Current Status of Research on Mechanisms and Treatment of Constipation in Type 2 Diabetes Mellitus
DOI: https://doi.org/10.62517/jmpe.202418102
Author(s)
Yao Xiao1, Rui Zhang2,*
Affiliation(s)
1Changchun University of Chinese Medicine, Changchun, Jilin, China
2Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun, Jilin, China
*Corresponding Author.
Abstract
Both the prevalence of Type 2 diabetes mellitus (T2DM) and the number of its complications have been rising over the past few years. Type 2 diabetes constipation (T2DC) is one of the most common gastrointestinal complications caused by diabetes mellitus, and the incidence is also increasing due to the high prevalence of T2DC. Morbidity is also increasing. This review outlines the pathogenesis of DM, which causes oxidative stress, alterations in the enteric nervous system and related structures, intestinal dysbiosis, rectal dysfunction, biochemical dysfunction, and constipation, to further characterize T2DC. At the same time, the disease is in urgent need of intervention to alleviate the pressure of constipation on the lives of patients. This overview also summarizes the understanding of T2DC by domestic and foreign medical practitioners and the therapeutic advances in the treatment of T2DC from the perspective of improving symptoms by controlling blood glucose, diet and exercise, and improving symptoms through laxatives and gastrointestinal motivation drugs in Western medicine.
Keywords
Type 2 Diabetes Mellitus; Constipation; Treatment Progress; Oxidative Stress; Enteric Nervous System
References
[1]Maritim AC, Sanders RA, Watkins JB. (2003). Diabetes, oxidative stress and antioxidants: a review J Biochem Mol Toxicol, 17(1): 24-38.
[2]Brownlee M. (2005). The pathobiology of diabetic complications: a unifying mechanism. Diabetes, 54(6): 1615-1625.
[3]Moriyama R, Tsukamura H, Kinoshita M, et al. (2004). In vitro increase in intracellular calcium concentrations induced by low or high extracellular glucose levels in ependymocytes and serotonergic neurons of the rat lower brainstem. Endocrinology. May; 145 (5): 2507-15
[4]Larsen N, V ogensen FK, van den Berg FW. (2010). Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLo S One.Feb5; 5(2):e9085.
[5]Bagyánszki M, Bódi N. (2012). Diabetes-related alterations in the enteric nervous system and its microenvironment. World J Diabetes. May 15; 3(5):80-93.
[6]Christoph A, Thaiss, Maayan Levy, Inna Grosheva, et al. Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection. Science 23 Mar 2018: Vol. 359, Issue 6382, pp.1376-1383.
[7]Vincent Andrea M, Hayes John M, Mc Lean Lisa L, et al. (2009). Dyslipidemia-induced neuropathy in mice: the role of ox LDL-C/LOX-1.Diabetes, 58(10):2376-85, 2018, 38(21):5169-5171.
[8]Rao SS, Singh S. Clinical utility of colonic and anorectal manometry in chronic constipation. J Clin Gastroenterol, 2010; 44(9): 597-609.
[9]Menke A, Casagrande S, Geiss L, et al. Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012.The Journal of the American Medical Association, 2015.
[10]Ueno N, Inui A, Satoh Y. The effect of mosapride citrate on constipation in patients with diabetes. Diabetes Res Clin Pract. 2010 Jan; 87(1):27-32.
[11]Camilleri M, Kerstens, René, Rykx A, et al. A Placebo-Controlled Trial of Prucalopride for Severe Chronic Constipation. New England Journal of Medicine, 2008, 358(22): 2344-2354.
[12]Xiaokang Wu, Chaofeng Ma, Lei Han, et al. Molecular Characterisation of the Faecal Microbiota in Patients with Type II Diabetes. 61(1):69-78.
[13]Ziegler D, Nowak H, Kempler P, et al, Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a meta-analysis. Diabet Med. 2004 Feb; 21(2):114-21.
[14]Nelson, A. D, Camilleri, M, Acosta A, et al. A single-center, prospective, double-blind, sham-controlled, randomized study of the effect of a vibrating capsule on colonic transit in patients with chronic constipation. Neurogastroenterol Motil.2017 Jul; 29(7).