Insulin Resistance and Colorectal Cancer Risk: the Role of Elevated Plasma Resistin Levels

Farahani, Hamid; Mahmoudi, Touraj; Asadi, Asadollah; Nobakht, Hossein; Dabiri, Reza; Hamta, Amir

doi:10.1007/s12029-019-00260-7

Cited by 33 publications

(22 citation statements)

References 30 publications

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“…Resistin, primarily produced by monocytes and macrophages, is another connecting point for IR and CRC, although the role of resistin in both pathophysiological processes is not fully explained. Resistin was reportedly increased in subjects with rectal cancer and in correlation with insulin levels in CRC patients [76]. Similarly, our study demonstrated increased levels of resistin and its receptor adenylate cyclase-associated protein 1 in CRC [77].…”

Section: Insulin Resistancesupporting

confidence: 80%

Diabetes and Colorectal Cancer Risk: A New Look at Molecular Mechanisms and Potential Role of Novel Antidiabetic Agents

Vekić

Stefanović

Giglio

et al. 2021

IJMS

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Epidemiological data have demonstrated a significant association between the presence of type 2 diabetes mellitus (T2DM) and the development of colorectal cancer (CRC). Chronic hyperglycemia, insulin resistance, oxidative stress, and inflammation, the processes inherent to T2DM, also play active roles in the onset and progression of CRC. Recently, small dense low-density lipoprotein (LDL) particles, a typical characteristic of diabetic dyslipidemia, emerged as another possible underlying link between T2DM and CRC. Growing evidence suggests that antidiabetic medications may have beneficial effects in CRC prevention. According to findings from a limited number of preclinical and clinical studies, glucagon-like peptide-1 receptor agonists (GLP-1RAs) could be a promising strategy in reducing the incidence of CRC in patients with diabetes. However, available findings are inconclusive, and further studies are required. In this review, novel evidence on molecular mechanisms linking T2DM with CRC development, progression, and survival will be discussed. In addition, the potential role of GLP-1RAs therapies in CRC prevention will also be evaluated.

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Section: Insulin Resistancesupporting

confidence: 80%

Diabetes and Colorectal Cancer Risk: A New Look at Molecular Mechanisms and Potential Role of Novel Antidiabetic Agents

Vekić

Stefanović

Giglio

et al. 2021

IJMS

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“…Moreover, T2D could decrease the survival of CRC patients. The evidence has shown that elevated insulin concentration is able to develop CRC cell growth, but the mechanism and molecular link between CRC and T2D are controversial ( 194 – 196 ). However, metabolic syndrome, especially insulin resistance and hyperglycemia, could explain the relationship between these diseases ( 197 , 198 ).…”

Section: Ages-rage Interaction Regard To T2d and Crc Associationmentioning

confidence: 99%

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

et al. 2020

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Receptor for advanced glycation end-products (RAGE) is a multiligand binding and single-pass transmembrane protein taken in diverse chronic inflammatory conditions. RAGE behaves as a pattern recognition receptor, which binds and is engaged in the cellular response to a variety of damage-associated molecular pattern molecules, as well as HMGB1, S100 proteins, and AGEs (advanced glycation end-products). The RAGE activation turns out to a formation of numerous intracellular signaling mechanisms, resulting in the progression and prolongation of colorectal carcinoma (CRC). The RAGE expression correlates well with the survival of colon cancer cells. RAGE is involved in the tumorigenesis, which increases and develops well in the stressed tumor microenvironment. In this review, we summarized downstream signaling cascade activated by the multiligand activation of RAGE, as well as RAGE ligands and their sources, clinical studies, and tumor markers related to RAGE particularly in the inflammatory tumor microenvironment in CRC. Furthermore, the role of RAGE signaling pathway in CRC patients with diabetic mellitus is investigated. RAGE has been reported to drive assorted signaling pathways, including activator protein 1, nuclear factor-κB, signal transducer and activator of transcription 3, SMAD family member 4 (Smad4), mitogen-activated protein kinases, mammalian target of rapamycin, phosphoinositide 3-kinases, reticular activating system, Wnt/β-catenin pathway, and Glycogen synthase kinase 3β, and even microRNAs.

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“…Adiponectin could reduce cell proliferation rate and induce cells apoptosis as demonstrated in many studies [27]. In the same vein, it was reported recently that higher plasma levels of resistin in connection with insulin resistance play a role in susceptibility to colorectal carcinoma [28].…”

Section: Despite Extensive Research Evaluated the Relation Of Obesitymentioning

confidence: 77%

Evaluation of Visceral Adiposity Index and Vitamin D Status in Colon Cancer: Is Visceral Obesity the Missing Link?

Aboelnaga

Abdelkhalek

et al. 2021

J Endocrinol Metab

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Insulin Resistance and Colorectal Cancer Risk: the Role of Elevated Plasma Resistin Levels

Cited by 33 publications

References 30 publications

Diabetes and Colorectal Cancer Risk: A New Look at Molecular Mechanisms and Potential Role of Novel Antidiabetic Agents

Diabetes and Colorectal Cancer Risk: A New Look at Molecular Mechanisms and Potential Role of Novel Antidiabetic Agents

Receptor for Advanced Glycation End Products Acts as a Fuel to Colorectal Cancer Development

Evaluation of Visceral Adiposity Index and Vitamin D Status in Colon Cancer: Is Visceral Obesity the Missing Link?

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