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Eksport do Mediów Społecznościowych

Eksport do Mediów Społecznościowych

Oś mikrobiota–jelita–mózg a zaburzenia poznawcze u chorych na cukrzycę: niezapomniana podróż

Srinidhi Rai1, Souparnika Sreelatha2, Nayana Devang3, Priya D. Alva1, Arkiath Veettil Raveendran4
Diabetologia Praktyczna 2024;10:9-20.

Streszczenie

Cel: Cukrzyca (DM, diabetes mellitus) wiąże się z powikłaniami wpływającymi na jakość życia. Co ciekawe, mikroflora jelitowa jest ściśle powiązana z metabolizmem glukozy. W tym przeglądzie narracyjnym przedstawiono charakterystykę mikrobioty jelitowej u chorych na cukrzycę, opisano modulację kontroli glikemii gospodarza przez mikrobiotę jelitową, charakterystykę nieszczelności jelit, mechanizmy zaburzeń poznawczych w cukrzycy (DCI, diabetic cognitive impairment) oraz rolę osi mózg–jelita–mikrobiota w DM. Materiał i metody: Przeszukano literaturę w bazach Medline, Scopus, WOS i PubMed, używając słów kluczowych: mikrobiota jelitowa, DM, nieszczelność jelit i DCI (ang. gut microbiota, DM, intestinal permeability, DCI). Wyniki: Dysbioza mikrobioty jelitowej powoduje przerwanie bariery jelitowej, skutkujące przedostaniem się bakterii jelitowych i ich metabolitów do układu krążenia, co może zaburzyć wrażliwość na insulinę, metabolizm glukozy i homeostazę immunologiczną. Mikrobiota jelitowa odgrywa kluczową rolę w regulacji ogólnoustrojowej wrażliwości na insulinę i metabolizmu energetycznego. Uważa się, że dysfunkcja bariery jelitowej wywołana hiperglikemią jest podstawowym mechanizmem infekcji ogólnoustrojowych i reakcji zapalnej u pacjentów z cukrzycą. Zarówno dysbakterioza, jak i cytokiny będą prowadzić do dysfunkcji bariery jelitowej i bariery krew–mózg, ułatwiając przenikanie szkodliwych substancji (końcowych produktów glikacji) do neuronów, a tym samym przyczyniając się do rozwoju DCI. Modulacja przepuszczalności jelit poprzez interwencje żywieniowe może stanowić potencjalny cel w zapobieganiu cukrzycy. Wnioski: Dowody kliniczne na związek między hiperglikemią a dysfunkcją bariery jelitowej u ludzi są nieliczne. Konieczne są dalsze badania kliniczne, aby uzyskać więcej informacji poprzez ocenę markerów integralności bariery jelitowej i statusu glikemicznego oraz ich związku z funkcjami poznawczymi.

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Referencje

  1. https://atlasbiomed.com/blog/11-ways-your-life-can-disrupt-the-gut-microbiome/ (22.02.2023).
  2. Wu Y, Ding Y, Tanaka Y, et al. Risk factors contributing to type 2 diabetes and recent advances in the treatment and prevention. Int J Med Sci. 2014; 11(11): 1185–1200.
  3. Integrative HMP (iHMP) Research Network Consortium. The Integrative Human Microbiome Project. Nature. 2019; 569(7758): 641–648.
  4. Zhang L, Chu J, Hao W, et al. Gut Microbiota and Type 2 Diabetes Mellitus: Association, Mechanism, and Translational Applications. Mediators Inflamm. 2021; 2021: 5110276.
  5. Sogin ML, Morrison HG, Huber JA, et al. Microbial diversity in the deep sea and the underexplored "rare biosphere". Proc Natl Acad Sci U S A. 2006; 103(32): 12115–12120.
  6. Turnbaugh PJ, Ley RE, Hamady M, et al. The human microbiome project. Nature. 2007; 449(7164): 804–810.
  7. Hooper LV, Gordon JI. Commensal host-bacterial relationships in the gut. Science. 2001; 292(5519): 1115–1118.
  8. Human Microbiome Project Consortium. Structure, function and diversity of the healthy human microbiome. Nature. 2012; 486(7402): 207–214.
  9. Larsen N, Vogensen FK, van den Berg FWJ, et al. Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLoS One. 2010; 5(2): e9085.
  10. Sedighi M, Razavi S, Navab-Moghadam F, et al. Comparison of gut microbiota in adult patients with type 2 diabetes and healthy individuals. Microb Pathog. 2017; 111: 362–369.
  11. Cunningham AL, Stephens JW, Harris DA. Gut microbiota influence in type 2 diabetes mellitus (T2DM). Gut Pathog. 2021; 13(1): 50.
  12. Furet JP, Kong LC, Tap J, et al. Differential adaptation of human gut microbiota to bariatric surgery-induced weight loss: links with metabolic and low-grade inflammation markers. Diabetes. 2010; 59(12): 3049–3057.
  13. Everard A, Belzer C, Geurts L, et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci U S A. 2013; 110(22): 9066–9071.
  14. Bäckhed F, Ding H, Wang T, et al. The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A. 2004; 101(44): 15718–15723.
  15. Dandona P, Aljada A, Bandyopadhyay A. Inflammation: the link between insulin resistance, obesity and diabetes. Trends Immunol. 2004; 25(1): 4–7.
  16. Ley RE. Obesity and the human microbiome. Curr Opin Gastroenterol. 2010; 26(1): 5–11.
  17. Chen X, Devaraj S. Gut Microbiome in Obesity, Metabolic Syndrome, and Diabetes. Curr Diab Rep. 2018; 18(12): 129.
  18. Saad MJA, Santos A, Prada PO. Linking Gut Microbiota and Inflammation to Obesity and Insulin Resistance. Physiology (Bethesda). 2016; 31(4): 283–293.
  19. Gurung M, Li Z, You H, et al. Role of gut microbiota in type 2 diabetes pathophysiology. EBioMedicine. 2020; 51: 102590.
  20. Kim SH, Huh CS, Choi ID, et al. The anti-diabetic activity of Bifidobacterium lactis HY8101 in vitro and in vivo. J Appl Microbiol. 2014; 117(3): 834–845.
  21. Paun A, Yau C, Danska JS. The Influence of the Microbiome on Type 1 Diabetes. J Immunol. 2017; 198(2): 590–595.
  22. Cunningham AL, Stephens JW, Harris DA. Gut microbiota influence in type 2 diabetes mellitus (T2DM). Gut Pathog. 2021; 13(1): 50.
  23. Nicholson JK, Holmes E, Kinross J, et al. Host-gut microbiota metabolic interactions. Science. 2012; 336(6086): 1262–1267.
  24. Yamagata K, Daitoku H, Shimamoto Y, et al. Bile acids regulate gluconeogenic gene expression via small heterodimer partner-mediated repression of hepatocyte nuclear factor 4 and Foxo1. J Biol Chem. 2004; 279(22): 23158–23165.
  25. Pelaseyed T, Bergström JH, Gustafsson JK, et al. The mucus and mucins of the goblet cells and enterocytes provide the first defense line of the gastrointestinal tract and interact with the immune system. Immunol Rev. 2014; 260(1): 8–20.
  26. Schroeder BO. Fight them or feed them: how the intestinal mucus layer manages the gut microbiota. Gastroenterol Rep (Oxf). 2019; 7(1): 3–12.
  27. Shifrin DA, McConnell RE, Nambiar R, et al. Enterocyte microvillus-derived vesicles detoxify bacterial products and regulate epithelial-microbial interactions. Curr Biol. 2012; 22(7): 627–631.
  28. Sorini C, Cosorich I, Lo Conte M, et al. Loss of gut barrier integrity triggers activation of islet-reactive T cells and autoimmune diabetes. Proc Natl Acad Sci U S A. 2019; 116(30): 15140–15149.
  29. Vaarala O, Atkinson MA, Neu J. The "perfect storm" for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability, and mucosal immunity. Diabetes. 2008; 57(10): 2555–2562.
  30. Chelakkot C, Ghim J, Ryu SHo. Mechanisms regulating intestinal barrier integrity and its pathological implications. Exp Mol Med. 2018; 50(8): 1–9.
  31. Xu J, Liang R, Zhang W, et al. Faecalibacterium prausnitzii-derived microbial anti-inflammatory molecule regulates intestinal integrity in diabetes mellitus mice via modulating tight junction protein expression. J Diabetes. 2020; 12(3): 224–236.
  32. Min XH, Yu T, Qing Q, et al. Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway. Cell Biol Int. 2014; 38(10): 1194–1204.
  33. Thaiss CA, Levy M, Grosheva I, et al. Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection. Science. 2018; 359(6382): 1376–1383.
  34. Yang Ge, Wei J, Liu P, et al. Role of the gut microbiota in type 2 diabetes and related diseases. Metabolism. 2021; 117: 154712.
  35. Pussinen PJ, Havulinna AS, Lehto M, et al. Endotoxemia is associated with an increased risk of incident diabetes. Diabetes Care. 2011; 34(2): 392–397.
  36. Cox AJ, Zhang P, Bowden DW, et al. Increased intestinal permeability as a risk factor for type 2 diabetes. Diabetes Metab. 2017; 43(2): 163–166.
  37. Shen L, Ao Li, Xu H, et al. Poor short-term glycemic control in patients with type 2 diabetes impairs the intestinal mucosal barrier: a prospective, single-center, observational study. BMC Endocr Disord. 2019; 19(1): 29.
  38. Horton F, Wright J, Smith L, et al. Increased intestinal permeability to oral chromium (51 Cr) -EDTA in human Type 2 diabetes. Diabet Med. 2014; 31(5): 559–563.
  39. Genser L, Aguanno D, Soula HA, et al. Increased jejunal permeability in human obesity is revealed by a lipid challenge and is linked to inflammation and type 2 diabetes. J Pathol. 2018; 246(2): 217–230.
  40. Creely SJ, McTernan PG, Kusminski CM, et al. Lipopolysaccharide activates an innate immune system response in human adipose tissue in obesity and type 2 diabetes. Am J Physiol Endocrinol Metab. 2007; 292(3): E740–E747.
  41. Trøseid M, Nestvold TK, Rudi K, et al. Plasma lipopolysaccharide is closely associated with glycemic control and abdominal obesity: evidence from bariatric surgery. Diabetes Care. 2013; 36(11): 3627–3632.
  42. Zhang D, Zhang L, Zheng Y, et al. Circulating zonulin levels in newly diagnosed Chinese type 2 diabetes patients. Diabetes Res Clin Pract. 2014; 106(2): 312–318.
  43. Moreno-Navarrete JM, Sabater M, Ortega F, et al. Circulating zonulin, a marker of intestinal permeability, is increased in association with obesity-associated insulin resistance. PLoS One. 2012; 7(5): e37160.
  44. Jayashree B, Bibin YS, Prabhu D, et al. Increased circulatory levels of lipopolysaccharide (LPS) and zonulin signify novel biomarkers of proinflammation in patients with type 2 diabetes. Mol Cell Biochem. 2014; 388(1-2): 203–210.
  45. Hoffmanová I, Sánchez D, Hábová V, et al. Serological markers of enterocyte damage and apoptosis in patients with celiac disease, autoimmune diabetes mellitus and diabetes mellitus type 2. Physiol Res. 2015; 64(4): 537–546.
  46. Yuan JH, Xie QS, Chen GC, et al. Impaired intestinal barrier function in type 2 diabetic patients measured by serum LPS, Zonulin, and IFABP. J Diabetes Complications. 2021; 35(2): 107766.
  47. Biessels GJ, van der Heide LP, Kamal A, et al. Ageing and diabetes: implications for brain function. Eur J Pharmacol. 2002; 441(1-2): 1–14.
  48. Rawlings AM, Sharrett AR, Schneider ALC, et al. Diabetes in midlife and cognitive change over 20 years: a cohort study. Ann Intern Med. 2014; 161(11): 785–793.
  49. Watson GS, Craft S. The role of insulin resistance in the pathogenesis of Alzheimer's disease: implications for treatment. CNS Drugs. 2003; 17(1): 27–45.
  50. Yaffe K, Blackwell T, Kanaya AM, et al. Diabetes, impaired fasting glucose, and development of cognitive impairment in older women. Neurology. 2004; 63(4): 658–663.
  51. Choi J, Chandrasekaran K, Demarest TG, et al. Brain diabetic neurodegeneration segregates with low intrinsic aerobic capacity. Ann Clin Transl Neurol. 2014; 1(8): 589–604.
  52. Launer LJ, Miller ME, Williamson JD, et al. ACCORD MIND investigators. Effects of intensive glucose lowering on brain structure and function in people with type 2 diabetes (ACCORD MIND): a randomised open-label substudy. Lancet Neurol. 2011; 10(11): 969–977.
  53. Mastrocola R, Restivo F, Vercellinatto I, et al. Oxidative and nitrosative stress in brain mitochondria of diabetic rats. J Endocrinol. 2005; 187(1): 37–44.
  54. Foster JA, McVey Neufeld KA. Gut-brain axis: how the microbiome influences anxiety and depression. Trends Neurosci. 2013; 36(5): 305–312.
  55. Xu Y, Zhou H, Zhu Q. The Impact of Microbiota-Gut-Brain Axis on Diabetic Cognition Impairment. Front Aging Neurosci. 2017; 9: 106.
  56. Hawkins BT, Lundeen TF, Norwood KM, et al. Increased blood-brain barrier permeability and altered tight junctions in experimental diabetes in the rat: contribution of hyperglycaemia and matrix metalloproteinases. Diabetologia. 2007; 50(1): 202–211.
  57. Strachan MWJ. R D Lawrence Lecture 2010. The brain as a target organ in Type 2 diabetes: exploring the links with cognitive impairment and dementia. Diabet Med. 2011; 28(2): 141–147.
  58. Shimizu F, Sano Y, Tominaga O, et al. Advanced glycation end-products disrupt the blood-brain barrier by stimulating the release of transforming growth factor-β by pericytes and vascular endothelial growth factor and matrix metalloproteinase-2 by endothelial cells in vitro. Neurobiol Aging. 2013; 34(7): 1902–1912.
  59. Mattson MP, Camandola S. NF-kappaB in neuronal plasticity and neurodegenerative disorders. J Clin Invest. 2001; 107(3): 247–254.
  60. Wong RH, Scholey A, Howe PR. Assessing premorbid cognitive ability in adults with type 2 diabetes mellitus--a review with implications for future intervention studies. Curr Diab Rep. 2014; 14(11): 547.
  61. Rdzak GM, Abdelghany O. Does insulin therapy for type 1 diabetes mellitus protect against Alzheimer's disease? Pharmacotherapy. 2014; 34(12): 1317–1323.
  62. Lochhead JJ, Kellohen KL, Ronaldson PT, et al. Distribution of insulin in trigeminal nerve and brain after intranasal administration. Sci Rep. 2019; 9(1): 2621.
  63. Rhea EM, Salameh TS, Banks WA. Routes for the delivery of insulin to the central nervous system: A comparative review. Exp Neurol. 2019; 313: 10–15.
  64. Craft S, Claxton A, Baker LD, et al. Effects of Regular and Long-Acting Insulin on Cognition and Alzheimer's Disease Biomarkers: A Pilot Clinical Trial. J Alzheimers Dis. 2017; 57(4): 1325–1334.
  65. Fan LW, Carter K, Bhatt A, et al. Rapid transport of insulin to the brain following intranasal administration in rats. Neural Regen Res. 2019; 14(6): 1046–1051.
  66. Yaribeygi H, Rashidy-Pour A, Atkin SL, et al. GLP-1 mimetics and cognition. Life Sci. 2021; 264: 118645.
  67. McClean PL, Hölscher C. Lixisenatide, a drug developed to treat type 2 diabetes, shows neuroprotective effects in a mouse model of Alzheimer's disease. Neuropharmacology. 2014; 86: 241–258.
  68. Pipatpiboon N, Pintana H, Pratchayasakul W, et al. DPP4-inhibitor improves neuronal insulin receptor function, brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption. Eur J Neurosci. 2013; 37(5): 839–849.
  69. Antal B, McMahon LP, Sultan SF, et al. Type 2 diabetes mellitus accelerates brain aging and cognitive decline: Complementary findings from UK Biobank and meta-analyses. Elife. 2022; 11.
  70. Naguib R, Soliman E, Neimatallah F, et al. Cognitive impairment among patients with diabetes in Saudi Arabia: a cross-sectional study. Middle East Current Psychiatry. 2020; 27(1).
  71. Varghese SM, Joy N, John AM, et al. Sweet Memories or Not? A Comparative Study on Cognitive Impairment in Diabetes Mellitus. Front Public Health. 2022; 10: 822062.
  72. Han E, Han Kd, Lee BW, et al. Severe Hypoglycemia Increases Dementia Risk and Related Mortality: A Nationwide, Population-based Cohort Study. J Clin Endocrinol Metab. 2022; 107(5): e1976–e1986.
  73. Malik A, Ahmed M, Mansoor S, et al. Cognitive Impairment in Type 2 Diabetes Mellitus. Cureus. 2022; 14(2): e22193.
  74. Frison E, Proust-Lima C, Mangin JF, et al. MEMENTO Cohort Study Group. Diabetes Mellitus and Cognition: Pathway Analysis in the MEMENTO Cohort. Neurology. 2021; 97(8): e836–e848.
  75. Lin CF, Liu HC, Lin SY. Kidney Function and Risk of Physical and Cognitive Impairment in Older Persons with Type 2 Diabetes at an Outpatient Clinic with Geriatric Assessment Implementation. Diabetes Metab Syndr Obes. 2022; 15: 79–91.
  76. Dove A, Shang Y, Xu W, et al. The impact of diabetes on cognitive impairment and its progression to dementia. Alzheimers Dement. 2021; 17(11): 1769–1778.
  77. Sun L, Diao X, Gang X, et al. Risk Factors for Cognitive Impairment in Patients with Type 2 Diabetes. J Diabetes Res. 2020; 2020: 4591938.
  78. Bercik P, Park AJ, Sinclair D, et al. The anxiolytic effect of Bifidobacterium longum NCC3001 involves vagal pathways for gut-brain communication. Neurogastroenterol Motil. 2011; 23(12): 1132–1139.
  79. Kim KA, Gu W, Lee IA, et al. High fat diet-induced gut microbiota exacerbates inflammation and obesity in mice via the TLR4 signaling pathway. PLoS One. 2012; 7(10): e47713.
  80. Chunchai T, Thunapong W, Yasom S, et al. Decreased microglial activation through gut-brain axis by prebiotics, probiotics, or synbiotics effectively restored cognitive function in obese-insulin resistant rats. J Neuroinflammation. 2018; 15(1): 11.
  81. Petra AI, Panagiotidou S, Hatziagelaki E, et al. Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation. Clin Ther. 2015; 37(5): 984–995.
  82. Socała K, Doboszewska U, Szopa A, et al. The role of microbiota-gut-brain axis in neuropsychiatric and neurological disorders. Pharmacol Res. 2021; 172: 105840.
  83. Allen NJ, Lyons DA. Glia as architects of central nervous system formation and function. Science. 2018; 362(6411): 181–185.
  84. Liddelow SA, Guttenplan KA, Clarke LE, et al. Neurotoxic reactive astrocytes are induced by activated microglia. Nature. 2017; 541(7638): 481–487.
  85. Barbierato M, Facci L, Argentini C, et al. Astrocyte-microglia cooperation in the expression of a pro-inflammatory phenotype. CNS Neurol Disord Drug Targets. 2013; 12(5): 608–618.
  86. Viana SD, Valero J, Rodrigues-Santos P, et al. Regulation of striatal astrocytic receptor for advanced glycation end-products variants in an early stage of experimental Parkinson's disease. J Neurochem. 2016; 138(4): 598–609.
  87. Mrak RE, Griffin WS. Glia and their cytokines in progression of neurodegeneration. Neurobiol Aging. 2005; 26(3): 349–354.
  88. Srinivasan M, Lahiri DK. Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis. Expert Opin Ther Targets. 2015; 19(4): 471–487.
  89. Klingelhoefer L, Reichmann H. Pathogenesis of Parkinson disease--the gut-brain axis and environmental factors. Nat Rev Neurol. 2015; 11(11): 625–636.
  90. Sharon G, Sampson TR, Geschwind DH, et al. The Central Nervous System and the Gut Microbiome. Cell. 2016; 167(4): 915–932.