Patients with type 2 diabetes (T2D) are at increased risk of developing cancer. This evidence arises from numerous epidemiologic studies that relate a positive association between T2D and cancer. In-vitro and several in-vivo experiments have attempted to discern the potential mechanistic factors involved in this relationship. Candidates include hyperinsulinemia, insulin-like growth factor-1 (IGF-1), and insulin-like growth factor-2 (IGF-2) signaling. These studies demonstrated that increased insulin, IGF-1, and IGF-2 signaling through the insulin receptor and IGF-1 receptor can induce cancer development and progression.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3678929PMC
http://dx.doi.org/10.5041/RMMJ.10043DOI Listing

Publication Analysis

Top Keywords

insulin-like growth
12
increased risk
8
igf-2 signaling
8
role insulin
4
insulin insulin-like
4
growth factors
4
factors increased
4
cancer
4
risk cancer
4
cancer diabetes
4

Similar Publications

Objectives: The gonadotropin-releasing hormone (GnRH) provocation test is crucial for diagnosing central precocious puberty (CPP). However, due to its invasion and high cost, it is essential to find a simpler biomarker. This study aimed to investigate the feasibility of fasting insulin (FINS) and insulin-like growth factor-1 (IGF-1) as potential biomarkers for diagnosing girls with CPP and to analyze their effects on puberty development.

View Article and Find Full Text PDF

Temporal and Spatial Metabolic Shifts Revealing the Transition from Ulcerative Colitis to Colitis-Associated Colorectal Cancer.

Adv Sci (Weinh)

January 2025

Key Laboratory of Drug Quality Control and Pharmacovigilance (Ministry of Education), State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, P. R. China.

Patients with ulcerative colitis (UC) have a higher risk of developing colorectal cancer (CRC), however, the metabolic shifts during the UC-to-CRC transition remain elusive. In this study, an AOM-DSS-induced three-stage colitis-associated colorectal cancer (CAC) model is constructed and targeted metabolomics analysis and pathway enrichment are performed, uncovering the metabolic changes in this transition. Spatial metabolic trajectories in the "normal-to-normal adjacent tissue (NAT)-to-tumor" transition, and temporal metabolic trajectories in the "colitis-to-dysplasia-to-carcinoma" transition are identified through K-means clustering of 74 spatially and 77 temporally differential metabolites, respectively.

View Article and Find Full Text PDF

Background: Pediatric growth hormone deficiency (GHD) is a disease resulting from the impaired growth hormone-insulin-like growth factor-1 (GH-IGF-1) axis, but the effects of GHD on children's behavior and brain microstructural structure alterations have not yet been fully clarified. We aimed to investigate the quantitative profiles of gray matter and white matter in pediatric GHD using synthetic magnetic resonance imaging (MRI).

Methods: The data of 50 children with GHD and 50 typically developing (TD) children were prospectively collected.

View Article and Find Full Text PDF

Objectives: To investigate the effects of selenium on functional and histopathological changes and mRNA expression levels of insulin-like growth factors 1 and 2 (IGF-1 and -2) and aquaporins 4 and 5 (AQP-4 and -5) in 131I-induced damaged rat parotid glands.

Methods: Rats were divided into three groups: iodotherapy-with-selenium, iodotherapy-only, and control. Rats in the iodotherapy-with-selenium group were intragastrically administered 131I on the first day and selenomethionine through drinking water.

View Article and Find Full Text PDF

Obesity is a modifiable risk factor for breast cancer. Yet, how obesity contributes to cancer initiation is not fully understood. The goal of this study was to determine if the body mass index (BMI) and metabolic hallmarks of obesity are related to DNA damage in normal breast tissue.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!