 05 Feb 2023

Cited by 15 | Viewed by 5760

Abstract

Polycystic ovary syndrome (PCOS) is the most common endocrine and metabolic disorder in women of reproductive age. Its heterogeneous clinical presentation is characterized by hyperandrogenemia, reproductive changes, polycystic ovary morphology, and insulin resistance (IR). The primary pathophysiological process in its multifactorial etiology has not yet been identified. However, the two most proposed core etiologies are the disruption of insulin metabolism and hyperandrogenemia, both of which begin to intertwine and propagate each other in the later stages of the disease. Insulin metabolism can be viewed as the interconnectedness of beta cell function, IR or insulin sensitivity, and insulin clearance. Previous studies of insulin metabolism in PCOS patients have yielded conflicting results, and literature reviews have focused mainly on the molecular mechanisms and clinical implications of IR. In this narrative review, we comprehensively explored the role of insulin secretion, clearance, and decreased sensitivity in target cells as a potential primary insult in PCOS pathogenesis, along with the molecular mechanism behind IR in PCOS. Full article

(This article belongs to the Special Issue New Advances in Insulin and Insulin Receptor Biology)

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