Type 2 Diabetes: An Updated Overview
- PMID: 32422019
- DOI: 10.1615/CritRevOncog.2019030976
Type 2 Diabetes: An Updated Overview
Abstract
The prevalence of type 2 diabetes (T2D) is increasing worldwide. This study provides essential information about the classification, diagnosis, pathogenesis, treatment, and complications of T2D. Glucose homeostasis is controlled by the rates of endogenous glucose production (EGP) and glucose utilization. EGP is ~2 mg/kg/min in humans and is equal to the rate of basal glucose utilization. During fasting, ~75-85% of EGP occurs in the liver and the remainder in the kidney. Hepatic glucose production is the main determinant of fasting blood glucose concentration. In the fed state, when insulin secretion is stimulated and glucagon secretion is inhibited, EGP decreases and glucose uptake in splanchnic (liver and gut) and peripheral (primarily muscle) tissues increases. β-cell dysfunction and insulin resistance represent core pathophysiological defects in T2D. Although the pathogenesis of T2D was previously focused on dysfunctions of "ominous triumvirate" (liver, skeletal muscle, and β-cell), it has been extended to "ominous octet," which includes defects in adipocytes (increased lipolysis), gastrointestinal tract (incretin deficiency/resistance), pancreatic α-cells (hyperglucagonemia), kidneys (increased glucose reabsorption), and brain (insulin resistance); endothelial dysfunction, inflammation, increased oxidative stress, and hypoxia are also involved in the pathogenesis of T2D. In conclusion, diabetes is one of the leading causes of morbidity and mortality worldwide. More insights into the pathophysiology of T2D necessitate revising the treatment approaches from only glycemic control to a pathophysiological-based view. In addition, new emerging complications of T2D such as cancer warrant further attention.
Similar articles
-
Role of reduced insulin-stimulated bone blood flow in the pathogenesis of metabolic insulin resistance and diabetic bone fragility.Med Hypotheses. 2016 Aug;93:81-6. doi: 10.1016/j.mehy.2016.05.008. Epub 2016 May 12. Med Hypotheses. 2016. PMID: 27372862
-
Diabetes and branched-chain amino acids: What is the link?J Diabetes. 2018 May;10(5):350-352. doi: 10.1111/1753-0407.12645. Epub 2018 Feb 13. J Diabetes. 2018. PMID: 29369529
-
Current issues in the treatment of type 2 diabetes. Overview of newer agents: where treatment is going.Am J Med. 2010 Mar;123(3 Suppl):S38-48. doi: 10.1016/j.amjmed.2009.12.008. Am J Med. 2010. PMID: 20206731 Review.
-
The entero-insular axis: implications for human metabolism.Clin Chem Lab Med. 2008;46(1):43-56. doi: 10.1515/CCLM.2008.008. Clin Chem Lab Med. 2008. PMID: 18020966 Review.
-
The Liver-α-Cell Axis and Type 2 Diabetes.Endocr Rev. 2019 Oct 1;40(5):1353-1366. doi: 10.1210/er.2018-00251. Endocr Rev. 2019. PMID: 30920583 Review.
Cited by
-
Anti-oxidant effect of nitrite in the pancreatic islets of type 2 diabetic male rats.Iran J Basic Med Sci. 2023 Apr;26(4):420-428. doi: 10.22038/IJBMS.2023.68245.14900. Iran J Basic Med Sci. 2023. PMID: 37009002 Free PMC article.
-
Streptozotocin as a tool for induction of rat models of diabetes: a practical guide.EXCLI J. 2023 Feb 21;22:274-294. doi: 10.17179/excli2022-5720. eCollection 2023. EXCLI J. 2023. PMID: 36998708 Free PMC article. Review.
-
Uric acid-induced pancreatic β-cell dysfunction.BMC Endocr Disord. 2021 Feb 16;21(1):24. doi: 10.1186/s12902-021-00698-6. BMC Endocr Disord. 2021. PMID: 33593356 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical