NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X
- PMID: 9389420
- DOI: 10.1007/s001250050822
NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X
Abstract
Non-insulin-dependent diabetes mellitus (NIDDM) is commonly associated with hypertriglyceridaemia, low serum HDL-cholesterol concentrations, hypertension, obesity and accelerated atherosclerosis (metabolic syndrome X). Since a similar dyslipidaemia occurs with the acute-phase response, we investigated whether elevated acute-phase/stress reactants (the innate immune system's response to environmental stress) and their major cytokine mediator (interleukin-6, IL-6) are associated with NIDDM and syndrome X, and may thus provide a unifying pathophysiological mechanism for these conditions. Two groups of Caucasian subjects with NIDDM were studied. Those with any 4 or 5 features of syndrome X (n = 19) were compared with a group with 0 or 1 feature of syndrome X (n = 25) but similar age, sex distribution, diabetes duration, glycaemic control and diabetes treatment. Healthy non-diabetic subjects of comparable age and sex acted as controls. Overnight urinary albumin excretion rate, a risk factor for cardiovascular disease, was also assayed in subjects to assess its relationship to the acute-phase response. Serum sialic acid was confirmed as a marker of the acute-phase response since serum concentrations were significantly related to established acute-phase proteins such as alpha-1 acid glycoprotein (r = 0.82, p < 0.0001). There was a significant graded increase of serum sialic acid, alpha-1 acid glycoprotein, IL-6 and urinary albumin excretion rate amongst the three groups, with the lowest levels in non-diabetic subjects, intermediate levels in NIDDM patients without syndrome X and highest levels in NIDDM patients with syndrome X. C-reactive protein and cortisol levels were also higher in syndrome X-positive compared to X-negative patients and serum amyloid A was higher in both diabetic groups than in the control group. We conclude that NIDDM is associated with an elevated acute-phase response, particularly in those with features of syndrome X. Abnormalities of the innate immune system may be a contributor to the hypertriglyceridaemia, low HDL cholesterol, hypertension, glucose intolerance, insulin resistance and accelerated atherosclerosis of NIDDM. Microalbuminuria may be a component of the acute-phase response.
Comment in
-
Innate immunity, insulin resistance and type 2 diabetes.Diabetologia. 2012 Feb;55(2):273-8. doi: 10.1007/s00125-011-2387-y. Epub 2011 Nov 30. Diabetologia. 2012. PMID: 22124608
Similar articles
-
Ethnic differences in correlates of microalbuminuria in NIDDM. The role of the acute-phase response.Diabetes Care. 1998 Mar;21(3):385-8. doi: 10.2337/diacare.21.3.385. Diabetes Care. 1998. PMID: 9540020
-
The innate immune response and type 2 diabetes: evidence that leptin is associated with a stress-related (acute-phase) reaction.Clin Endocrinol (Oxf). 2000 Jan;52(1):107-12. doi: 10.1046/j.1365-2265.2000.00921.x. Clin Endocrinol (Oxf). 2000. PMID: 10651761
-
Serum amyloid A protein in patients with non-insulin-dependent diabetes mellitus.Clin Biochem. 1994 Dec;27(6):469-73. doi: 10.1016/0009-9120(94)00044-v. Clin Biochem. 1994. PMID: 7535207
-
Is type II diabetes mellitus a disease of the innate immune system?Diabetologia. 1998 Oct;41(10):1241-8. doi: 10.1007/s001250051058. Diabetologia. 1998. PMID: 9794114 Review.
-
The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X.Brain Behav Immun. 2003 Oct;17(5):350-64. doi: 10.1016/s0889-1591(03)00048-5. Brain Behav Immun. 2003. PMID: 12946657 Review.
Cited by
-
Short-term high-fat feeding induces islet macrophage infiltration and β-cell replication independently of insulin resistance in mice.Am J Physiol Endocrinol Metab. 2016 Oct 1;311(4):E763-E771. doi: 10.1152/ajpendo.00092.2016. Epub 2016 Aug 30. Am J Physiol Endocrinol Metab. 2016. PMID: 27577853 Free PMC article.
-
Insights into the Immunopathophysiology of Severe COVID-19 in Metabolic Disorders.Ann Natl Acad Med Sci. 2020 Apr;56(2):112-115. doi: 10.1055/s-0040-1713346. Ann Natl Acad Med Sci. 2020. PMID: 33082620 Free PMC article.
-
Diabetes is a proinflammatory state: a translational perspective.Expert Rev Endocrinol Metab. 2010 Jan 1;5(1):19-28. doi: 10.1586/eem.09.44. Expert Rev Endocrinol Metab. 2010. PMID: 20204165 Free PMC article.
-
Type 2 diabetes mellitus is associated with impaired cytokine response and adhesion molecule expression in human endotoxemia.Intensive Care Med. 2010 Sep;36(9):1548-55. doi: 10.1007/s00134-010-1845-1. Epub 2010 Mar 13. Intensive Care Med. 2010. PMID: 20229041 Clinical Trial.
-
Diabetic periodontitis: a model for activated innate immunity and impaired resolution of inflammation.Periodontol 2000. 2007;43:233-44. doi: 10.1111/j.1600-0757.2006.00168.x. Periodontol 2000. 2007. PMID: 17214841 Free PMC article. Review. No abstract available.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials