Chronic mild inflammation links obesity, metabolic syndrome, atherosclorosis and diabetes
Authors:
M. Anděl 1,2,4; J. Polák 1,3,4; P. Kraml 1,4; P. Dlouhý 1,2; V. Štich 1,3
Authors‘ workplace:
Centrum pro výzkum diabetu, metabolismu a výživy 3. lékařské fakulty UK a FN Královské Vinohrady Praha, vedoucí prof. MUDr. Michal Anděl, CSc.
1; Ústav výživy 3. lékařské fakulty UK a FN Královské Vinohrady, Praha, přednosta prof. MUDr. Michal Anděl, CSc.
2; Ústav tělovýchovného lékařství 3. lékařské fakulty UK a FN Královské Vinohrady, Praha, přednosta doc. MUDr. Vladimír Štich, Ph. D.
3; II. interní klinika 3. lékařské fakulty UK a FN Královské Vinohrady, Praha, přednosta prof. MUDr. Michal Anděl, CSc.
4
Published in:
Vnitř Lék 2009; 55(7-8): 659-665
Category:
134th Internal Medicine Day - 23rd Vanysek's Day Brno 2009 - Vanysek's Lecture
Overview
Chronic low grade inflammation is relatively new concept in metabolic medicine. This concept describes the relations between the inflammation and adipose tissue, insulin resistence, atherosclerosis and type 2 diabetes mellitus. Macrophages and lymphocytes deposed in adipose tissue produce proinflammatory cytokines which directly or through the CRP liver secretion are targeting endothelial cells, hepatocytes and β cells of Langerhans islets of pancreas. The dysfunction of these cells follows often further disturbances and in case of β cells – the cell death. The connection between the adipose tissue insulin resistence, atherosclerosis and type 2 diabetes was earlier described with endocrine and metabolic descriptors. The concept of chronic low grade inflammation creates also another description of multilateral connections in metabolic syndome. The salicylates and the drugs related to them seem to have some glucose lowering properties. The recent development in the field of chronic low grade inflammation represents also certain therapeutic hope for antiinflammatory intervention in type 2 diabetes.
Key words:
chronic low grade inflammation – metabolic syndrome – type 2 diabetes mellitus – cytokines
Sources
1. Altannavch TS, Roubalová K, Kucera P et al. Effect of high glucose concentrations on expression of ELAM-1, VCAM‑1 and ICAM‑1 in HUVEC with and without cytokine activation. Physiol Res 2004; 53: 77–82.
2. Anděl M, Kraml P, Dlouhý P et al. Patogeneze aterosklerózy – od metabolických změn k chronickému zánětu s aspekty střádavého onemocnění. Prak Lékař 1997; 77: 266–274.
3. Anděl M, Tsevegjav A, Roubalová K et al. Infekční a zánětlivé faktory v patogenezi aterosklerózy. Vnitř Lék 2003; 49: 960–966.
4. Avalos I, Rho YH, Chung CP et al. Atherosclerosis in rheumatoid arthritis and systemic lupus erythematosus. Clin Exp Rheumatol 2008; 26 (5 Suppl 51): S5–S13.
5. Bannerman DD, Goldblum SE. Direct effects of endotoxin on the endothelium: barrier function and injury. Lab Invest 1999; 79: 1181–1199.
6. Bastard JP, Maachi M, Lagathu C et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw 2006; 17: 4–12.
7. Bednář B. Úvod do patologie. Praha: Avicenum 1982.
8. Bláha F. O patogenezi aterosklerózy. Čas Lék Čes 1958; 97: 85–89.
9. Cinti S, Mitchell G, Barbatelli G et al. Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 2005; 46: 2347–2355.
10. de Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS Lett 2008; 582: 97–105.
11. Donath MY, Schumann DM, Faulenbach M et al. Islet inflammation in type 2 diabetes: from metabolic stress to therapy. Diabetes Care 2008; 31 (Suppl 2): S161–S164.
12. Ebstein W. Therapie des Diabetes mellitus, insbesondere über die Anwendung des salicylsauren Natron bei demselben. Berl Klin Wochenschr 1897; 13: 337–340.
13. Ehses JA, Böni-Schnetzler M, Faulenbach M et al. Macrophages, cytokines and beta‑cell death in Type 2 diabetes. Biochem Soc Trans 2008; 36: 340–342.
14. Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis: emerging mechanistic paradigms. Circulation 1999; 100: e20–e28.
15. Farmer SR. Transcriptional control of adipocyte formation. Cell Metab 2006; 4: 263–273.
16. Fleischman A, Shoelson SE, Bernier R et al. Salsalate improves glycaemia and inflammatory parameters in obese young adults. Diabetes care 2008; 31: 289–294.
17. Festa A, Hanley AJ, Tracy RP et al. Inflammation in the prediabetic state is related to increased insulin resistance rather than decreased insulin secretion. Circulation 2003; 108: 1822–1830.
18. Gregor MF, Hotamisligil GS. Thematic review series: Adipocyte Biology. Adipocyte stress: the endoplasmic reticulum and metabolic disease. J Lipid Res 2007; 48: 1905–1914.
19. Haque WA, Shimomura I, Matsuzawa Y et al. Serum adiponectin and leptin levels in patients with lipodystrophies. J Clin Endocrinol Metab 2002; 87: 2395.
20. Heilbronn LK, Campbell LV. Adipose tissue macrophages, low grade inflammation and insulin resistance in human obesity. Curr Pharm Des 2008; 14: 1225–1230.
21. Heilbronn L, Smith SR, Ravussin E. Failure of fat cell proliferation, mitochondrial function and fat oxidation results in ectopic fat storage, insulin resistance and type II diabetes mellitus. Int J Obes Relat Metab Disord 2004; 28 (Suppl 4): S12–S21.
22. Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006; 444: 860–867.
23. Hotta K, Funahashi T, Arita Y et al. Plasma concentrations of a novel, adipose‑specific protein, adiponectin, in type 2 diabetic patients. Arterioscler Thromb Vasc Biol 2000; 20: 1595–1599.
24. Hung CF, Huang TF, Chen BH et al. Lycopene inhibits TNF‑alpha‑induced endothelial ICAM‑1 expression and monocyte-endothelial adhesion. Eur J Pharmacol 2008; 586: 275–282.
25. Hsieh PS, Chan JY, Shyu JF et al. Mild portal endotoxaemia induces subacute hepatic inflammation and pancreatic beta‑cell dysfunction in rats. Eur J Clin Invest 2008; 38: 640–648.
26. Irie F, Fitzpatrick AL, Lopez OL et al. Enhanced risk for Alzheimer disease in persons with type 2 diabetes and APOE epsilon4: the Cardiovascular Health Study Cognition Study. Arch Neurol 2008; 65: 89–93.
27. Kol A, Sukhova GK, Lichtman AH et al. Chlamydial heat shock protein 60 localizes in human atheroma and regulates macrophage tumor necrosis factor‑alpha and matrix metalloproteinase expression. Circulation 1998; 98: 300–307.
28. Koska J, Ortega E, Bunt JC et al. The effect of salsalate on insulin action and glucose tolerance in obese non‑diabetic patients: result of a randomised double-blind placebo-controlled study. Diabetologia 2009; 52: 385–393.
29. Kraml PJ, Roubalová K, Bulvas M. Markers of Chlamydia pneumoniae and human cytomegalovirus infection in patients with chronic peripheral vascular disease and their relation to inflammation, endothelial dysfunction and changes in lipid metabolism. Folia Microbiol (Praha) 2008; 53: 551–557.
30. Lee CC, Adler AI, Sandhu MS et al. Association of C – reactive protein with type 2 diabetes: prospective analysis and meta‑analysis. Diabetologia 2009; 52: 1040–1047.
31. Lee JY, Hwang DH. The modulation of inflammatory gene expression by lipids: mediation through Toll‑like receptors. Mol Cells 2006; 21: 174–185.
32. Levine JA, Jensen MD, Eberhardt NL et al. Adipocyte macrophage colony-stimulating factor is a mediator of adipose tissue growth. J Clin Invest 1998; 101: 1557–1564.
33. Maixner E. Patologie a terapie vnitřních nemocí, část prvá Nemoci srdce a cévstva. Praha: Bursík a Kohout 1912.
34. Matsuura E, Kobayashi K, Lopez LR. Atherosclerosis in autoimmune disease. Curr Rheumatol Rep 2009; 11: 61–69.
35. Osborn O, Brownell SE, Sanchez-Alavez M et al. Treatment with an Interleukin 1 beta antibody improves glycemic control in diet‑induced obesity. Cytokine 2008; 44: 141–148.
36. Ozcan U, Cao Q, Yilmaz E et al. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science 2004; 306: 457–461.
37. Pfützner A, Weber MM, Forst T. A biomarker concept for assessment of insulin resistance, beta‑cell function and chronic systemic inflammation in type 2 diabetes mellitus. Clin Lab 2008; 54: 485–490.
38. Pickup JC, Crook MA. Is type II diabetes mellitus a disease of the innate immune system? Diabetologia 1998; 41: 1241–1248.
39. Pittenger MF, Mackay AM, Beck SC et al. Multilineage potential of adult human mesenchymal stem cells. Science 1999; 284: 143–147.
40. Plomgaard P, Bouzakri K, Krogh-Madsen R et al. Tumor necrosis factor‑alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation. Diabetes 2005; 54: 2939–2945.
41. Poitou C, Viguerie N, Cancello R et al. Serum amyloid A: production by human white adipocyte and regulation by obesity and nutrition. Diabetologia 2005; 48: 519–528.
42. Prince RL, Larkins RG, Alford FP. The effect of acetylsalicylic acid on plasma glucose and the response of glucose regulatory hormones to intravenous glucose and arginine in insulin treated diabetics and normal subjects. Metabolism 1981; 30: 293–298.
43. Randle PJ, Garland PB, Hales CN et al. The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1963; 13: 785–789.
44. Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 1988; 37: 1595–1607.
45. Reid J, Macdougall AI, Andrews MM. Aspirin and diabetes mellitus. Br Med J 1957; 2: 1071–1074.
46. Robertson RP, Harmon J, Tran PO et al. Beta‑cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes. Diabetes 2004; 53 (Suppl 1): S119–S124.
47. Rosen ED, MacDougald OA. Adipocyte differentiation from the inside out. Nat Rev Mol Cell Biol 2006; 7: 885–896.
48. Saran AM, DuBose TD Jr. Cardiovascular disease in chronic kidney disease. Ther Adv Cardiovasc Dis 2008; 2: 425–434.
49. Schrauwen P, Hesselink MK. Oxidative capacity, lipotoxicity, and mitochondrial damage in type 2 diabetes. Diabetes 2004; 53: 1412–1417.
50. Simons PJ, van den Pangaart PS, Aerts JM et al. Pro‑inflammatory delipidizing cytokines reduce adiponectin secretion from human adipocytes without affecting adiponectin oligomerization. J Endokrinol 2007; 192: 289–299.
51. Skurk T, Herder C, Kräft I et al. Production and release of macrophage migration inhibitory factor from human adipocytes. Endocrinology 2005; 146: 1006–1011.
52. Thomayer J. Pathologie a a terapie nemocí vnitřních. 3. vydání. Praha: Bursík a Kohout 1909.
53. Toso C, Emamaullee JA, Merani S et al. The role of macrophage migration inhibitory factor on glucose metabolism and diabetes. Diabetologia 2008; 51: 1937–1946.
54. van Harmelen V, Skurk T, Röhrig K et al. Effect of BMI and age on adipose tissue cellularity and differentiation capacity in women. Int J Obes Relat Metab Disord 2003; 27: 889–895.
55. Vozarova B, Weyer C, Lindsay RS et al. High white blood cell count is associates with a worsening of insulin sensitivity and predicts the development of type 2 diabetes. Diabetes 2002; 51: 455–461.
56. Wajchenberg BL. Beta‑cell failure in diabetes and preservation by clinical treatment. Endocr Rev 2007; 28: 187–218.
57. Wang P, Mariman E, Renes J et al. The secretory function of adipocytes in the physiology of white adipose tissue. J Cell Physiol 2008; 216: 3–13.
58. Weisberg SP, McCann D, Desai M et al. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest 2003; 112: 1796–1808.
59. Williamson RT. On the treatment of glycosuria and diabetes mellitus with sodium salicylate. Br Med J 1901; 1: 760–762.
60. Wititsuwannakul D, Kim KH. Mechanism of palmityl coenzyme A inhibition of liver glycogen synthase. J Biol Chem 1977; 252: 7812–7817.
61. Xu WL, von Strauss EW, Qiu CX et al. Uncontrolled diabetes increases the risk of Alzheimer disease: a population‑based cohort study. Diabetologia 2009; 52: 1031–1039.
62. Zhu J, Quyyumi AA, Norman JE et al. Effects of total pathogen burden on coronary artery disease risk and C‑reactive protein levels. Am J Cardiol 2000; 85: 140–146.
Labels
Diabetology Endocrinology Internal medicineArticle was published in
Internal Medicine
2009 Issue 7-8
Most read in this issue
- Metabolic syndrome and the liver (NAFLD/NASH)
- Anxious-depressive disorders and metabolic syndrome
- Chronic mild inflammation links obesity, metabolic syndrome, atherosclorosis and diabetes
- Laboratory markers of metabolic syndrome in clinical practice