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Review
- Metabolic Risk/Epidemiology
- Hepatic Fibrosis and Cancer: The Silent Threats of Metabolic Syndrome
- Scott L. Friedman
- Diabetes Metab J. 2024;48(2):161-169. Published online January 26, 2024
- DOI: https://doi.org/10.4093/dmj.2023.0240
- 2,465 View
- 294 Download
-
Abstract
PDF
PubReader 
ePub - Metabolic dysfunction-associated steatotic (fatty) liver disease (MASLD), previously termed non-alcoholic fatty liver disease, is a worldwide epidemic that can lead to hepatic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). The disease is typically a component of the metabolic syndrome that accompanies obesity, and is often overlooked because the liver manifestations are clinically silent until late-stage disease is present (i.e., cirrhosis). Moreover, Asian populations, including Koreans, have a higher fraction of patients who are lean, yet their illness has the same prognosis or worse than those who are obese. Nonetheless, ongoing injury can lead to hepatic inflammation and ballooning of hepatocytes as classic features. Over time, fibrosis develops following activation of hepatic stellate cells, the liver’s main fibrogenic cell type. The disease is usually more advanced in patients with type 2 diabetes mellitus, indicating that all diabetic patients should be screened for liver disease. Although there has been substantial progress in clarifying pathways of injury and fibrosis, there no approved therapies yet, but current research seeks to uncover the pathways driving hepatic inflammation and fibrosis, in hopes of identifying new therapeutic targets. Emerging molecular methods, especially single cell sequencing technologies, are revolutionizing our ability to clarify mechanisms underlying MASLD-associated fibrosis and HCC.
Original Article
- Metabolic Risk/Epidemiology
- Association of Measures of Glucose Metabolism with Colorectal Cancer Risk in Older Chinese: A 13-Year Follow-up of the Guangzhou Biobank Cohort Study-Cardiovascular Disease Substudy and Meta-Analysis
- Shu Yi Wang, Wei Sen Zhang, Chao Qiang Jiang, Ya Li Jin, Tong Zhu, Feng Zhu, Lin Xu
- Diabetes Metab J. 2024;48(1):134-145. Published online January 3, 2024
- DOI: https://doi.org/10.4093/dmj.2022.0383
- 1,158 View
- 141 Download
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Abstract
PDF
Supplementary MaterialPubReader ePub - Background
Abnormal glucose metabolism is a risk factor for colorectal cancer (CRC). However, association of glycosylated hemoglobin (HbA1c) with CRC risk remains under-reported. We examined the association between glycemic indicators (HbA1c, fasting plasma glucose, fasting insulin, 2-hour glucose, 2-hour insulin, and homeostasis model of risk assessment-insulin resistance index) and CRC risk using prospective analysis and meta-analysis.
Methods
Participants (n=1,915) from the Guangzhou Biobank Cohort Study-Cardiovascular Disease Substudy were included. CRC events were identified through record linkage. Cox regression was used to assess the associations of glycemic indicators with CRC risk. A meta-analysis was performed to investigate the association between HbA1c and CRC risk.
Results
During an average of 12.9 years follow-up (standard deviation, 2.8), 42 incident CRC cases occurred. After adjusting for potential confounders, the hazard ratio (95% confidence interval [CI]) of CRC for per % increment in HbA1c was 1.28 (95% CI, 1.01 to 1.63) in overall population, 1.51 (95% CI, 1.13 to 2.02) in women and 1.06 (95% CI, 0.68 to 1.68) in men. No significant association of other measures of glycemic indicators and baseline diabetes with CRC risk was found. Meta-analyses of 523,857 participants including our results showed that per % increment of HbA1c was associated with 13% higher risk of CRC, with the pooled risk ratio being 1.13 (95% CI, 1.01 to 1.27). Subgroupanalyses found stronger associations in women, colon cancer, Asians, and case-control studies.
Conclusion
Higher HbA1c was a significant predictor of CRC in the general population. Our findings shed light on the pathology of glucose metabolism and CRC, which warrants more in-depth investigation.
Reviews
- Pathophysiology
- Immune-Checkpoint Inhibitors-Induced Type 1 Diabetes Mellitus: From Its Molecular Mechanisms to Clinical Practice
- Yun Kyung Cho, Chang Hee Jung
- Diabetes Metab J. 2023;47(6):757-766. Published online July 24, 2023
- DOI: https://doi.org/10.4093/dmj.2023.0072
- 2,851 View
- 330 Download
- 2 Crossref
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Abstract
PDFPubReader ePub
- With the increasing use of immune-checkpoint inhibitors (ICIs), such as anti-cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) and anti-programmed cell death-1 (PD-1), for the treatment of malignancies, cases of ICI-induced type 1 diabetes mellitus (ICI-T1DM) have been reported globally. This review focuses on the features and pathogenesis of this disease. T1DM is an immune-related adverse event that occurs following the administration of anti-PD-1 or anti-programmed death ligand-1 (PDL1) alone or in combination with anti-CTLA-4. More than half of the reported cases presented as abrupt-onset diabetic ketoacidosis. The primary mechanism of ICI-T1DM is T-cell stimulation, which results from the loss of interaction between PD-1 and PD-L1 in pancreatic islet. The similarities and differences between ICI-T1DM and classical T1DM may provide insights into this disease entity. ICI-T1DM is a rare but often life-threatening medical emergency that healthcare professionals and patients need to be aware of. Early detection of and screening for this disease is imperative. At present, the only known treatment for ICI-T1DM is insulin injection. Further research into the mechanisms and risk factors associated with ICI-T1DM development may contribute to a better understanding of this disease entity and the identification of possible preventive strategies.
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Citations
Citations to this article as recorded by
- Research Advances of Immune Checkpoint Inhibitors Related Endocrine Adverse Events
晶晶 王
Advances in Clinical Medicine.2024; 14(02): 2706. CrossRef - Immune checkpoint inhibitor‑associated diabetes mellitus in patients with HCC: Report of three cases and literature review
Gaocheng Wang, Jingjing Wang, Shuilin Dong, Zhanguo Zhang, Wanguang Zhang, Jianping Zhao
Experimental and Therapeutic Medicine.2024;[Epub] CrossRef
- Research Advances of Immune Checkpoint Inhibitors Related Endocrine Adverse Events
- Metabolic risk/Epidemiology
- Obesity, Diabetes, and Increased Cancer Progression
- Dae-Seok Kim, Philipp E. Scherer
- Diabetes Metab J. 2021;45(6):799-812. Published online November 22, 2021
- DOI: https://doi.org/10.4093/dmj.2021.0077
- 14,241 View
- 669 Download
- 71 Web of Science
- 77 Crossref
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Graphical Abstract
Abstract
PDFPubReader ePub - Rates of obesity and diabetes have increased significantly over the past decades and the prevalence is expected to continue to rise further in the coming years. Many observations suggest that obesity and diabetes are associated with an increased risk of developing several types of cancers, including liver, pancreatic, endometrial, colorectal, and post-menopausal breast cancer. The path towards developing obesity and diabetes is affected by multiple factors, including adipokines, inflammatory cytokines, growth hormones, insulin resistance, and hyperlipidemia. The metabolic abnormalities associated with changes in the levels of these factors in obesity and diabetes have the potential to significantly contribute to the development and progression of cancer through the regulation of distinct signaling pathways. Here, we highlight the cellular and molecular pathways that constitute the links between obesity, diabetes, cancer risk and mortality. This includes a description of the existing evidence supporting the obesity-driven morphological and functional alternations of cancer cells and adipocytes through complex interactions within the tumor microenvironment.
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Citations
Citations to this article as recorded by- Triglyceride‐glucose index (TyG index) and endometrial carcinoma risk: A retrospective cohort study
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International Journal of Molecular Sciences.2023; 24(4): 3283. CrossRef - Hormonal Gut–Brain Signaling for the Treatment of Obesity
Eun Roh, Kyung Mook Choi
International Journal of Molecular Sciences.2023; 24(4): 3384. CrossRef - A novel five-gene metabolism-related risk signature for predicting prognosis and immune infiltration in endometrial cancer: A TCGA data mining
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Computers in Biology and Medicine.2023; 155: 106632. CrossRef - Green Antimicrobials as Therapeutic Agents for Diabetic Foot Ulcers
Ines D. Teixeira, Eugenia Carvalho, Ermelindo C. Leal
Antibiotics.2023; 12(3): 467. CrossRef - Impact of abdominal obesity on the risk of glioma development in patients with diabetes: A nationwide population-based cohort study in Korea
Hyunji Sang, Yun Kyung Cho, Kyungdo Han, Eun Hee Koh, Sandar Tin Tin
PLOS ONE.2023; 18(3): e0283023. CrossRef - Relationship Between Physical Exercise and Cognitive Impairment Among Older Adults with Type 2 Diabetes: Chain Mediating Roles of Sleep Quality and Depression
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Psychology Research and Behavior Management.2023; Volume 16: 817. CrossRef - The Mediterranean Lifestyle to Contrast Low-Grade Inflammation Behavior in Cancer
Rosa Divella, Graziella Marino, Stefania Infusino, Laura Lanotte, Gaia Gadaleta-Caldarola, Gennaro Gadaleta-Caldarola
Nutrients.2023; 15(7): 1667. CrossRef - Distribution of ABO blood groups and Rh factor in benign and malign thyroid nodules
Muzaffer Serdar DENİZ
Journal of Health Sciences and Medicine.2023; 6(2): 462. CrossRef - The Role of Selected Adipocytokines in Ovarian Cancer and Endometrial Cancer
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Diabetes Research and Clinical Practice.2023; 200: 110684. CrossRef - Prediction of Hypoglycemia in Diabetic Patients During Colonoscopy
Preparation
Xiaohua Lu, Lingqiao Xie, Wane Zhao, Chuangbiao Zhang, Xixi Luo, Yan Zhou
Experimental and Clinical Endocrinology & Diabetes.2023; 131(05): 274. CrossRef - Interplay of skeletal muscle and adipose tissue: sarcopenic obesity
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Metabolism.2023; 144: 155577. CrossRef - PIK3CA mutation in endometriotic epithelial cells promotes viperin-dependent inflammatory response to insulin
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路路 潘
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Biomedicines.2022; 10(11): 2891. CrossRef - Targeting Adiponectin in Breast Cancer
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Biomedicines.2022; 10(11): 2958. CrossRef - Multidisciplinary Progress in Obesity Research
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Environmental Science and Pollution Research.2022; 30(11): 31395. CrossRef - The crosstalk within the breast tumor microenvironment in type II diabetes: Implications for cancer disparities
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Frontiers in Endocrinology.2022;[Epub] CrossRef
- Triglyceride‐glucose index (TyG index) and endometrial carcinoma risk: A retrospective cohort study
- Pathophysiology
- Hyperinsulinemia in Obesity, Inflammation, and Cancer
- Anni M.Y. Zhang, Elizabeth A. Wellberg, Janel L. Kopp, James D. Johnson
- Diabetes Metab J. 2021;45(3):285-311. Published online March 29, 2021
- DOI: https://doi.org/10.4093/dmj.2020.0250
- Correction in: Diabetes Metab J 2021;45(4):622
- 23,327 View
- 904 Download
- 81 Web of Science
- 88 Crossref
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Graphical Abstract
Abstract
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- The relative insufficiency of insulin secretion and/or insulin action causes diabetes. However, obesity and type 2 diabetes mellitus can be associated with an absolute increase in circulating insulin, a state known as hyperinsulinemia. Studies are beginning to elucidate the cause-effect relationships between hyperinsulinemia and numerous consequences of metabolic dysfunctions. Here, we review recent evidence demonstrating that hyperinsulinemia may play a role in inflammation, aging and development of cancers. In this review, we will focus on the consequences and mechanisms of excess insulin production and action, placing recent findings that have challenged dogma in the context of the existing body of literature. Where relevant, we elaborate on the role of specific signal transduction components in the actions of insulin and consequences of chronic hyperinsulinemia. By discussing the involvement of hyperinsulinemia in various metabolic and other chronic diseases, we may identify more effective therapeutics or lifestyle interventions for preventing or treating obesity, diabetes and cancer. We also seek to identify pertinent questions that are ripe for future investigation.
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Citations
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- Histone Deacetylase 9: Its Role in the Pathogenesis of Diabetes and Other Chronic Diseases
- Siqi Hu, Eun-Hee Cho, Ji-Young Lee
- Diabetes Metab J. 2020;44(2):234-244. Published online March 24, 2020
- DOI: https://doi.org/10.4093/dmj.2019.0243
- 6,396 View
- 161 Download
- 20 Web of Science
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Abstract
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As a member of the class IIa histone deacetylases (HDACs), HDAC9 catalyzes the deacetylation of histones and transcription factors, commonly leading to the suppression of gene transcription. The activity of HDAC9 is regulated transcriptionally and post-translationally. HDAC9 is known to play an essential role in regulating myocyte and adipocyte differentiation and cardiac muscle development. Also, recent studies have suggested that HDAC9 is involved in the pathogenesis of chronic diseases, including cardiovascular diseases, osteoporosis, autoimmune disease, cancer, obesity, insulin resistance, and liver fibrosis. HDAC9 modulates the expression of genes related to the pathogenesis of chronic diseases by altering chromatin structure in their promotor region or reducing the transcriptional activity of their respective transcription factors. This review summarizes the current knowledge of the regulation of HDAC9 expression and activity. Also, the roles of HDAC9 in the pathogenesis of chronic diseases are discussed, along with potential underlying mechanisms.
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- Diabetes and Cancer: Cancer Should Be Screened in Routine Diabetes Assessment
- Sunghwan Suh, Kwang-Won Kim
- Diabetes Metab J. 2019;43(6):733-743. Published online December 23, 2019
- DOI: https://doi.org/10.4093/dmj.2019.0177
- 8,669 View
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Abstract
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Cancer incidence appears to be increased in both type 1 and type 2 diabetes mellitus (DM). DM represents a risk factor for cancer, particularly hepatocellular, hepatobiliary, pancreas, breast, ovarian, endometrial, and gastrointestinal cancers. In addition, there is evidence showing that DM is associated with increased cancer mortality. Common risk factors such as age, obesity, physical inactivity and smoking may contribute to increased cancer risk in patients with DM. Although the mechanistic process that may link diabetes to cancer is not completely understood yet, biological mechanisms linking DM and cancer are hyperglycemia, hyperinsulinemia, increased bioactivity of insulin-like growth factor 1, oxidative stress, dysregulations of sex hormones, and chronic inflammation. However, cancer screening rate is significantly lower in people with DM than that in people without diabetes. Evidence from previous studies suggests that some medications used to treat DM are associated with either increased or reduced risk of cancer. However, there is no strong evidence supporting the association between the use of anti-hyperglycemic medication and specific cancer. In conclusion, all patients with DM should be undergo recommended age- and sex appropriate cancer screenings to promote primary prevention and early detection. Furthermore, cancer should be screened in routine diabetes assessment.
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Original Articles
- The Relationship between Metformin and Cancer in Patients with Type 2 Diabetes
- Hyun Hee Chung, Jun Sung Moon, Ji Sung Yoon, Hyoung Woo Lee, Kyu Chang Won
- Diabetes Metab J. 2013;37(2):125-131. Published online April 16, 2013
- DOI: https://doi.org/10.4093/dmj.2013.37.2.125
- 3,563 View
- 29 Download
- 13 Crossref
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Abstract
PDFPubReader
Background Recently, several studies reported that the cancer incidence in type 2 diabetes patients is higher than in the general population. Although a number of risks are shared between cancer and diabetes patients, there have been few studies of its correlation. We evaluated the influences of several factors including low density lipoprotein cholesterol (LDL-C), albuminuria and use of metformin on the risk of cancer in patients with type 2 diabetes.
Methods We enrolled 1,320 patients with at least 5 years of follow-up and 73 patients were diagnosed with cancer during this period. The associations of the risk factors with cancer incidence were evaluated by multiple regression analysis. The subjects were placed into two subgroups based on metformin dosage (<1,000 mg/day, ≥1,000 mg/day) and we compared cancer incidence using analysis of covariance.
Results LDL-C and albuminuria were not significantly correlated with cancer risk. In contrast, metformin showed a reverse correlation with cancer risk (
P =0.006; relative risk, 0.574). In the metformin nonadministration group, smoking, male gender, and high triglyceride levels tended to be contributing factors without statistical significance. Cancer occurence was lower in the low dose metformin group (less than 1,000 mg/day) (P =0.00).Conclusion These results suggest that the administration of low dose metformin in patients with type 2 diabetes may be associated with a reduced risk of cancer.
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Sudhir Manickavel, Yolanda Hartman, Andrew Burns, Manuel A. Lora Gonzalez, Jason Warram, Erika Walsh, Jacob B. Hunter, Daniel E. Killeen
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Diabetes & Metabolism Journal.2013; 37(2): 113. CrossRef
- Metformin Reduces Tumor Growth in a Murine Flank Schwannoma Model
- The Risk of Bladder Cancer in Korean Diabetic Subjects Treated with Pioglitazone
- Sun Ok Song, Kwang Joon Kim, Byung-Wan Lee, Eun Seok Kang, Bong Soo Cha, Hyun Chul Lee
- Diabetes Metab J. 2012;36(5):371-378. Published online October 18, 2012
- DOI: https://doi.org/10.4093/dmj.2012.36.5.371
- 4,152 View
- 30 Download
- 30 Crossref
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Abstract
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Background There is growing concern regarding the increased incidence of bladder cancer in diabetic patients using pioglitazone. This study aimed to investigate the association between bladder cancer and the use of pioglitazone in Korean diabetics.
Methods This retrospective, matched case-control study included a case group (
n =329) of diabetic patients with bladder cancer who presented at the Severance Hospital from November 2005 to June 2011. The control group consisted of patients without bladder cancer (1:2 ratio matching for sex and age,n =658) who were listed on the Severance Hospital diabetes registry.Results The percentage of subjects who had ever used pioglitazone was significantly lower in the case group than in the control group (6.4% vs. 15.0%,
P <0.001). Multivariate conditional logistic analysis revealed that independent factors affecting bladder cancer were smoking (odds ratio [OR], 11.64; 95% confidence interval [CI], 6.56 to 20.66;P <0.001), coexisting cancer (OR, 6.11; 95% CI, 2.25 to 16.63;P <0.001), and hemoglobin levels (OR, 0.78; 95% CI, 0.69 to 0.88;P <0.001). The OR of the history of pioglitazone use was 2.09 and was not significantly different between the two groups (95% CI, 0.26 to 16.81;P =0.488).Conclusion A relationship between pioglitazone use and incidence of bladder cancer was not observed in Korean diabetic patients. This suggests that the risk for bladder cancer in Korean diabetic subjects treated with pioglitazone might be different from that of Caucasian populations. Large-scale, well-designed and multi-center studies are needed to further evaluate this relationship.
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