Dataset Information

Potential Role of Insulin Growth-Factor-Binding Protein 2 as Therapeutic Target for Obesity-Related Insulin Resistance.

ABSTRACT: Evidence from observational and in vitro studies suggests that insulin growth-factor-binding protein type 2 (IGFBP2) is a promising protein in non-communicable diseases, such as obesity, insulin resistance, metabolic syndrome, or type 2 diabetes. Accordingly, great efforts have been carried out to explore the role of IGFBP2 in obesity state and insulin-related diseases, which it is typically found decreased. However, the physiological pathways have not been explored yet, and the relevance of IGFBP2 as an important pathway integrator of metabolic disorders is still unknown. Here, we review and discuss the molecular structure of IGFBP2 as the first element of regulating the expression of IGFBP2. We highlight an update of the association between low serum IGFBP2 and an increased risk of obesity, type 2 diabetes, metabolic syndrome, and low insulin sensitivity. We hypothesize mechanisms of IGFBP2 on the development of obesity and insulin resistance in an insulin-independent manner, which meant that could be evaluated as a therapeutic target. Finally, we cover the most interesting lifestyle modifications that regulate IGFBP2, since lifestyle factors (diet and/or physical activity) are associated with important variations in serum IGFBP2.

SUBMITTER: Boughanem H

PROVIDER: S-EPMC7865532 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Potential Role of Insulin Growth-Factor-Binding Protein 2 as Therapeutic Target for Obesity-Related Insulin Resistance.

Boughanem Hatim H Yubero-Serrano Elena M EM López-Miranda José J Tinahones Francisco J FJ Macias-Gonzalez Manuel M

International journal of molecular sciences 20210124 3

Evidence from observational and in vitro studies suggests that insulin growth-factor-binding protein type 2 (IGFBP2) is a promising protein in non-communicable diseases, such as obesity, insulin resistance, metabolic syndrome, or type 2 diabetes. Accordingly, great efforts have been carried out to explore the role of IGFBP2 in obesity state and insulin-related diseases, which it is typically found decreased. However, the physiological pathways have not been explored yet, and the relevance of IGF ...[more]

PMID: 33498859

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Project description:The present study aimed to reveal the metabolic alterations of the extracellular matrix (ECM) in uterosacral ligament (USL) with pelvic organ prolapse (POP) and to explore the role of transforming growth factor‑β1 (TGF‑β1) in pathogenesis of POP. For this purpse, 60 participants who underwent hysterectomy for benign indications were enrolled, 30 of which had symptomatic POP (grade II, III or IV) and composed the POP group, and the other 30 had asymptomatic POP (grade I or less) and served as the controls. Collagen fibers, elastin,matrix metalloproteinase (MMP)‑2/9, tissue inhibitor of matrix metalloproteinases (TIMP)‑2 and TGF‑β1 were examined by Masson's trichrome staining, immunohistochemistry and RT-qPCR using USL biopsies. In vitro, human USL fibroblasts (hUSLFs) were primary cultured, pre-treated with recombinant TGF‑β1 (0, 5, or 10 ng/ml) and then subjected to cyclic mechanical stretching (CMS; 0 or 5,333 µε strain). Changes in the expression levels of collagen type I/III, elastin, TIMP‑2, MMP‑2/9 and Smad were detected. Our results revealed that at the tissue level, the expression of collagen fibers, elastin, TIMP‑2 and TGF‑β1 was significantly reduced in the POP group, while the activities of MMP‑2/9 were significantly upregulated, compared with the control group. Statistical analysis indicated that the mRNA expression of TGF‑β1 inversely correlated with the severity of POP partially. Our in vitro experimental data demonstrated that a CMS of 5333 µε strain promoted the degradation of ECM proteins, inhibited the synthesis of TIMP‑2, and upregulated the proteolytic activities of MMP‑2/9. Pre-treatment with TGF‑β1 attenuated the loss of ECM by stimulating the synthesis of TIMP‑2 and inhibiting the activities of MMP‑2/9 through the TGF‑β1/Smad3 signaling pathway. On the whole, our data indicate that the reduced anabolism and increased catabolism of ECM proteins in USL are the pathological characteristics of POP. TGF‑β1 not only has a specific value in predicting the severity of POP, but should also be considered as a novel therapeutic target for POP.

Dataset Information

Potential Role of Insulin Growth-Factor-Binding Protein 2 as Therapeutic Target for Obesity-Related Insulin Resistance.

Publications

Potential Role of Insulin Growth-Factor-Binding Protein 2 as Therapeutic Target for Obesity-Related Insulin Resistance.

Similar Datasets

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